MEpedia - User contributions [en]

Positron emission tomography

2019-02-27T04:42:28Z

Paulitasofia1:created the page

Positron emission tomography, commonly referred to as PET, is a method of biomedical imaging. It uses nuclear functional imaging techniques to observe metabolic processes in the body. In clinical settings, it is predominantly used in oncology for tumor metastasis imaging, neurology, and cardiology.<ref>{{Cite web|url=https://www.sciencedirect.com/science/article/pii/S0001299800800355|title=ScienceDirect|website=www.sciencedirect.com|access-date=2019-02-27}}</ref>
[[File:PET scanner.jpg|left|thumb|PET scanner]]

== How it works ==
PET uses radioactive tracers (also called radiotracer or radioligand), which are chemical compounds that are biologically active, meaning that the compound functions/reacts/ has a biological purpose in the body. These compounds have been altered such that their structure includes a positron-emitting radioisotope (a radioactive atom). This means that the radiotracer’s movement and activity throughout the body can be detected with a PET machine. Many biological compounds have been made into a radiotracer, which allows for observation of how that compound acts throughout a region of the body.
[[File:FDG.png|left|thumb|400x400px|A normal glucose molecule (left) and an 18-F labeled FDG molecule (right) used for PET scans.<ref>{{Cite web|url=https://maxfacts.uk/diagnosis/tests/pet-scans|title=PET scans|website=maxfacts.uk|access-date=2019-02-27}}</ref>]]

=== FDG ===
For example, fludeoxyglucose (FDG), an analogue of glucose, is a commonly used measure of metabolism; detection of FDG correlates with regional glucose uptake. Glucose metabolism is an important measure because cancer cells increase their metabolism to support their increased rates of proliferation and distribution throughout the body. Increased metabolic activity is usually accomplished through increased glucose-uptake. Because cancerous tumors have higher levels of metabolic activity, tumors can usually be detected with FDG-PET. In fact, around 90% of clinical PET imaging uses FDG to monitor cancer metastasis.<ref>{{Cite web|url=https://www.ncbi.nlm.nih.gov/pubmed/20473153|title=Glucose metabolism in cancer cells. - PubMed - NCBI|last=C|first=Annibaldi A and Widmann|website=www.ncbi.nlm.nih.gov|language=en|access-date=2019-02-27}}</ref>

== The procedure ==
A small amount of radiotracer is introduced into the subject’s body via injection, and the subject then enters the PET machine. As the radiotracer breaks down, it emits gamma rays which are picked up by the machine, and then translated into a 3-dimensional image of radiotracer concentration throughout the body. The resulting image can be thought of as a heat map, showing areas of high concentration as more brightly lit.
[[File:Fdg lung.jpg|thumb|500x500px|FDG-PET image portraying a cancerous tumor in the lung.<ref>{{Cite web|url=https://www.sciencedirect.com/science/article/pii/S0001299800800355|title=ScienceDirect|website=www.sciencedirect.com|access-date=2019-02-27}}</ref>]]
[[File:Positron emission tomography.png|left|thumb|600x600px|Principle of positron emission tomography (PET).<ref>{{Cite web|url=https://www.sciencedirect.com/science/article/pii/S0001299800800355|title=ScienceDirect|website=www.sciencedirect.com|access-date=2019-02-27}}</ref>]]

== Clinical reasons for getting a PET scan: ==
* Generally, to evaluate the function of organs such as the heart and brain
** I.e., measuring perfusion of the heart muscle
* To diagnose neurological conditions such as Alzheimer’s, Huntington’s, Parkinson’s, epilepsy, and stroke
* To detect the spread of cancer
* To evaluate cancer treatment efficacy
* To locate the specific site for surgery prior to the surgical procedure
* To evaluate the brain after trauma<ref>{{Cite web|url=https://www.hopkinsmedicine.org/healthlibrary/test_procedures/neurological/positron_emission_tomography_pet_92,p07654|title=How Does a PET Scan Work?|website=www.hopkinsmedicine.org|language=en|access-date=2019-02-27}}</ref>

== Risks ==
The risks for the amount of radiotracer injected into the body is small enough that there is usually no need to take precautions against radioactive exposure. If you are pregnant or breastfeeding, you should notify the doctor/researcher to protect against injury to the fetus or contaminating breastmilk.<ref>{{Cite web|url=https://www.hopkinsmedicine.org/healthlibrary/test_procedures/neurological/positron_emission_tomography_pet_92,p07654|title=How Does a PET Scan Work?|website=www.hopkinsmedicine.org|language=en|access-date=2019-02-27}}</ref>

== PET research in ME ==
[[File:PBR28 Alzheimers.jpg|thumb|PET image depicting neuroinflammation in Alzheimer’s disease (left) versus healthy controls (right) using PBR28, a second-generation TSPO-binding radioligand.<ref>{{Cite web|url=https://www.sciencedirect.com/science/article/pii/S0001299800800355|title=ScienceDirect|website=www.sciencedirect.com|access-date=2019-02-27}}</ref>]]
PET research in ME has focused on measures of neuroinflammation. This has been done using a TSPO-binding radioligand to measure microglial activation. TSPO (translocator protein) is a protein that is produced when microglia, the resident macrophages of the brain, become activated. Microglial activation is a commonly used measure of neuroinflammation. Further research using high-quality PET/TSPO methodology is needed to better understand the pathophysiology of neuroinflammation in ME.<ref>{{Cite journal|last=Lara Mejia|first=Paula S.|last2=Brumfield|first2=Sydney A.|last3=VanElzakker|first3=Michael B.|date=2019|title=Neuroinflammation and Cytokines in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): A Critical Review of Research Methods|url=https://www.frontiersin.org/articles/10.3389/fneur.2018.01033/full#B8|journal=Frontiers in Neurology|language=English|volume=9|doi=10.3389/fneur.2018.01033|issn=1664-2295}}</ref>

=== Nakatomi et al. 2014 ===
Nakatomi et al. 2014 was the first case-control study using PET to measure neuroinflammation through TSPO expression in ME. They used PK11195, a first generation TSPO-binding radioligand. They found increased PK11195 in cingulate cortex, hippocampus, amygdala, thalamus, midbrain, and pons. PK11195 concentrations in certain regions were found to have positive correlations with cognitive impairment scores (related to brain fog), pain scores, and depression scores. The study concludes that neuroinflammation seems to be present in ME patients and is associated with neuropsychological symptoms.<ref>{{Cite journal|last=Watanabe|first=Yasuyoshi|last2=Kuratsune|first2=Hirohiko|last3=Inaba|first3=Masaaki|last4=Yamaguti|first4=Kouzi|last5=Shiomi|first5=Susumu|last6=Kataoka|first6=Yosky|last7=Takahashi|first7=Kazuhiro|last8=Kawabe|first8=Joji|last9=Fukuda|first9=Sanae|date=2014-06-01|title=Neuroinflammation in Patients with Chronic Fatigue Syndrome/Myalgic Encephalomyelitis: An 11C-(R)-PK11195 PET Study|url=http://jnm.snmjournals.org/content/55/6/945|journal=Journal of Nuclear Medicine|language=en|volume=55|issue=6|pages=945–950|doi=10.2967/jnumed.113.131045|issn=0161-5505|pmid=24665088}}</ref>
[[File:PK11195.gif|left|thumb|400x400px|Statistical parametric maps showing areas of significant contrast of PK11195 in ME/CFS versus healthy controls.<ref>{{Cite web|url=https://www.sciencedirect.com/science/article/pii/S0001299800800355|title=ScienceDirect|website=www.sciencedirect.com|access-date=2019-02-27}}</ref>]]

== Learn more: ==
[https://www.nimh.nih.gov/research-priorities/therapeutics/cns-radiotracer-table.shtml List of PET radiotracers used in research]

== References ==
<references />

File:PK11195.gif

2019-02-27T04:27:37Z

Paulitasofia1:

PK11195 Nakatomi et al

File:Pbr28.gif

2019-02-27T04:19:10Z

Paulitasofia1:

Pbr28

Varicella zoster virus

2018-12-14T03:44:43Z

Paulitasofia1:adding to page

'''Varicella zoster virus (VZV)''' is one of eight herpesviruses (HHV 3) and is known to only infect humans. It causes varicella (chickenpox) upon initial infection, and can reactivate to cause herpes zoster (shingles). After initial infection, VZV establishes a latent infection in the body.

== Initial infection ==
Varicella, or more commonly referred to as chickenpox, usually lasts 5-7 days. Typical signs and symptoms include:
* A rash that turns into itchy, fluid-filled blisters (turn into scabs after a week)
* Fever
* Tiredness
* Loss of appetite
* Headache
People who have been vaccinated against varicella can still get the disease, but it is usually a milder form. Complications can occur, but are not common in healthy, vaccinated people who get the disease. People who are at risk for complications include infants, adolescents, adults, pregnant women, and people with weakened immune systems. Complications include:
* Bacterial infections of the skin and soft tissues
* Pneumonia
* infection/inflammation of the brain
* Bleeding problems
* Sepsis
* Dehydration <ref name=":0">{{Cite web|url=https://www.cdc.gov/chickenpox/about/symptoms.html|title=Chickenpox {{!}} Signs and Symptoms {{!}} Varicella {{!}} CDC|website=www.cdc.gov|access-date=2018-12-14}}</ref>

== Age of infection ==
Similar to [[Epstein-Barr virus]], the age of initial infection affects the severity of the infection. In childhood (except for in infants), varicella is usually significantly less severe than in adolescence and adulthood. As a result, adolescents and adults are at risk for complications. Reactivation (zoster/shingles) also continues this pattern; older adults are more likely to have complications, with longer lasting and more severe pain.<ref name=":0" />

==Reactivation: Zoster/Shingles ==
About 1 in 3 people in the U.S. will develop zoster/shingles in their lifetime. Anybody who has had varicella/chickenpox may develop zoster (including children). People who have weakened immune systems or use immunosuppressive drugs (e.g., steroids) are at higher risk to develop zoster. Most people only have one episode of zoster, but multiple reactivations may occur. Zoster causes a painful rash on one side of the face or body. The rash consists of blisters that are accompanied by pain, itching, or tingling. Other symptoms can include fever, headache, chills, and an upset stomach.<ref name=":0" />

== Transmission of VZV ==
VZV is a highly contagious virus that spreads through touching or breathing in the virus particles that come from the chickenpox blisters. VZV can also be spread from people with zoster/shingles via the same methods of transmission, resulting in varicella/chickenpox. For most people, getting varicella/chickenpox once provides immunity for life, meaning they will not get chickenpox twice.

The best method of prevention is the chickenpox vaccine.<ref name=":0" />

== Latency and reactivation ==
After initial infection, VZV establishes a latent infection in the trigeminal nerve and dorsal root ganglia, most predominantly in 87% of the nuclei of neurons of the trigeminal ganglia, as VZV is neurotropic (preferentially targets neural tissue). VZV infects less than 0.1% of non-neuronal cells. It is present in the ganglia of more than 90% of adults.<ref name=":1">{{Cite journal|last=Kennedy|first=Peter G. E.|last2=Gilden|first2=Donald H.|last3=Cohrs|first3=Randall J.|last4=Bloom|first4=David C.|last5=Mitchell|first5=Bradley M.|date=2003-03-01|title=Herpes simplex virus-1 and varicella-zoster virus latency in ganglia|url=https://link.springer.com/article/10.1080/13550280390194000|journal=Journal of NeuroVirology|language=en|volume=9|issue=2|pages=194–204|doi=10.1080/13550280390194000|issn=1538-2443}}</ref>

Virus gene transcription during latency is epigenetically regulated by at least 6 genes. The expression of gene 63 is the indicator of VZV latency.<ref>{{Cite journal|last=Cohrs|first=Randall J.|last2=Kennedy|first2=Peter GE|date=2010-11-01|title=Varicella-zoster virus human ganglionic latency: a current summary|url=https://link.springer.com/article/10.1007/BF03210846|journal=Journal of NeuroVirology|language=en|volume=16|issue=6|pages=411–418|doi=10.1007/BF03210846|issn=1538-2443}}</ref> Thus, reactivation can occur either spontaneously or following a triggering factor.<ref name=":1" />

The latency burden of VZV seems to correlate with the severity of the primary illness.<ref>{{Cite journal|last=Levin|first=Myron J.|last2=Smith|first2=Jeffrey G.|last3=Kaufhold|first3=Robin M.|last4=Barber|first4=Debra|last5=Hayward|first5=Anthony R.|last6=Chan|first6=Christina Y.|last7=Chan|first7=Ivan S. F.|last8=Li|first8=David J. J.|last9=Wang|first9=William|date=2003-11-01|title=Decline in varicella-zoster virus (VZV)-specific cell-mediated immunity with increasing age and boosting with a high-dose VZV vaccine|url=https://www.ncbi.nlm.nih.gov/pubmed/14593591|journal=The Journal of Infectious Diseases|volume=188|issue=9|pages=1336–1344|doi=10.1086/379048|issn=0022-1899|pmid=14593591}}</ref>

== Complications ==
Neurological complications may follow reactivation (zoster/shingles), especially in immunocompromised individuals. These complications include:
* Encephalitis
* Segmental motor weakness
* Myelitis
* Asteritis
* postherpetic neuralgia
* Vasculopathy
* Viral infection of cerebral arteries
* Vision loss
* Hearing problems <ref>{{Cite journal|last=Kennedy|first=Peter G. E.|last2=Gilden|first2=Donald H.|last3=Cohrs|first3=Randall J.|last4=Bloom|first4=David C.|last5=Mitchell|first5=Bradley M.|date=2003-03-01|title=Herpes simplex virus-1 and varicella-zoster virus latency in ganglia|url=https://link.springer.com/article/10.1080/13550280390194000|journal=Journal of NeuroVirology|language=en|volume=9|issue=2|pages=194–204|doi=10.1080/13550280390194000|issn=1538-2443}}</ref>

== Treatment ==
Antiviral treatment can be curative, even after weeks to months of chronic VZV infection.<ref>{{Cite journal|last=Kennedy|first=Peter G. E.|last2=Gilden|first2=Donald H.|last3=Cohrs|first3=Randall J.|last4=Bloom|first4=David C.|last5=Mitchell|first5=Bradley M.|date=2003-03-01|title=Herpes simplex virus-1 and varicella-zoster virus latency in ganglia|url=https://link.springer.com/article/10.1080/13550280390194000|journal=Journal of NeuroVirology|language=en|volume=9|issue=2|pages=194–204|doi=10.1080/13550280390194000|issn=1538-2443}}</ref>

== VZV in ME/CFS ==
Other herpesviruses have been linked to ME.<ref>{{Cite book|url=https://www.ncbi.nlm.nih.gov/books/NBK284894/|title=Review of the Evidence on Other ME/CFS Symptoms and Manifestations|last=Medicine|first=Institute of|last2=Populations|first2=Board on the Health of Select|last3=Syndrome|first3=Committee on the Diagnostic Criteria for Myalgic Encephalomyelitis/Chronic Fatigue|date=2015-02-10|publisher=National Academies Press (US)|language=en}}</ref>

One medical hypothesis states that for some patients, CFS is a result of infection by a neurotropic virus, particularly VZV. Shapiro argues that virtually all CFS symptoms could be produced by infection of the peripheral ganglia. He further argues that the chronic course of CFS could be explained by how infections of the peripheral ganglia can cause long-term nerve dysfunction.<ref>{{Cite journal|date=2009-11-01|title=Does varicella-zoster virus infection of the peripheral ganglia cause Chronic Fatigue Syndrome?|url=https://www.sciencedirect.com/science/article/pii/S0306987709003065|journal=Medical Hypotheses|language=en|volume=73|issue=5|pages=728–734|doi=10.1016/j.mehy.2009.04.043|issn=0306-9877}}</ref>

=== Studies ===
A population cohort study followed a group of VZV-infected and non-infected individuals, and found that the incidence of CFS was higher among the VZV-infected cohort. The authors report that the VZV-infected patients that used antiviral treatment had a 15% reduced risk of CFS compared to patients without antiviral treatment. Overall they concluded that VZV infection may be associated with the risk of CFS, even without a comorbidity.<ref>{{Cite journal|last=Kao|first=C.-H.|last2=Kuo|first2=C.-N.|last3=Shen|first3=W.-C.|last4=Lin|first4=W.-M.|last5=Chen|first5=C.-S.|last6=Chen|first6=H.-J.|last7=Yang|first7=T.-Y.|last8=Tsai|first8=S.-Y.|date=2014-09-01|title=Increased risk of chronic fatigue syndrome following herpes zoster: a population-based study|url=https://link.springer.com/article/10.1007/s10096-014-2095-x|journal=European Journal of Clinical Microbiology & Infectious Diseases|language=en|volume=33|issue=9|pages=1653–1659|doi=10.1007/s10096-014-2095-x|issn=1435-4373}}</ref>

==Lyme Disease==
Several herpesviruses including [[varicella-zoster virus]]<ref name="Feder" /><ref name="Woelfle" /> may cause false positives on [[Lyme Disease]] tests.

==Prevalence==
*2001, In a Belgian study, 26.8% of patients meeting the [[Fukuda criteria]] and 30.7% of patients meeting the [[Holmes criteria]], in a cohort of 2073 [[CFS]] patients, reported cold sores and /or shingles.<ref name="symptoms2001" />

==Learn more==
*[https://en.wikipedia.org/wiki/Varicella_zoster_virus Wikipedia - Varicella zoster virus]

==See also==
*[[Herpesvirus]]

== References ==
<references>
<ref name="Feder">Feder HM Jr, Gerber MA, Luger SW, Ryan RW. False-positive serologic tests for Lyme disease after varicella infection. N Engl J Med 1991;325:1886-7</ref>
<ref name="Woelfle">Woelfle J, Wilske B, Haverkamp F, Bialek R. False-positive serological tests for Lyme disease in facial palsy and varicella zoster meningo-encephalitis. Eur J Pediatr 1998;157:953-4.</ref>
<ref name="symptoms2001">{{citation
| last1 = De Becker | first1 = P | authorlink1 = Pascale De Becker
| last2 = McGregor | first2 = N | authorlink2 = Neil McGregor
| last3 = De Meirleir | first3 = K | authorlink3 = Kenny de Meirleir
| title = A definition-based analysis of symptoms in a large cohort of patients with chronic fatigue syndrome.
| journal = Journal of Internal Medicine | volume = 250 | issue = 3 | page = 234-240
| date = Sep 2001
| pmid = 11555128
| url = http://www.ncbi.nlm.nih.gov/pubmed/11555128
}}</ref>
</references>
[[Category:Infectious agents]]
[[Category:Triggers and risk factors]]
[[Category:Virology]]

Varicella zoster virus

2018-12-14T03:13:42Z

Paulitasofia1:adding to page

Sarcoidosis

2018-12-14T02:48:10Z

Paulitasofia1:created sarcoidosis page

'''Sarcoidosis''' is a systemic disease which is characterized by the accumulation of immune cells (activated T cells and macrophages) in various organs throughout the body, forming lumps called granulomas. Granulomas are most commonly found in the lungs and lymphatic system. The formation of granulomas is thought to be triggered by ongoing inflammation. Although the exact cause of sarcoidosis is unknown, many studies suggest that it is due to an exaggerated immune response.<ref>{{Cite web|url=https://www.nhlbi.nih.gov/health-topics/sarcoidosis|title=Sarcoidosis {{!}} National Heart, Lung, and Blood Institute (NHLBI)|website=www.nhlbi.nih.gov|access-date=2018-12-14}}</ref><ref>{{Cite journal|last=Nambiar|first=Anoop M.|last2=Peters|first2=Jay I.|last3=Soto-Gomez|first3=Natalia|date=2016-05-15|title=Diagnosis and Management of Sarcoidosis|url=https://www.aafp.org/afp/2016/0515/p840.html|journal=American Family Physician|language=en|volume=93|issue=10|pages=840–848|issn=1532-0650}}</ref>

== Clinical presentation ==
Early detection of sarcoidosis continues to be a challenge, because the signs and symptoms of sarcoidosis vary depending on the location of the granulomas. Many people show no signs or symptoms. General signs and symptoms include:
* Fatigue
* Fever
* Malaise
* Pain and swelling in the joints
* Weight loss
People with sarcoidosis in the lungs may present with wheezing, unexplained cough, chest pain, or shortness of breath. If the granulomas affect other parts of the body, the clinical presentation will likely be related to those organs.
[[File:Sarcoidosis.jpg|none|thumb|683x683px|The signs and symptoms of sarcoidosis and the organs it affects.<ref>{{Cite web|url=https://www.nhlbi.nih.gov/health-topics/sarcoidosis|title=Sarcoidosis {{!}} National Heart, Lung, and Blood Institute (NHLBI)|website=www.nhlbi.nih.gov|access-date=2018-12-14}}</ref>]]

File:Sarcoidosis.jpg

2018-12-14T02:45:52Z

Paulitasofia1:

The signs and symptoms of sarcoidosis and the organs it affects.

Dysautonomia

2018-12-14T02:22:25Z

Paulitasofia1:linked to other pages

Dysautonomia describes several different medical conditions that involve dysregulation of the autonomic nervous system. People with dysautonomia have problems regulating autonomic functions, including heart rate, blood pressure, body temperature, and digestion. Thus, dysautonomia can present with various symptoms, such as lightheadedness, fainting, unstable blood pressure, and orthostatic intolerance.<ref name=":0">{{Cite web|url=http://www.dysautonomiainternational.org/page.php?ID=34|title=Dysautonomia International:|website=www.dysautonomiainternational.org|access-date=2018-12-12}}</ref>

== Types of dysautonomia ==
More than 70 million people have dysautonomia. There are various types of dysautonomia, each presenting with different underlying mechanisms as well as some overlapping mechanisms. Forms of dysautonomia include:
* '''[[Postural orthostatic tachycardia syndrome|Postural orthostatic tachycardia syndrome (POTS)]]''', a form of orthostatic intolerance that can cause lightheadedness, fainting, tachycardia, chest pains, exercise intolerance, temperature sensitivity, and more.
* '''[[Neurocardiogenic syncope]]''' is the most common form of dysautonomia, with many individuals having a mild case (fainting once or twice in their lifetime). Severe cases can result in fainting several times per day.
* '''[[Multiple system atrophy|Multiple system atrophy (MSA)]]''', a fatal and rare form of dysautonomia, affects 350,000 people worldwide. It is a neurodegenerative disorder occurring in adults over the age of 40. MSA progresses rapidly; patients usually become bedridden within 2 years of diagnosis.
* '''[[Familial dysautonomia]] (FD)''' is a rare genetic disorder in persons of Ashkenazi Jewish descent. It is a very serious condition, consisting of abnormal development, progressive degeneration of the sensory and autonomic nervous systems, and is inevitably fatal. FD is caused by a point mutation in the ''IKBAP'' gene, resulting in the severe reduction of the IKAP protein, which is involved in many intracellular processes.<ref>{{Cite journal|last=Dragatsis|first=Ioannis|last2=Dietrich|first2=Paula|last3=Dragatsis|first3=Ioannis|last4=Dietrich|first4=Paula|date=2016-12|title=Familial Dysautonomia: Mechanisms and Models|url=http://www.scielo.br/scielo.php?script=sci_abstract&pid=S1415-47572016000400497&lng=en&nrm=iso&tlng=en|journal=Genetics and Molecular Biology|volume=39|issue=4|pages=497–514|doi=10.1590/1678-4685-gmb-2015-0335|issn=1415-4757}}</ref>
* '''[[Autonomic dysreflexia]] (AD)''' is a form of dysautonomia associated with spinal cord injuries, affecting the communication of the autonomic nervous system.
* '''[[Baroreflex failure]]'''; the baroreflex is the body’s homeostatic mechanism for maintaining blood pressure. If the baroreceptor or its system fails, patients experience inappropriate blood pressure.
* '''[[Cerebral salt wasting syndrome]]''' is a condition in response to physical injury or the presence of tumors in the brain, presenting as hyponatremia (excessive sodium secretion from the kidney) and dehydration.
* '''[[Diabetic autonomic neuropathy]]''' is a very common form of dysautonomia, affecting 69 million people worldwide (20% of diabetics). It is a serious complication of diabetes, associated with an increased risk of cardiovascular mortality.
* '''Panayiotopoulos syndrome''', also known as autonomic epilepsy is a childhood-specific seizure disorder consisting of seizures with predominantly autonomic symptoms (without convulsing).<ref>{{Cite journal|last=Covanis|first=Athanasios|date=2006-10-01|title=Panayiotopoulos Syndrome: A Benign Childhood Autonomic Epilepsy Frequently Imitating Encephalitis, Syncope, Migraine, Sleep Disorder, or Gastroenteritis|url=http://pediatrics.aappublications.org/content/118/4/e1237|journal=Pediatrics|language=en|volume=118|issue=4|pages=e1237–e1243|doi=10.1542/peds.2006-0623|issn=1098-4275|pmid=16950946}}</ref>
* '''Reflex sympathetic dystrophy''' is a an extremely painful neurological condition that is sometimes considered a form of dysautonomia.
Dysautonomia can occur independently or secondary to other medical conditions, such as diabetes, [[Multiple sclerosis|MS]], rheumatoid arthritis, and [[Systemic lupus erythematosus|lupus]].<ref name=":0" />

== Comorbidities/causes of dysautonomia ==
Comorbidities and causes of dysautonomia include:<ref name=":0" />
* [[Amyloidosis]]
** A group of rare disorders caused by the accumulation of amyloid protein in various tissues throughout the body. If the amyloid accumulation occurs in the heart or on peripheral nerves, it can cause dysautonomia.
* [[Celiac|Celiac disease]]
* [[Charcot-Marie-Tooth disease]]
* [[Chiari malformation]]
* Chronic inflammatory demyelinating polyneuropathy
* [[Inflammatory bowel disease]] (such as Crohn’s and ulcerative colitis)<ref>{{Cite journal|last=Lindgren|first=S.|last2=Lilja|first2=B.|last3=Rosén|first3=I.|last4=Sundkvist|first4=G.|date=1991-4|title=Disturbed autonomic nerve function in patients with Crohn's disease|url=https://www.ncbi.nlm.nih.gov/pubmed/2034989|journal=Scandinavian Journal of Gastroenterology|volume=26|issue=4|pages=361–366|issn=0036-5521|pmid=2034989}}</ref><ref>{{Cite journal|last=Lindgren|first=S.|last2=Stewenius|first2=J.|last3=Sjölund|first3=K.|last4=Lilja|first4=B.|last5=Sundkvist|first5=G.|date=1993-7|title=Autonomic vagal nerve dysfunction in patients with ulcerative colitis|url=https://www.ncbi.nlm.nih.gov/pubmed/8362220|journal=Scandinavian Journal of Gastroenterology|volume=28|issue=7|pages=638–642|issn=0036-5521|pmid=8362220}}</ref>
* [[Deconditioning]]
** The physical change in the way the body functions due to a decrease in activity. The most common cause of deconditioning is bed rest. Due to debilitating symptoms, patients with various chronic illnesses may experience deconditioning, which can exacerbate symptoms. It is important to take steps to prevent and/or reverse deconditioning. <ref>{{Cite journal|last=Dyckman|first=Damian J.|last2=Sauder|first2=Charity L.|last3=Ray|first3=Chester A.|date=2012-01-01|title=Effects of short-term and prolonged bed rest on the vestibulosympathetic reflex|url=https://www.ncbi.nlm.nih.gov/pubmed/22021328|journal=American Journal of Physiology. Heart and Circulatory Physiology|volume=302|issue=1|pages=H368–374|doi=10.1152/ajpheart.00193.2011|issn=1522-1539|pmc=3334249|pmid=22021328}}</ref>
* [[Diabetes]]<ref>{{Cite journal|last=Vinik|first=Aaron I|last2=Erbas|first2=Tomris|last3=Casellini|first3=Carolina M|date=2013-01-29|title=Diabetic cardiac autonomic neuropathy, inflammation and cardiovascular disease|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3580884/|journal=Journal of Diabetes Investigation|volume=4|issue=1|pages=4–18|doi=10.1111/jdi.12042|issn=2040-1116|pmc=3580884|pmid=23550085}}</ref>
* [[Ehlers-Danlos syndrome]]<ref>{{Cite journal|date=1999-10-01|title=Orthostatic intolerance and chronic fatigue syndrome associated with Ehlers-Danlos syndrome|url=https://www.sciencedirect.com/science/article/pii/S0022347699701733|journal=The Journal of Pediatrics|language=en|volume=135|issue=4|pages=494–499|doi=10.1016/S0022-3476(99)70173-3|issn=0022-3476}}</ref>
* [[Mast cell activation syndrome|Mast cell disorders]]
* Mitochondrial diseases<ref>{{Cite journal|last=Kanjwal|first=Khalil|last2=Karabin|first2=Beverly|last3=Kanjwal|first3=Yousuf|last4=Saeed|first4=Bilal|last5=Grubb|first5=Blair P.|date=2010-10|title=Autonomic dysfunction presenting as orthostatic intolerance in patients suffering from mitochondrial cytopathy|url=https://www.ncbi.nlm.nih.gov/pubmed/20960537|journal=Clinical Cardiology|volume=33|issue=10|pages=626–629|doi=10.1002/clc.20805|issn=1932-8737|pmid=20960537}}</ref>
* Paraneoplastic syndrome<ref>{{Cite journal|last=Koike|first=Haruki|last2=Tanaka|first2=Fumiaki|last3=Sobue|first3=Gen|date=2011-10|title=Paraneoplastic neuropathy: wide-ranging clinicopathological manifestations|url=https://www.ncbi.nlm.nih.gov/pubmed/21799410|journal=Current Opinion in Neurology|volume=24|issue=5|pages=504–510|doi=10.1097/WCO.0b013e32834a87b7|issn=1473-6551|pmid=21799410}}</ref>
* Parkinson’s disease<ref>{{Cite journal|last=Goldstein|first=David S|date=2014-4|title=Dysautonomia in Parkinson’s disease: neurocardiological abnormalities|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4222515/|journal=Comprehensive Physiology|volume=4|issue=2|pages=805–826|doi=10.1002/cphy.c130026|issn=2040-4603|pmc=4222515|pmid=24715569}}</ref>
* [[Sarcoidosis]]<ref>{{Cite journal|last=Bakkers|first=M.|last2=Faber|first2=C. G.|last3=Drent|first3=M.|last4=Hermans|first4=M. C. E.|last5=van Nes|first5=S. I.|last6=Lauria|first6=G.|last7=De Baets|first7=M.|last8=Merkies|first8=I. S. J.|date=2010-12|title=Pain and autonomic dysfunction in patients with sarcoidosis and small fibre neuropathy|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2993892/|journal=Journal of Neurology|volume=257|issue=12|pages=2086–2090|doi=10.1007/s00415-010-5664-7|issn=0340-5354|pmc=2993892|pmid=20644950}}</ref>
* [[Sjogren’s syndrome]]<ref>{{Cite journal|last=Ng|first=W.-F.|last2=Stangroom|first2=A. J.|last3=Davidson|first3=A.|last4=Wilton|first4=K.|last5=Mitchell|first5=S.|last6=Newton|first6=J. L.|date=2012-12|title=Primary Sjogrens syndrome is associated with impaired autonomic response to orthostasis and sympathetic failure|url=https://www.ncbi.nlm.nih.gov/pubmed/22976617|journal=QJM: monthly journal of the Association of Physicians|volume=105|issue=12|pages=1191–1199|doi=10.1093/qjmed/hcs172|issn=1460-2393|pmc=3508582|pmid=22976617}}</ref>
* Physical trauma or surgery<ref>{{Cite journal|last=Kanjwal|first=Khalil|last2=Karabin|first2=Beverly|last3=Kanjwal|first3=Yousuf|last4=Grubb|first4=Blair P.|date=2010|title=Autonomic dysfunction presenting as postural tachycardia syndrome following traumatic brain injury|url=https://www.ncbi.nlm.nih.gov/pubmed/20865679|journal=Cardiology Journal|volume=17|issue=5|pages=482–487|issn=1897-5593|pmid=20865679}}</ref><ref>{{Cite journal|last=Billakanty|first=Sreedhar R.|last2=Kligman|first2=Mark D.|last3=Kanjwal|first3=Yousuf M.|last4=Kosinski|first4=Daniel J.|last5=Maly|first5=George T.|last6=Karabin|first6=Beverly|last7=Grubb|first7=Blair P.|date=2008-7|title=New-onset orthostatic intolerance following bariatric surgery|url=https://www.ncbi.nlm.nih.gov/pubmed/18684286|journal=Pacing and clinical electrophysiology: PACE|volume=31|issue=7|pages=884–888|doi=10.1111/j.1540-8159.2008.01103.x|issn=1540-8159|pmid=18684286}}</ref>
* Vitamin deficiencies
* Patients have also reported dysautonomia caused by viral infections

== Treatment ==
There are currently no cures for dysautonomia, as it is an umbrella term that covers many conditions related to the dysfunction of the autonomic system. Therefore, there are treatments that are used to improve quality of life by treating specific symptoms, or treating the underlying disease that is causing the dysautonomia. Further treatments are used to improve quality of life.<ref>{{Cite web|url=http://www.dysautonomiainternational.org/page.php?ID=34|title=Dysautonomia International:|website=www.dysautonomiainternational.org|access-date=2018-12-12}}</ref>

== Dysautonomia in ME ==
[[File:Dysautonomia1.png|thumb|Symptoms of autonomic dysfunction are correlated with severity of fatigue in CFS patients.<ref>{{Cite journal|last=Jones|first=D. E. J.|last2=Shin|first2=J.|last3=Seth|first3=A.|last4=Sutcliffe|first4=K.|last5=Okonkwo|first5=O.|last6=Newton|first6=J. L.|date=2007-08-01|title=Symptoms of autonomic dysfunction in chronic fatigue syndrome|url=https://academic.oup.com/qjmed/article/100/8/519/1521818|journal=QJM: An International Journal of Medicine|language=en|volume=100|issue=8|pages=519–526|doi=10.1093/qjmed/hcm057|issn=1460-2725}}</ref>]]
Many people with ME experience autonomic dysfunction. Symptoms of autonomic dysfunction in ME include altered blood pressure, heart rate, digestion, body temperature, exercise intolerance, and neurological correlates with [[autonomic nervous system]] (ANS) dysfunction (for a complete list, see our [[Autonomic nervous system|Autonomic Nervous System page]]).

Some researchers suggest that dysautonomia is central to the pathophysiology of ME.<ref>{{Cite journal|date=2004-02-01|title=Dysautonomia in chronic fatigue syndrome: facts, hypotheses, implications|url=https://www.sciencedirect.com/science/article/pii/S0306987703003311|journal=Medical Hypotheses|language=en|volume=62|issue=2|pages=203–206|doi=10.1016/S0306-9877(03)00331-1|issn=0306-9877}}</ref> Various studies have investigated the efficacy of treating ME patients by targeting autonomic symptoms (e.g., <ref>{{Cite journal|last=Straus|first=Stephen E.|last2=Wolff|first2=Mark|last3=Lucas|first3=Katherine E.|last4=Snader|first4=Sally|last5=Hohman|first5=Patricia|last6=Soto|first6=Norberto|last7=Cuccherini|first7=Brenda A.|last8=Sharma|first8=Geetika|last9=Anand|first9=Ravinder|date=2001-01-03|title=Fludrocortisone Acetate to Treat Neurally Mediated Hypotension in Chronic Fatigue Syndrome: A Randomized Controlled Trial|url=https://jamanetwork.com/journals/jama/fullarticle/193426|journal=JAMA|language=en|volume=285|issue=1|pages=52–59|doi=10.1001/jama.285.1.52|issn=0098-7484}}</ref>) without significant success.

=== Studies on Dysautonomia and ME ===
One study (Orjatsalo et al. 2018) has looked at autonomic cardiac function in different sleep stages of people with CFS. They found that people with CFS had higher nocturnal systolic and mean BP and lower heart rate than controls, suggesting a nocturnal dysfunction of the cardiac ANS in CFS. This means that patients have a lower parasympathetic tone and higher sympathetic tone during sleep.<ref>{{Cite journal|last=Orjatsalo|first=Maija|last2=Alakuijala|first2=Anniina|last3=Partinen|first3=Markku|date=2018-02-15|title=Autonomic Nervous System Functioning Related to Nocturnal Sleep in Patients With Chronic Fatigue Syndrome Compared to Tired Controls|url=https://www.ncbi.nlm.nih.gov/pubmed/29246267|journal=Journal of clinical sleep medicine: JCSM: official publication of the American Academy of Sleep Medicine|volume=14|issue=2|pages=163–171|doi=10.5664/jcsm.6924|issn=1550-9397|pmc=5786834|pmid=29246267}}</ref>
[[File:Dysautonomia2.png|thumb|Difference in total autonomic dysfunction (depicted by COMPASS score) between healthy controls (left), CFS patients (middle), and patients with primary biliary cirrhosis (PBC, a condition in which there is strong evidence of a causal link between fatigue and autonomic dysfunction; right). COMPASS scores were significantly higher in the CFS group.<ref>{{Cite journal|last=Jones|first=D. E. J.|last2=Shin|first2=J.|last3=Seth|first3=A.|last4=Sutcliffe|first4=K.|last5=Okonkwo|first5=O.|last6=Newton|first6=J. L.|date=2007-08-01|title=Symptoms of autonomic dysfunction in chronic fatigue syndrome|url=https://academic.oup.com/qjmed/article/100/8/519/1521818|journal=QJM: An International Journal of Medicine|language=en|volume=100|issue=8|pages=519–526|doi=10.1093/qjmed/hcm057|issn=1460-2725}}</ref>]]
Another study ([[Kunihisa Miwa|Miwa]] 2016) investigated POTS in patients with both ME and orthostatic intolerance. They hypothesized that the characteristics of sympathetic activation may differ between these patients’ “good days” and “bad days”. Patients were characterized with an active standing test and an echocardiography. Their results indicated that ME patients may experience exaggerated activation of the sympathetic nervous system. They suggest that sympathetic activation in ME is impaired and is associated with preload failure.<ref>{{Cite journal|last=Miwa|first=Kunihisa|date=2016-9|title=Variability of postural orthostatic tachycardia in patients with myalgic encephalomyelitis and orthostatic intolerance|url=https://www.ncbi.nlm.nih.gov/pubmed/26374335|journal=Heart and Vessels|volume=31|issue=9|pages=1522–1528|doi=10.1007/s00380-015-0744-3|issn=1615-2573|pmid=26374335|quote=|author-link=Kunihisa Miwa|author-link2=|author-link3=|author-link4=|author-link5=|via=}}</ref>

Newton et al. aimed to determine the prevalence of autonomic dysfunction in CFS using the Composite Autonomic Symptom Scale (COMPASS) and the Fatigue Impact Scale (FIS). The study included a healthy control group and a control group of patients with primary biliary cirrhosis (PBC; where 60% of patients experience significant fatigue and some experience autonomic dysfunction). Their results indicated that symptoms of autonomic dysfunction were strongly associated with the presence of CFS or PBC (in some but not all patients), and that symptoms correlated with severity of fatigue. COMPASS scores were significantly higher for the CFS group than for the PBC group and healthy control group.<ref>{{Cite journal|last=Jones|first=D. E. J.|last2=Shin|first2=J.|last3=Seth|first3=A.|last4=Sutcliffe|first4=K.|last5=Okonkwo|first5=O.|last6=Newton|first6=J. L.|date=2007-08-01|title=Symptoms of autonomic dysfunction in chronic fatigue syndrome|url=https://academic.oup.com/qjmed/article/100/8/519/1521818|journal=QJM: An International Journal of Medicine|language=en|volume=100|issue=8|pages=519–526|doi=10.1093/qjmed/hcm057|issn=1460-2725|quote=|author-link=|author-link2=|author-link3=|author-link4=|author-link5=|via=|author-link6=Julia Newton}}</ref>

== References==
<references />

[[Category:Diagnoses]]
[[Category:Comorbidities]]
[[Category:Signs and symptoms]]
[[Category:Neurology]]

Dysautonomia

2018-12-12T16:32:20Z

Paulitasofia1:

{{stub}}
Dysautonomia describes several different medical conditions that involve dysregulation of the autonomic nervous system. People with dysautonomia have problems regulating autonomic functions, including heart rate, blood pressure, body temperature, and digestion. Thus, dysautonomia can present with various symptoms, such as lightheadedness, fainting, unstable blood pressure, and orthostatic intolerance.<ref name=":0">{{Cite web|url=http://www.dysautonomiainternational.org/page.php?ID=34|title=Dysautonomia International:|website=www.dysautonomiainternational.org|access-date=2018-12-12}}</ref>

== Types of dysautonomia ==
More than 70 million people have dysautonomia. There are various types of dysautonomia, each presenting with different underlying mechanisms as well as some overlapping mechanisms. Forms of dysautonomia include:
* '''Postural orthostatic tachycardia syndrome (POTS)''', a form of orthostatic intolerance that can cause lightheadedness, fainting, tachycardia, chest pains, exercise intolerance, temperature sensitivity, and more.
* '''Neurocardiogenic syncope''' is the most common form of dysautonomia, with many individuals having a mild case (fainting once or twice in their lifetime). Severe cases can result in fainting several times per day.
* '''Multiple system atrophy (MSA)''', a fatal and rare form of dysautonomia, affects 350,000 people worldwide. It is a neurodegenerative disorder occurring in adults over the age of 40. MSA progresses rapidly; patients usually become bedridden within 2 years of diagnosis.
* '''Familial dysautonomia (FD)''' is a rare genetic disorder in persons of Ashkenazi Jewish descent. It is a very serious condition, consisting of abnormal development, progressive degeneration of the sensory and autonomic nervous systems, and is inevitably fatal. FD is caused by a point mutation in the ''IKBAP'' gene, resulting in the severe reduction of the IKAP protein, which is involved in many intracellular processes.<ref>{{Cite journal|last=Dragatsis|first=Ioannis|last2=Dietrich|first2=Paula|last3=Dragatsis|first3=Ioannis|last4=Dietrich|first4=Paula|date=2016-12|title=Familial Dysautonomia: Mechanisms and Models|url=http://www.scielo.br/scielo.php?script=sci_abstract&pid=S1415-47572016000400497&lng=en&nrm=iso&tlng=en|journal=Genetics and Molecular Biology|volume=39|issue=4|pages=497–514|doi=10.1590/1678-4685-gmb-2015-0335|issn=1415-4757}}</ref>
* '''Autonomic dysreflexia (AD)''' is a form of dysautonomia associated with spinal cord injuries, affecting the communication of the autonomic nervous system.
* '''Baroreflex failure'''; the baroreflex is the body’s homeostatic mechanism for maintaining blood pressure. If the baroreceptor or its system fails, patients experience inappropriate blood pressure.
* '''Cerebral salt wasting syndrome''' is a condition in response to physical injury or the presence of tumors in the brain, presenting as hyponatremia (excessive sodium secretion from the kidney) and dehydration.
* '''Diabetic autonomic neuropathy''' is a very common form of dysautonomia, affecting 69 million people worldwide (20% of diabetics). It is a serious complication of diabetes, associated with an increased risk of cardiovascular mortality.
* '''Panayiotopoulos syndrome''', also known as autonomic epilepsy is a childhood-specific seizure disorder consisting of seizures with predominantly autonomic symptoms (without convulsing).<ref>{{Cite journal|last=Covanis|first=Athanasios|date=2006-10-01|title=Panayiotopoulos Syndrome: A Benign Childhood Autonomic Epilepsy Frequently Imitating Encephalitis, Syncope, Migraine, Sleep Disorder, or Gastroenteritis|url=http://pediatrics.aappublications.org/content/118/4/e1237|journal=Pediatrics|language=en|volume=118|issue=4|pages=e1237–e1243|doi=10.1542/peds.2006-0623|issn=1098-4275|pmid=16950946}}</ref>
* '''Reflex sympathetic dystrophy''' is a an extremely painful neurological condition that is sometimes considered a form of dysautonomia.
Dysautonomia can occur independently or secondary to other medical conditions, such as diabetes, MS, rheumatoid arthritis, and lupus.<ref name=":0" />

== Comorbidities/causes of dysautonomia ==
Comorbidities and causes of dysautonomia include:<ref name=":0" />
* Amyloidosis
** A group of rare disorders caused by the accumulation of amyloid protein in various tissues throughout the body. If the amyloid accumulation occurs in the heart or on peripheral nerves, it can cause dysautonomia.
* Celiac disease
* Charcot-Marie-Tooth disease
* Chiari malformation
* Chronic inflammatory demyelinating polyneuropathy
* Inflammatory bowel disease (such as Crohn’s and ulcerative colitis)<ref>{{Cite journal|last=Lindgren|first=S.|last2=Lilja|first2=B.|last3=Rosén|first3=I.|last4=Sundkvist|first4=G.|date=1991-4|title=Disturbed autonomic nerve function in patients with Crohn's disease|url=https://www.ncbi.nlm.nih.gov/pubmed/2034989|journal=Scandinavian Journal of Gastroenterology|volume=26|issue=4|pages=361–366|issn=0036-5521|pmid=2034989}}</ref><ref>{{Cite journal|last=Lindgren|first=S.|last2=Stewenius|first2=J.|last3=Sjölund|first3=K.|last4=Lilja|first4=B.|last5=Sundkvist|first5=G.|date=1993-7|title=Autonomic vagal nerve dysfunction in patients with ulcerative colitis|url=https://www.ncbi.nlm.nih.gov/pubmed/8362220|journal=Scandinavian Journal of Gastroenterology|volume=28|issue=7|pages=638–642|issn=0036-5521|pmid=8362220}}</ref>
* Deconditioning
** The physical change in the way the body functions due to a decrease in activity. The most common cause of deconditioning is bed rest. Due to debilitating symptoms, patients with various chronic illnesses may experience deconditioning, which can exacerbate symptoms. It is important to take steps to prevent and/or reverse deconditioning. <ref>{{Cite journal|last=Dyckman|first=Damian J.|last2=Sauder|first2=Charity L.|last3=Ray|first3=Chester A.|date=2012-01-01|title=Effects of short-term and prolonged bed rest on the vestibulosympathetic reflex|url=https://www.ncbi.nlm.nih.gov/pubmed/22021328|journal=American Journal of Physiology. Heart and Circulatory Physiology|volume=302|issue=1|pages=H368–374|doi=10.1152/ajpheart.00193.2011|issn=1522-1539|pmc=PMC3334249|pmid=22021328}}</ref>
* Diabetes<ref>{{Cite journal|last=Vinik|first=Aaron I|last2=Erbas|first2=Tomris|last3=Casellini|first3=Carolina M|date=2013-01-29|title=Diabetic cardiac autonomic neuropathy, inflammation and cardiovascular disease|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3580884/|journal=Journal of Diabetes Investigation|volume=4|issue=1|pages=4–18|doi=10.1111/jdi.12042|issn=2040-1116|pmc=PMC3580884|pmid=23550085}}</ref>
* Ehlers-Danlos syndrome<ref>{{Cite journal|date=1999-10-01|title=Orthostatic intolerance and chronic fatigue syndrome associated with Ehlers-Danlos syndrome|url=https://www.sciencedirect.com/science/article/pii/S0022347699701733|journal=The Journal of Pediatrics|language=en|volume=135|issue=4|pages=494–499|doi=10.1016/S0022-3476(99)70173-3|issn=0022-3476}}</ref>
* Mast cell disorders
* Mitochondrial diseases<ref>{{Cite journal|last=Kanjwal|first=Khalil|last2=Karabin|first2=Beverly|last3=Kanjwal|first3=Yousuf|last4=Saeed|first4=Bilal|last5=Grubb|first5=Blair P.|date=2010-10|title=Autonomic dysfunction presenting as orthostatic intolerance in patients suffering from mitochondrial cytopathy|url=https://www.ncbi.nlm.nih.gov/pubmed/20960537|journal=Clinical Cardiology|volume=33|issue=10|pages=626–629|doi=10.1002/clc.20805|issn=1932-8737|pmid=20960537}}</ref>
* Paraneoplastic syndrome<ref>{{Cite journal|last=Koike|first=Haruki|last2=Tanaka|first2=Fumiaki|last3=Sobue|first3=Gen|date=2011-10|title=Paraneoplastic neuropathy: wide-ranging clinicopathological manifestations|url=https://www.ncbi.nlm.nih.gov/pubmed/21799410|journal=Current Opinion in Neurology|volume=24|issue=5|pages=504–510|doi=10.1097/WCO.0b013e32834a87b7|issn=1473-6551|pmid=21799410}}</ref>
* Parkinson’s disease<ref>{{Cite journal|last=Goldstein|first=David S|date=2014-4|title=Dysautonomia in Parkinson’s disease: neurocardiological abnormalities|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4222515/|journal=Comprehensive Physiology|volume=4|issue=2|pages=805–826|doi=10.1002/cphy.c130026|issn=2040-4603|pmc=PMC4222515|pmid=24715569}}</ref>
* Sarcoidosis<ref>{{Cite journal|last=Bakkers|first=M.|last2=Faber|first2=C. G.|last3=Drent|first3=M.|last4=Hermans|first4=M. C. E.|last5=van Nes|first5=S. I.|last6=Lauria|first6=G.|last7=De Baets|first7=M.|last8=Merkies|first8=I. S. J.|date=2010-12|title=Pain and autonomic dysfunction in patients with sarcoidosis and small fibre neuropathy|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2993892/|journal=Journal of Neurology|volume=257|issue=12|pages=2086–2090|doi=10.1007/s00415-010-5664-7|issn=0340-5354|pmc=PMC2993892|pmid=20644950}}</ref>
* Sjogren’s syndrome<ref>{{Cite journal|last=Ng|first=W.-F.|last2=Stangroom|first2=A. J.|last3=Davidson|first3=A.|last4=Wilton|first4=K.|last5=Mitchell|first5=S.|last6=Newton|first6=J. L.|date=2012-12|title=Primary Sjogrens syndrome is associated with impaired autonomic response to orthostasis and sympathetic failure|url=https://www.ncbi.nlm.nih.gov/pubmed/22976617|journal=QJM: monthly journal of the Association of Physicians|volume=105|issue=12|pages=1191–1199|doi=10.1093/qjmed/hcs172|issn=1460-2393|pmc=PMC3508582|pmid=22976617}}</ref>
* Physical trauma or surgery<ref>{{Cite journal|last=Kanjwal|first=Khalil|last2=Karabin|first2=Beverly|last3=Kanjwal|first3=Yousuf|last4=Grubb|first4=Blair P.|date=2010|title=Autonomic dysfunction presenting as postural tachycardia syndrome following traumatic brain injury|url=https://www.ncbi.nlm.nih.gov/pubmed/20865679|journal=Cardiology Journal|volume=17|issue=5|pages=482–487|issn=1897-5593|pmid=20865679}}</ref><ref>{{Cite journal|last=Billakanty|first=Sreedhar R.|last2=Kligman|first2=Mark D.|last3=Kanjwal|first3=Yousuf M.|last4=Kosinski|first4=Daniel J.|last5=Maly|first5=George T.|last6=Karabin|first6=Beverly|last7=Grubb|first7=Blair P.|date=2008-7|title=New-onset orthostatic intolerance following bariatric surgery|url=https://www.ncbi.nlm.nih.gov/pubmed/18684286|journal=Pacing and clinical electrophysiology: PACE|volume=31|issue=7|pages=884–888|doi=10.1111/j.1540-8159.2008.01103.x|issn=1540-8159|pmid=18684286}}</ref>
* Vitamin deficiencies
* Patients have also reported dysautonomia caused by viral infections

== Treatment ==
There are currently no cures for dysautonomia, as it is an umbrella term that covers many conditions related to the dysfunction of the autonomic system. Therefore, there are treatments that are used to improve quality of life by treating specific symptoms, or treating the underlying disease that is causing the dysautonomia. Further treatments are used to improve quality of life.<ref>{{Cite web|url=http://www.dysautonomiainternational.org/page.php?ID=34|title=Dysautonomia International:|website=www.dysautonomiainternational.org|access-date=2018-12-12}}</ref>

== Dysautonomia in ME ==
[[File:Dysautonomia1.png|thumb|Symptoms of autonomic dysfunction are correlated with severity of fatigue in CFS patients.<ref>{{Cite journal|last=Jones|first=D. E. J.|last2=Shin|first2=J.|last3=Seth|first3=A.|last4=Sutcliffe|first4=K.|last5=Okonkwo|first5=O.|last6=Newton|first6=J. L.|date=2007-08-01|title=Symptoms of autonomic dysfunction in chronic fatigue syndrome|url=https://academic.oup.com/qjmed/article/100/8/519/1521818|journal=QJM: An International Journal of Medicine|language=en|volume=100|issue=8|pages=519–526|doi=10.1093/qjmed/hcm057|issn=1460-2725}}</ref>]]
Many people with ME experience autonomic dysfunction. Symptoms of autonomic dysfunction in ME include altered blood pressure, heart rate, digestion, body temperature, exercise intolerance, and neurological correlates with ANS dysfunction (for a complete list, see our Autonomic Nervous System page).

Some researchers suggest that dysautonomia is central to the pathophysiology of ME.<ref>{{Cite journal|date=2004-02-01|title=Dysautonomia in chronic fatigue syndrome: facts, hypotheses, implications|url=https://www.sciencedirect.com/science/article/pii/S0306987703003311|journal=Medical Hypotheses|language=en|volume=62|issue=2|pages=203–206|doi=10.1016/S0306-9877(03)00331-1|issn=0306-9877}}</ref> Various studies have investigated the efficacy of treating ME patients by targeting autonomic symptoms (e.g., <ref>{{Cite journal|last=Straus|first=Stephen E.|last2=Wolff|first2=Mark|last3=Lucas|first3=Katherine E.|last4=Snader|first4=Sally|last5=Hohman|first5=Patricia|last6=Soto|first6=Norberto|last7=Cuccherini|first7=Brenda A.|last8=Sharma|first8=Geetika|last9=Anand|first9=Ravinder|date=2001-01-03|title=Fludrocortisone Acetate to Treat Neurally Mediated Hypotension in Chronic Fatigue Syndrome: A Randomized Controlled Trial|url=https://jamanetwork.com/journals/jama/fullarticle/193426|journal=JAMA|language=en|volume=285|issue=1|pages=52–59|doi=10.1001/jama.285.1.52|issn=0098-7484}}</ref>) without significant success.

=== Studies on Dysautonomia and ME ===
One study (Orjatsalo et al. 2018) has looked at autonomic cardiac function in different sleep stages of people with CFS. They found that people with CFS had higher nocturnal systolic and mean BP and lower heart rate than controls, suggesting a nocturnal dysfunction of the cardiac ANS in CFS. This means that patients have a lower parasympathetic tone and higher sympathetic tone during sleep.<ref>{{Cite journal|last=Orjatsalo|first=Maija|last2=Alakuijala|first2=Anniina|last3=Partinen|first3=Markku|date=2018-02-15|title=Autonomic Nervous System Functioning Related to Nocturnal Sleep in Patients With Chronic Fatigue Syndrome Compared to Tired Controls|url=https://www.ncbi.nlm.nih.gov/pubmed/29246267|journal=Journal of clinical sleep medicine: JCSM: official publication of the American Academy of Sleep Medicine|volume=14|issue=2|pages=163–171|doi=10.5664/jcsm.6924|issn=1550-9397|pmc=PMC5786834|pmid=29246267}}</ref>
[[File:Dysautonomia2.png|thumb|Difference in total autonomic dysfunction (depicted by COMPASS score) between healthy controls (left), CFS patients (middle), and patients with primary biliary cirrhosis (PBC, a condition in which there is strong evidence of a causal link between fatigue and autonomic dysfunction; right). COMPASS scores were significantly higher in the CFS group.<ref>{{Cite journal|last=Jones|first=D. E. J.|last2=Shin|first2=J.|last3=Seth|first3=A.|last4=Sutcliffe|first4=K.|last5=Okonkwo|first5=O.|last6=Newton|first6=J. L.|date=2007-08-01|title=Symptoms of autonomic dysfunction in chronic fatigue syndrome|url=https://academic.oup.com/qjmed/article/100/8/519/1521818|journal=QJM: An International Journal of Medicine|language=en|volume=100|issue=8|pages=519–526|doi=10.1093/qjmed/hcm057|issn=1460-2725}}</ref>]]
Another study (Miwa 2016) investigated POTS in patients with both ME and orthostatic intolerance. They hypothesized that the characteristics of sympathetic activation may differ between these patients’ “good days” and “bad days”. Patients were characterized with an active standing test and an echocardiography. Their results indicated that ME patients may experience exaggerated activation of the sympathetic nervous system. They suggest that sympathetic activation in ME is impaired and is associated with preload failure.<ref>{{Cite journal|last=Miwa|first=Kunihisa|date=2016-9|title=Variability of postural orthostatic tachycardia in patients with myalgic encephalomyelitis and orthostatic intolerance|url=https://www.ncbi.nlm.nih.gov/pubmed/26374335|journal=Heart and Vessels|volume=31|issue=9|pages=1522–1528|doi=10.1007/s00380-015-0744-3|issn=1615-2573|pmid=26374335}}</ref>

Newton et al. aimed to determine the prevalence of autonomic dysfunction in CFS using the Composite Autonomic Symptom Scale (COMPASS) and the Fatigue Impact Scale (FIS). The study included a healthy control group and a control group of patients with primary biliary cirrhosis (PBC; where 60% of patients experience significant fatigue and some experience autonomic dysfunction). Their results indicated that symptoms of autonomic dysfunction were strongly associated with the presence of CFS or PBC (in some but not all patients), and that symptoms correlated with severity of fatigue. COMPASS scores were significantly higher for the CFS group than for the PBC group and healthy control group.<ref>{{Cite journal|last=Jones|first=D. E. J.|last2=Shin|first2=J.|last3=Seth|first3=A.|last4=Sutcliffe|first4=K.|last5=Okonkwo|first5=O.|last6=Newton|first6=J. L.|date=2007-08-01|title=Symptoms of autonomic dysfunction in chronic fatigue syndrome|url=https://academic.oup.com/qjmed/article/100/8/519/1521818|journal=QJM: An International Journal of Medicine|language=en|volume=100|issue=8|pages=519–526|doi=10.1093/qjmed/hcm057|issn=1460-2725}}</ref>

== References==
<references />

[[Category:Diagnoses]]
[[Category:Comorbidities]]
[[Category:Signs and symptoms]]
[[Category:Neurology]]

File:Dysautonomia2.png

2018-12-12T16:29:03Z

Paulitasofia1:

Difference in total autonomic dysfunction (depicted by COMPASS score) between healthy controls (left), CFS patients (middle), and patients with primary biliary cirrhosis (PBC, a condition in which there is strong evidence of a causal link between fatigue and autonomic dysfunction; right). COMPASS scores were significantly higher in the CFS group.

File:Dysautonomia1.png

2018-12-12T16:27:41Z

Paulitasofia1:

Symptoms of autonomic dysfunction are correlated with severity of fatigue in CFS patients.

File:Autonomic dysfunction scores in CFS.png

2018-12-12T16:25:56Z

Paulitasofia1:

Symptoms of autonomic dysfunction are correlated with severity of fatigue in CFS patients.

File:Autonomic dysfunction scores.ppt

2018-12-12T16:23:59Z

Paulitasofia1:

Symptoms of autonomic dysfunction are correlated with severity of fatigue in CFS patients.

Dysautonomia

2018-12-12T16:20:56Z

Paulitasofia1:Expanded the stub

{{stub}}
Dysautonomia describes several different medical conditions that involve dysregulation of the autonomic nervous system. People with dysautonomia have problems regulating autonomic functions, including heart rate, blood pressure, body temperature, and digestion. Thus, dysautonomia can present with various symptoms, such as lightheadedness, fainting, unstable blood pressure, and orthostatic intolerance.<ref name=":0">{{Cite web|url=http://www.dysautonomiainternational.org/page.php?ID=34|title=Dysautonomia International:|website=www.dysautonomiainternational.org|access-date=2018-12-12}}</ref>

== Types of dysautonomia ==
More than 70 million people have dysautonomia. There are various types of dysautonomia, each presenting with different underlying mechanisms as well as some overlapping mechanisms. Forms of dysautonomia include:
* '''Postural orthostatic tachycardia syndrome (POTS)''', a form of orthostatic intolerance that can cause lightheadedness, fainting, tachycardia, chest pains, exercise intolerance, temperature sensitivity, and more.
* '''Neurocardiogenic syncope''' is the most common form of dysautonomia, with many individuals having a mild case (fainting once or twice in their lifetime). Severe cases can result in fainting several times per day.
* '''Multiple system atrophy (MSA)''', a fatal and rare form of dysautonomia, affects 350,000 people worldwide. It is a neurodegenerative disorder occurring in adults over the age of 40. MSA progresses rapidly; patients usually become bedridden within 2 years of diagnosis.
* '''Familial dysautonomia (FD)''' is a rare genetic disorder in persons of Ashkenazi Jewish descent. It is a very serious condition, consisting of abnormal development, progressive degeneration of the sensory and autonomic nervous systems, and is inevitably fatal. FD is caused by a point mutation in the ''IKBAP'' gene, resulting in the severe reduction of the IKAP protein, which is involved in many intracellular processes.<ref>{{Cite journal|last=Dragatsis|first=Ioannis|last2=Dietrich|first2=Paula|last3=Dragatsis|first3=Ioannis|last4=Dietrich|first4=Paula|date=2016-12|title=Familial Dysautonomia: Mechanisms and Models|url=http://www.scielo.br/scielo.php?script=sci_abstract&pid=S1415-47572016000400497&lng=en&nrm=iso&tlng=en|journal=Genetics and Molecular Biology|volume=39|issue=4|pages=497–514|doi=10.1590/1678-4685-gmb-2015-0335|issn=1415-4757}}</ref>
* '''Autonomic dysreflexia (AD)''' is a form of dysautonomia associated with spinal cord injuries, affecting the communication of the autonomic nervous system.
* '''Baroreflex failure'''; the baroreflex is the body’s homeostatic mechanism for maintaining blood pressure. If the baroreceptor or its system fails, patients experience inappropriate blood pressure.
* '''Cerebral salt wasting syndrome''' is a condition in response to physical injury or the presence of tumors in the brain, presenting as hyponatremia (excessive sodium secretion from the kidney) and dehydration.
* '''Diabetic autonomic neuropathy''' is a very common form of dysautonomia, affecting 69 million people worldwide (20% of diabetics). It is a serious complication of diabetes, associated with an increased risk of cardiovascular mortality.
* '''Panayiotopoulos syndrome''', also known as autonomic epilepsy is a childhood-specific seizure disorder consisting of seizures with predominantly autonomic symptoms (without convulsing).<ref>{{Cite journal|last=Covanis|first=Athanasios|date=2006-10-01|title=Panayiotopoulos Syndrome: A Benign Childhood Autonomic Epilepsy Frequently Imitating Encephalitis, Syncope, Migraine, Sleep Disorder, or Gastroenteritis|url=http://pediatrics.aappublications.org/content/118/4/e1237|journal=Pediatrics|language=en|volume=118|issue=4|pages=e1237–e1243|doi=10.1542/peds.2006-0623|issn=1098-4275|pmid=16950946}}</ref>
* '''Reflex sympathetic dystrophy''' is a an extremely painful neurological condition that is sometimes considered a form of dysautonomia.
Dysautonomia can occur independently or secondary to other medical conditions, such as diabetes, MS, rheumatoid arthritis, and lupus.<ref name=":0" />

== Comorbidities/causes of dysautonomia ==
Comorbidities and causes of dysautonomia include:<ref name=":0" />
* Amyloidosis
** A group of rare disorders caused by the accumulation of amyloid protein in various tissues throughout the body. If the amyloid accumulation occurs in the heart or on peripheral nerves, it can cause dysautonomia.
* Celiac disease
* Charcot-Marie-Tooth disease
* Chiari malformation
* Chronic inflammatory demyelinating polyneuropathy
* Inflammatory bowel disease (such as Crohn’s and ulcerative colitis)<ref>{{Cite journal|last=Lindgren|first=S.|last2=Lilja|first2=B.|last3=Rosén|first3=I.|last4=Sundkvist|first4=G.|date=1991-4|title=Disturbed autonomic nerve function in patients with Crohn's disease|url=https://www.ncbi.nlm.nih.gov/pubmed/2034989|journal=Scandinavian Journal of Gastroenterology|volume=26|issue=4|pages=361–366|issn=0036-5521|pmid=2034989}}</ref><ref>{{Cite journal|last=Lindgren|first=S.|last2=Stewenius|first2=J.|last3=Sjölund|first3=K.|last4=Lilja|first4=B.|last5=Sundkvist|first5=G.|date=1993-7|title=Autonomic vagal nerve dysfunction in patients with ulcerative colitis|url=https://www.ncbi.nlm.nih.gov/pubmed/8362220|journal=Scandinavian Journal of Gastroenterology|volume=28|issue=7|pages=638–642|issn=0036-5521|pmid=8362220}}</ref>
* Deconditioning
** The physical change in the way the body functions due to a decrease in activity. The most common cause of deconditioning is bed rest. Due to debilitating symptoms, patients with various chronic illnesses may experience deconditioning, which can exacerbate symptoms. It is important to take steps to prevent and/or reverse deconditioning. <ref>{{Cite journal|last=Dyckman|first=Damian J.|last2=Sauder|first2=Charity L.|last3=Ray|first3=Chester A.|date=2012-01-01|title=Effects of short-term and prolonged bed rest on the vestibulosympathetic reflex|url=https://www.ncbi.nlm.nih.gov/pubmed/22021328|journal=American Journal of Physiology. Heart and Circulatory Physiology|volume=302|issue=1|pages=H368–374|doi=10.1152/ajpheart.00193.2011|issn=1522-1539|pmc=PMC3334249|pmid=22021328}}</ref>
* Diabetes<ref>{{Cite journal|last=Vinik|first=Aaron I|last2=Erbas|first2=Tomris|last3=Casellini|first3=Carolina M|date=2013-01-29|title=Diabetic cardiac autonomic neuropathy, inflammation and cardiovascular disease|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3580884/|journal=Journal of Diabetes Investigation|volume=4|issue=1|pages=4–18|doi=10.1111/jdi.12042|issn=2040-1116|pmc=PMC3580884|pmid=23550085}}</ref>
* Ehlers-Danlos syndrome<ref>{{Cite journal|date=1999-10-01|title=Orthostatic intolerance and chronic fatigue syndrome associated with Ehlers-Danlos syndrome|url=https://www.sciencedirect.com/science/article/pii/S0022347699701733|journal=The Journal of Pediatrics|language=en|volume=135|issue=4|pages=494–499|doi=10.1016/S0022-3476(99)70173-3|issn=0022-3476}}</ref>
* Mast cell disorders
* Mitochondrial diseases<ref>{{Cite journal|last=Kanjwal|first=Khalil|last2=Karabin|first2=Beverly|last3=Kanjwal|first3=Yousuf|last4=Saeed|first4=Bilal|last5=Grubb|first5=Blair P.|date=2010-10|title=Autonomic dysfunction presenting as orthostatic intolerance in patients suffering from mitochondrial cytopathy|url=https://www.ncbi.nlm.nih.gov/pubmed/20960537|journal=Clinical Cardiology|volume=33|issue=10|pages=626–629|doi=10.1002/clc.20805|issn=1932-8737|pmid=20960537}}</ref>
* Paraneoplastic syndrome<ref>{{Cite journal|last=Koike|first=Haruki|last2=Tanaka|first2=Fumiaki|last3=Sobue|first3=Gen|date=2011-10|title=Paraneoplastic neuropathy: wide-ranging clinicopathological manifestations|url=https://www.ncbi.nlm.nih.gov/pubmed/21799410|journal=Current Opinion in Neurology|volume=24|issue=5|pages=504–510|doi=10.1097/WCO.0b013e32834a87b7|issn=1473-6551|pmid=21799410}}</ref>
* Parkinson’s disease<ref>{{Cite journal|last=Goldstein|first=David S|date=2014-4|title=Dysautonomia in Parkinson’s disease: neurocardiological abnormalities|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4222515/|journal=Comprehensive Physiology|volume=4|issue=2|pages=805–826|doi=10.1002/cphy.c130026|issn=2040-4603|pmc=PMC4222515|pmid=24715569}}</ref>
* Sarcoidosis<ref>{{Cite journal|last=Bakkers|first=M.|last2=Faber|first2=C. G.|last3=Drent|first3=M.|last4=Hermans|first4=M. C. E.|last5=van Nes|first5=S. I.|last6=Lauria|first6=G.|last7=De Baets|first7=M.|last8=Merkies|first8=I. S. J.|date=2010-12|title=Pain and autonomic dysfunction in patients with sarcoidosis and small fibre neuropathy|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2993892/|journal=Journal of Neurology|volume=257|issue=12|pages=2086–2090|doi=10.1007/s00415-010-5664-7|issn=0340-5354|pmc=PMC2993892|pmid=20644950}}</ref>
* Sjogren’s syndrome<ref>{{Cite journal|last=Ng|first=W.-F.|last2=Stangroom|first2=A. J.|last3=Davidson|first3=A.|last4=Wilton|first4=K.|last5=Mitchell|first5=S.|last6=Newton|first6=J. L.|date=2012-12|title=Primary Sjogrens syndrome is associated with impaired autonomic response to orthostasis and sympathetic failure|url=https://www.ncbi.nlm.nih.gov/pubmed/22976617|journal=QJM: monthly journal of the Association of Physicians|volume=105|issue=12|pages=1191–1199|doi=10.1093/qjmed/hcs172|issn=1460-2393|pmc=PMC3508582|pmid=22976617}}</ref>
* Physical trauma or surgery<ref>{{Cite journal|last=Kanjwal|first=Khalil|last2=Karabin|first2=Beverly|last3=Kanjwal|first3=Yousuf|last4=Grubb|first4=Blair P.|date=2010|title=Autonomic dysfunction presenting as postural tachycardia syndrome following traumatic brain injury|url=https://www.ncbi.nlm.nih.gov/pubmed/20865679|journal=Cardiology Journal|volume=17|issue=5|pages=482–487|issn=1897-5593|pmid=20865679}}</ref><ref>{{Cite journal|last=Billakanty|first=Sreedhar R.|last2=Kligman|first2=Mark D.|last3=Kanjwal|first3=Yousuf M.|last4=Kosinski|first4=Daniel J.|last5=Maly|first5=George T.|last6=Karabin|first6=Beverly|last7=Grubb|first7=Blair P.|date=2008-7|title=New-onset orthostatic intolerance following bariatric surgery|url=https://www.ncbi.nlm.nih.gov/pubmed/18684286|journal=Pacing and clinical electrophysiology: PACE|volume=31|issue=7|pages=884–888|doi=10.1111/j.1540-8159.2008.01103.x|issn=1540-8159|pmid=18684286}}</ref>
* Vitamin deficiencies
* Patients have also reported dysautonomia caused by viral infections

== Treatment ==
There are currently no cures for dysautonomia, as it is an umbrella term that covers many conditions related to the dysfunction of the autonomic system. Therefore, there are treatments that are used to improve quality of life by treating specific symptoms, or treating the underlying disease that is causing the dysautonomia. Further treatments are used to improve quality of life.<ref>{{Cite web|url=http://www.dysautonomiainternational.org/page.php?ID=34|title=Dysautonomia International:|website=www.dysautonomiainternational.org|access-date=2018-12-12}}</ref>

== Dysautonomia in ME ==
Many people with ME experience autonomic dysfunction. Symptoms of autonomic dysfunction in ME include altered blood pressure, heart rate, digestion, body temperature, exercise intolerance, and neurological correlates with ANS dysfunction (for a complete list, see our Autonomic Nervous System page).

Some researchers suggest that dysautonomia is central to the pathophysiology of ME.<ref>{{Cite journal|date=2004-02-01|title=Dysautonomia in chronic fatigue syndrome: facts, hypotheses, implications|url=https://www.sciencedirect.com/science/article/pii/S0306987703003311|journal=Medical Hypotheses|language=en|volume=62|issue=2|pages=203–206|doi=10.1016/S0306-9877(03)00331-1|issn=0306-9877}}</ref> Various studies have investigated the efficacy of treating ME patients by targeting autonomic symptoms (e.g., <ref>{{Cite journal|last=Straus|first=Stephen E.|last2=Wolff|first2=Mark|last3=Lucas|first3=Katherine E.|last4=Snader|first4=Sally|last5=Hohman|first5=Patricia|last6=Soto|first6=Norberto|last7=Cuccherini|first7=Brenda A.|last8=Sharma|first8=Geetika|last9=Anand|first9=Ravinder|date=2001-01-03|title=Fludrocortisone Acetate to Treat Neurally Mediated Hypotension in Chronic Fatigue Syndrome: A Randomized Controlled Trial|url=https://jamanetwork.com/journals/jama/fullarticle/193426|journal=JAMA|language=en|volume=285|issue=1|pages=52–59|doi=10.1001/jama.285.1.52|issn=0098-7484}}</ref>) without significant success.

=== Studies on Dysautonomia and ME ===
One study (Orjatsalo et al. 2018) has looked at autonomic cardiac function in different sleep stages of people with CFS. They found that people with CFS had higher nocturnal systolic and mean BP and lower heart rate than controls, suggesting a nocturnal dysfunction of the cardiac ANS in CFS. This means that patients have a lower parasympathetic tone and higher sympathetic tone during sleep.<ref>{{Cite journal|last=Orjatsalo|first=Maija|last2=Alakuijala|first2=Anniina|last3=Partinen|first3=Markku|date=2018-02-15|title=Autonomic Nervous System Functioning Related to Nocturnal Sleep in Patients With Chronic Fatigue Syndrome Compared to Tired Controls|url=https://www.ncbi.nlm.nih.gov/pubmed/29246267|journal=Journal of clinical sleep medicine: JCSM: official publication of the American Academy of Sleep Medicine|volume=14|issue=2|pages=163–171|doi=10.5664/jcsm.6924|issn=1550-9397|pmc=PMC5786834|pmid=29246267}}</ref>

Another study (Miwa 2016) investigated POTS in patients with both ME and orthostatic intolerance. They hypothesized that the characteristics of sympathetic activation may differ between these patients’ “good days” and “bad days”. Patients were characterized with an active standing test and an echocardiography. Their results indicated that ME patients may experience exaggerated activation of the sympathetic nervous system. They suggest that sympathetic activation in ME is impaired and is associated with preload failure.<ref>{{Cite journal|last=Miwa|first=Kunihisa|date=2016-9|title=Variability of postural orthostatic tachycardia in patients with myalgic encephalomyelitis and orthostatic intolerance|url=https://www.ncbi.nlm.nih.gov/pubmed/26374335|journal=Heart and Vessels|volume=31|issue=9|pages=1522–1528|doi=10.1007/s00380-015-0744-3|issn=1615-2573|pmid=26374335}}</ref>

Newton et al. aimed to determine the prevalence of autonomic dysfunction in CFS using the Composite Autonomic Symptom Scale (COMPASS) and the Fatigue Impact Scale (FIS). The study included a healthy control group and a control group of patients with primary biliary cirrhosis (PBC; where 60% of patients experience significant fatigue and some experience autonomic dysfunction). Their results indicated that symptoms of autonomic dysfunction were strongly associated with the presence of CFS or PBC (in some but not all patients), and that symptoms correlated with severity of fatigue. COMPASS scores were significantly higher for the CFS group than for the PBC group and healthy control group.<ref>{{Cite journal|last=Jones|first=D. E. J.|last2=Shin|first2=J.|last3=Seth|first3=A.|last4=Sutcliffe|first4=K.|last5=Okonkwo|first5=O.|last6=Newton|first6=J. L.|date=2007-08-01|title=Symptoms of autonomic dysfunction in chronic fatigue syndrome|url=https://academic.oup.com/qjmed/article/100/8/519/1521818|journal=QJM: An International Journal of Medicine|language=en|volume=100|issue=8|pages=519–526|doi=10.1093/qjmed/hcm057|issn=1460-2725}}</ref>

*[[Orthostatic intolerance]]
*[[Postural orthostatic tachycardia syndrome]]
== References==
<references />

[[Category:Diagnoses]]
[[Category:Comorbidities]]
[[Category:Signs and symptoms]]
[[Category:Neurology]]

Pregnancy

2018-11-15T02:05:27Z

Paulitasofia1:changes after meeting with Jaime

Research on outcomes of pregnancy for women with ME is limited. There is some evidence of symptom improvement or remission in various inflammatory and autoimmune diseases during pregnancy. This may be due to hormonal or immune changes.<ref>{{Cite journal|date=2013-08-01|title=Do pregnancy-related changes in the microbiome stimulate innate immunity?|url=https://www.sciencedirect.com/science/article/pii/S1471491413001093|journal=Trends in Molecular Medicine|language=en|volume=19|issue=8|pages=454–459|doi=10.1016/j.molmed.2013.06.002|issn=1471-4914}}</ref>

== Biological changes during pregnancy ==

===Development of the placenta===

The placenta is a vascular organ that develops during pregnancy, attaching to the wall of the uterus. The umbilical cord connects the placenta to the developing fetus, allowing for blood to pass from the mother. The placenta allows for nutrient supply, thermoregulation, waste elimination, and gas exchange for the developing fetus, as well as production of hormones that support pregnancy for the mother. Towards the end of the pregnancy, the placenta provides antibodies to the fetus for protection against infectious pathogens after birth.<ref name=":4">{{Cite web|url=https://www.pregnancybirthbaby.org.au/what-is-the-placenta|title=What is the placenta?|last=|first=|date=July 2017|website=Pregnancy, Birth & Baby|archive-url=|archive-date=|dead-url=|access-date=11/14/2018}}</ref>

The fetus and the placenta may be detected as foreign threat by the mother's immune system. To prevent this from happening, the placenta secretes molecules containing Neurokinin-B. This is the same mechanism that parasitic nematodes use to evade detection by the host immune system. Additionally, there is a presence of lymphocytic suppressor cells in the fetus, which can inhibit maternal cytotoxic T cells.<ref name=":4" /><ref>{{Cite journal|date=2018-05-16|title=Immune tolerance in pregnancy|url=https://en.wikipedia.org/w/index.php?title=Immune_tolerance_in_pregnancy&oldid=841525208|journal=Wikipedia|language=en}}</ref><ref>{{Cite journal|last=Sakamoto|first=Rie|last2=Osada|first2=Hisao|last3=Iitsuka|first3=Yoshinori|last4=Masuda|first4=Kentarou|last5=Kaku|first5=Kenshi|last6=Seki|first6=Katsuyoshi|last7=Sekiya|first7=Souei|date=2003-5|title=Profile of neurokinin B concentrations in maternal and cord blood in normal pregnancy|url=https://www.ncbi.nlm.nih.gov/pubmed/12699441|journal=Clinical Endocrinology|volume=58|issue=5|pages=597–600|issn=0300-0664|pmid=12699441}}</ref> [[File:Pregnant non pregnant histamine ascorbic acid.jpg|right|350x350px]]

===Immune system===

As a prerequisite for a successful pregnancy, the [[immune system]] undergoes changes so that the mother's body will not reject the fetus.<ref name=":2">{{Cite journal|last=Reinhard|first=G.|last2=Noll|first2=A.|last3=Schlebusch|first3=H.|last4=Mallmann|first4=P.|last5=Ruecker|first5=A. V.|date=1998-04-28|title=Shifts in the TH1/TH2 balance during human pregnancy correlate with apoptotic changes|url=https://www.ncbi.nlm.nih.gov/pubmed/9588218|journal=Biochemical and Biophysical Research Communications|volume=245|issue=3|pages=933–938|doi=10.1006/bbrc.1998.8549|issn=0006-291X|pmid=9588218}}</ref> To do so, there is a general shift of the immune system from the a pro-inflammatory state (Th1) to an anti-inflammatory state (Th2) during pregnancy. Helper T cells (Th) of the immune system are divided into two main categories, Th1 and Th2, that have opposite functional activity. An immune response can be categorized as a Th1 response (pro-inflammatory, usually in response to pathogens or injury) or a Th2 response (anti-inflammatory, can be used to down-regulate the Th1 state). While both Th1 and Th2 responses are at play, the immune system tends to be dominated by one or the other depending on the Th1/Th2 balance.<ref>{{Cite journal|last=Kidd|first=Parris|date=2003-8|title=Th1/Th2 balance: the hypothesis, its limitations, and implications for health and disease|url=https://www.ncbi.nlm.nih.gov/pubmed/12946237|journal=Alternative Medicine Review: A Journal of Clinical Therapeutic|volume=8|issue=3|pages=223–246|issn=1089-5159|pmid=12946237}}</ref>

One study has shown that T cells from pregnant women produce less Th1 cytokines and more Th2 cytokines, indicating a general shift toward the Th2 anti-inflammatory state. Additionally, levels of regulatory T cells [[Treg|(Tregs)]], progesterone, and estrogen increase during pregnancy, which have anti-inflammatory properties.<ref>{{Cite journal|last=Munoz-Suano|first=Alba|last2=Hamilton|first2=Alexander B.|last3=Betz|first3=Alexander G.|date=May 2011|title=Gimme shelter: the immune system during pregnancy|url=http://www.ncbi.nlm.nih.gov/pubmed/21488887|journal=Immunological Reviews|volume=241|issue=1|pages=20–38|doi=10.1111/j.1600-065X.2011.01002.x|issn=1600-065X|pmid=21488887}}</ref>

In contrast, the T cells in women with recurrent spontaneous abortions produce normal, non-pregnancy levels of Th1 and Th2 cytokines, indicating a Th1 pro-inflammatory state in unsuccessful pregnancies.<ref name=":2" /> In this way, many spontaneous abortions are similar to organ transplant rejections; a Th2 state is required for successful pregnancies and organ transplants, and failed organ transplants usually occur in people who remain in a Th1 dominant state.<ref name=":2" />

==Pregnancy and ME/CFS ==

=== Fertility ===

Women with [[chronic fatigue syndrome]] report higher rates of [[polycystic ovarian syndrome]] (PCOS) and anovulatory cycles, higher rates of [[dysmenorrhea]] and higher rates of [[endometriosis]].<ref name=":0">{{Cite journal|last=Allen|first=Peggy Rosati|date=2008-7|title=Chronic fatigue syndrome: implications for women and their health care providers during the childbearing years|url=https://www.ncbi.nlm.nih.gov/pubmed/18586181|journal=Journal of Midwifery & Women's Health|volume=53|issue=4|pages=289–301; quiz 399|doi=10.1016/j.jmwh.2007.12.001|issn=1542-2011|pmid=18586181}}</ref>

=== Symptoms during pregnancy ===

There has been very little research on pregnancy and ME/CFS. One retrospective survey found that 41% of respondents reported no change in symptoms during pregnancy, 30% improved and 39% got worse.<ref name=":1">{{Cite journal|last=Schacterle|first=Richard S.|last2=Komaroff|first2=Anthony L.|date=2004-02-23|title=A Comparison of Pregnancies That Occur Before and After the Onset of Chronic Fatigue Syndrome|url=http://archinte.jamanetwork.com/article.aspx?articleid=216675|journal=Archives of Internal Medicine|language=en|volume=164|issue=4|pages=401|doi=10.1001/archinte.164.4.401|issn=0003-9926}}</ref>

In clinical practice, Dr. [[Nancy Klimas]], Dr. [[Lucinda Bateman]], and Dr. [[Charles Lapp]] report higher rates of improvement or remission during pregnancy. Klimas reports that in the 20 women she has followed through pregnancy, improvement in symptoms during pregnancy was "almost universal" and in some cases resulted in total temporary remission. Dr. Lapp reported that 25 out of 27 patients in his practice felt better during pregnancy. Dr. Klimas suggests that improvement may be due to increased blood volume during pregnancy or hormonal changes.<ref name=":0" />

=== Postpartum ===

In one survey, after delivery, 30% had no change in symptoms, 20% improved, and 20% got worse. Dr. Klimas reports that her patients typically do well postpartum until about 3 to 6 months after at which time there is often a severe relapse.<ref name=":0" /> Another study indicates that postpartum relapse or worsening of symptoms is likely due to the extra effort of taking care of a baby, as well as the shift away from pregnancy-related hormones and the TH2 state.<ref name=":3" />

Postpartum depression is two to three times more common in mothers with ME/CFS compared to healthy mothers.<ref name=":3" />

=== Complications ===

When comparing these women's pregnancies after illness onset to pregnancies before illness onset (but not to healthy controls), the rate of complications were similar. In pregnancies occurring after illness onset, there was a higher rate of miscarriages (30% vs. 8%) and development delays or learning disabilities (21% vs. 8%).<ref name=":1" /> However, this may be explained by maternal age (pregnancies before illness onset occurred when women were younger than pregnancies occurring after illness onset).<ref name=":1" />

== Significant studies ==

===Schacterle and Komaroff (2004) ===
Schacterle and Komaroff (2004) conducted a retrospective study on women with ME/CFS who had undergone pregnancy before and/or after onset of illness. Many women with ME/CFS have to make the difficult decision of whether to have a child, and concern due to illness has resulted in lower rates of pregnancy. Of interest, "women who had children before the onset of CFS and decided to continue to have children had more pregnancies after the onset. Among the 19 patients (22%) who reported pregnancies both before and after the onset of CFS, 30 pregnancies occurred before and 46 occurred after the onset."

The study showed that during pregnancy, symptoms were unchanged or improved in 71% of women with ME/CFS. After pregnancy, symptoms were unchanged or improved in 50% of patients. Many women report concern over adverse outcomes for their children, yet there is little evidence that this occurs. Importantly, most maternal and offspring outcomes from pregnancies that occurred after illness onset were not systematically worse than pregnancies occurring prior to illness onset. These data are overall encouraging for women with ME/CFS considering pregnancy. <ref name=":1" />

== Pregnancy in other conditions ==

In general, [[Th1]] dominant immune disorders tend to improve during pregnancy while [[Th2]] dominant immune disorders tend to worsen.<ref>{{Cite journal|last=ØSTENSEN|first=MONICA|date=1999-06-01|title=Sex Hormones and Pregnancy in Rheumatoid Arthritis and Systemic Lupus Erythematosus|url=http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.1999.tb07630.x/abstract?userIsAuthenticated=false&deniedAccessCustomisedMessage=|journal=Annals of the New York Academy of Sciences|language=en|volume=876|issue=1|doi=10.1111/j.1749-6632.1999.tb07630.x/abstract|issn=1749-6632}}</ref> For example, in a study of women with [[rheumatoid arthritis]] 75% of patients experienced remission of their RA during pregnancy and 62% experienced a worsening of symptoms after delivery.<ref>{{Cite journal|last=Østensen|first=Monika|last2=Aune|first2=Berit|last3=Husby|first3=Gunnar|date=Jan 1983|title=Effect of Pregnancy and Hormonal Changes on the Activity of Rheumatoid Arthritis|url=http://www.tandfonline.com/doi/abs/10.3109/03009748309102886|journal=Scandinavian Journal of Rheumatology|language=en|volume=12|issue=2|pages=69–72|doi=10.3109/03009748309102886|issn=0300-9742}}</ref> 92% of pregnant women with RA relapse within the first three months after delivery.<ref>{{Cite journal|date=2010-01-01|title=The impact of pregnancy on rheumatoid arthritis outcome: The role of maternofetal HLA class II disparity|url=https://www.sciencedirect.com/science/article/pii/S1297319X09001997|journal=Joint Bone Spine|language=en|volume=77|issue=1|pages=36–40|doi=10.1016/j.jbspin.2009.11.009|issn=1297-319X}}</ref> The course of [[Crohn's disease]] and [[ulcerative colitis]] improves during and after pregnancy.<ref>{{Cite journal|date=2013-08-01|title=Do pregnancy-related changes in the microbiome stimulate innate immunity?|url=https://www.sciencedirect.com/science/article/pii/S1471491413001093|journal=Trends in Molecular Medicine|language=en|volume=19|issue=8|pages=454–459|doi=10.1016/j.molmed.2013.06.002|issn=1471-4914}}</ref> In relapsing-remitting [[multiple sclerosis]], rates of relapse decrease during the first two trimesters and increase significantly postpartum.<ref>{{Cite journal|last=Confavreux|first=Christian|last2=Hutchinson|first2=Michael|last3=Hours|first3=Martine Marie|last4=Cortinovis-Tourniaire|first4=Patricia|last5=Moreau|first5=Thibault|date=1998-07-30|title=Rate of Pregnancy-Related Relapse in Multiple Sclerosis|url=http://www.nejm.org/doi/full/10.1056/nejm199807303390501|journal=New England Journal of Medicine|language=EN|volume=339|issue=5|pages=285–291|doi=10.1056/nejm199807303390501|issn=0028-4793}}</ref>

By contrast, pregnancy increases rates of [[lupus]] flares.<ref>{{Cite journal|last=Ruiz-Irastorza|first=G.|last2=Lima|first2=F.|last3=Alves|first3=J.|last4=Khamashta|first4=M. A.|last5=Simpson|first5=J.|last6=Hughes|first6=G. R. V.|last7=Buchanan|first7=N. M. M.|date=1996-02-01|title=INCREASED RATE OF LUPUS FLARE DURING PREGNANCY AND THE PUERPERIUM: A PROSPECTIVE STUDY OF 78 PREGNANCIES|url=https://academic.oup.com/rheumatology/article/35/2/133/1782393|journal=Rheumatology|language=en|volume=35|issue=2|pages=133–138|doi=10.1093/rheumatology/35.2.133|issn=1462-0324}}</ref> In a retrospective study of [[fibromyalgia]] patients based on personal interviews, nearly all patients surveyed experienced a worsening of symptoms during pregnancy, especially during the third trimester. Fibromyalgia did not appear to have an adverse effect on the outcome of pregnancy or the health of the baby.<ref>{{Cite journal|last=Østensen|first=Monika|last2=Rugelsjoen|first2=Anne|last3=Wigers|first3=Sigrid Horven|date=Jan 1997|title=The Effect of Reproductive Events and Alterations of Sex Hormone Levels on the Symptoms of Fibromyalgia|url=http://www.tandfonline.com/doi/abs/10.3109/03009749709065698|journal=Scandinavian Journal of Rheumatology|language=en|volume=26|issue=5|pages=355–360|doi=10.3109/03009749709065698|issn=0300-9742}}</ref>

== Related potential therapy ==

===Human Placental Extract===

HPE is used as a type of Complementary and Alternative Medicine therapy in various conditions involving chronic inflammation for its anti-inflammatory properties. In one interventional trial, injections of subcutaneous human placental extract (HPE) were found to improve symptoms in ME/CFS patients. Of note, the study did not find a difference between HPE injections and placebo. <ref>{{Cite journal|last=Park|first=Sat Byul|last2=Kim|first2=Kyu-Nam|last3=Sung|first3=Eunju|last4=Lee|first4=Suk Young|last5=Shin|first5=Ho Cheol|date=2016|title=Human Placental Extract as a Subcutaneous Injection Is Effective in Chronic Fatigue Syndrome: A Multi-Center, Double-Blind, Randomized, Placebo-Controlled Study|url=https://www.jstage.jst.go.jp/article/bpb/advpub/0/advpub_b15-00623/_article|journal=Biological & Pharmaceutical Bulletin|language=en|volume=39|issue=5|pages=674–679|doi=10.1248/bpb.b15-00623|issn=0918-6158}}</ref>
== See also ==

*[[Menstrual cycle]]
==Learn more==
*[http://emerge.org.au/about-mecfs/diagnosis/managing-symptoms-daily-basis/pregnancy-motherhood-mecfs/#.Vkp1cLSYe6x Pregnancy, Motherhood, Parenthood and ME/CFS]<ref>{{Cite news|url=http://emerge.org.au/about-mecfs/diagnosis/managing-symptoms-daily-basis/pregnancy-motherhood-mecfs/#.Vkp1cLSYe6x|title=Pregnancy, Motherhood, Parenthood and ME/CFS - Emerge Australia|work=Emerge Australia|access-date=2018-08-11|language=en-US}}</ref>
*2010, [http://www.njcfsa.org/wp-content/uploads/2010/09/Pregnancy-in-Women-with-ME-CFS.pdf Pregnancy in Women with Chronic Fatigue Syndrome (ME/CFS)]<ref name=":3">{{Cite news|url=http://www.njcfsa.org/wp-content/uploads/2010/09/Pregnancy-in-Women-with-ME-CFS.pdf|title=Pregnancy in Women with Chronic Fatigue Syndrome (ME/CFS)|last=Underhill|first=Rosemary|date=|work=NJCFSA|access-date=|archive-url=|archive-date=|dead-url=|publisher=New Jersey Chronic Fatigue Syndrome Association|format=PDF}}</ref>
*2016, [https://batemanhornecenter.org/pregnancy-and-mecfs/ Pregnancy and ME/CFS]<ref>{{Cite news|url=https://batemanhornecenter.org/pregnancy-and-mecfs/|title=Pregnancy and ME/CFS|last=Reynolds|first=Leigh|date=2016-07-06|work=Bateman Horne Center|access-date=2018-08-11|archive-url=|archive-date=|dead-url=|publisher=Bateman Horne Center|language=en-US}}</ref>
*[https://www.healthrising.org/blog/2014/03/02/pregnancy-chronic-fatigue-syndrome-four-mothers-talk-offer/ Pregnancy and Chronic Fatigue Syndrome-- Four Mothers Who've Been Through It Talk]

==References==
<references />
[[Category:Triggers and risk factors]]
[[Reproductive system‎]]

Pregnancy

2018-11-15T01:05:43Z

Paulitasofia1:/* Schacterle and Komaroff (2004) */

Research on outcomes of pregnancy for women with [[chronic fatigue syndrome]] is limited.

There is some evidence of symptom improvement or remission in various inflammatory and autoimmune diseases during pregnancy. This may be due to hormonal or immune changes.<ref>{{Cite journal|date=2013-08-01|title=Do pregnancy-related changes in the microbiome stimulate innate immunity?|url=https://www.sciencedirect.com/science/article/pii/S1471491413001093|journal=Trends in Molecular Medicine|language=en|volume=19|issue=8|pages=454–459|doi=10.1016/j.molmed.2013.06.002|issn=1471-4914}}</ref>

== Biological changes during pregnancy ==

===Development of the placenta===

The placenta is a vascular organ that develops during pregnancy, attaching to the wall of the uterus. The umbilical cord connects the placenta to the developing fetus, allowing for blood to pass from the mother. The placenta allows for nutrient supply, thermoregulation, waste elimination, and gas exchange for the developing fetus, as well as production of hormones that support pregnancy for the mother. Towards the end of the pregnancy, the placenta provides antibodies to the fetus for postpartum protection.<ref name=":4">{{Cite web|url=https://www.pregnancybirthbaby.org.au/what-is-the-placenta|title=What is the placenta?|last=|first=|date=July 2017|website=Pregnancy, Birth & Baby|archive-url=|archive-date=|dead-url=|access-date=11/14/2018}}</ref>

The fetus and the placenta may be detected as foreign allograft by the mother's immune system. To prevent this from happening, the placenta secretes molecules containing Neurokinin-B. This is the same mechanism that parasitic nematodes use to evade detection by the host immune system. Additionally, there is a presence of lymphocytic suppressor cells in the fetus, which can inhibit maternal cytotoxic T cells.<ref name=":4" /><ref>{{Cite journal|date=2018-05-16|title=Immune tolerance in pregnancy|url=https://en.wikipedia.org/w/index.php?title=Immune_tolerance_in_pregnancy&oldid=841525208|journal=Wikipedia|language=en}}</ref><ref>{{Cite journal|last=Sakamoto|first=Rie|last2=Osada|first2=Hisao|last3=Iitsuka|first3=Yoshinori|last4=Masuda|first4=Kentarou|last5=Kaku|first5=Kenshi|last6=Seki|first6=Katsuyoshi|last7=Sekiya|first7=Souei|date=2003-5|title=Profile of neurokinin B concentrations in maternal and cord blood in normal pregnancy|url=https://www.ncbi.nlm.nih.gov/pubmed/12699441|journal=Clinical Endocrinology|volume=58|issue=5|pages=597–600|issn=0300-0664|pmid=12699441}}</ref> [[File:Pregnant non pregnant histamine ascorbic acid.jpg|right]]

===Immune system===

As a prerequisite for a successful pregnancy, the [[immune system]] undergoes changes so that the mother's body will not reject the fetus.<ref name=":2">{{Cite journal|last=Reinhard|first=G.|last2=Noll|first2=A.|last3=Schlebusch|first3=H.|last4=Mallmann|first4=P.|last5=Ruecker|first5=A. V.|date=1998-04-28|title=Shifts in the TH1/TH2 balance during human pregnancy correlate with apoptotic changes|url=https://www.ncbi.nlm.nih.gov/pubmed/9588218|journal=Biochemical and Biophysical Research Communications|volume=245|issue=3|pages=933–938|doi=10.1006/bbrc.1998.8549|issn=0006-291X|pmid=9588218}}</ref> One study has shown that T cells from pregnant women produce less TH1 cytokines and more TH2 cytokines, indicating a general shift toward the TH2 anti-inflammatory state. In contrast, the T cells in women with recurrent spontaneous abortions produce normal, non-pregnancy levels of TH1 and TH2 cytokines, indicating a shift towards the TH1 pro-inflammatory state in unsuccessful pregnancies.<ref name=":2" /> (Many spontaneous abortions are similar to organ transplant rejections.) Additionally, levels of [[Treg]]s, progesterone, and estrogen increase during pregnancy, which have anti-inflammatory properties.<ref>{{Cite journal|last=Munoz-Suano|first=Alba|last2=Hamilton|first2=Alexander B.|last3=Betz|first3=Alexander G.|date=May 2011|title=Gimme shelter: the immune system during pregnancy|url=http://www.ncbi.nlm.nih.gov/pubmed/21488887|journal=Immunological Reviews|volume=241|issue=1|pages=20–38|doi=10.1111/j.1600-065X.2011.01002.x|issn=1600-065X|pmid=21488887}}</ref>

==Pregnancy and ME/CFS ==

=== Fertility ===

Women with [[chronic fatigue syndrome]] report higher rates of [[polycystic ovarian syndrome]] (PCOS) and anovulatory cycles, higher rates of [[dysmenorrhea]] and higher rates of [[endometriosis]].<ref name=":0" />

=== Symptoms during pregnancy ===

There has been very little research on pregnancy and ME/CFS. One retrospective survey found that 41% of respondents reported no change in symptoms during pregnancy, 30% improved and 39% got worse.<ref name=":1">{{Cite journal|last=Schacterle|first=Richard S.|last2=Komaroff|first2=Anthony L.|date=2004-02-23|title=A Comparison of Pregnancies That Occur Before and After the Onset of Chronic Fatigue Syndrome|url=http://archinte.jamanetwork.com/article.aspx?articleid=216675|journal=Archives of Internal Medicine|language=en|volume=164|issue=4|pages=401|doi=10.1001/archinte.164.4.401|issn=0003-9926}}</ref>

In clinical practice, Dr. [[Nancy Klimas]], Dr. [[Lucinda Bateman]], and Dr. [[Charles Lapp]] report higher rates of improvement or remission during pregnancy. Klimas reports that in the 20 women she has followed through pregnancy, improvement in symptoms during pregnancy was "almost universal" and in some cases resulted in total temporary remission. Dr. Lapp reported that 25 out of 27 patients in his practice felt better during pregnancy. Dr. Klimas suggests that improvement may be due to increased blood volume during pregnancy or hormonal changes.<ref name=":0">{{Cite web|url=http://www.medscape.com/viewarticle/576986_6|title=Chronic Fatigue Syndrome: Implications for Women and Their Health Care Providers During the Childbearing Years|website=www.medscape.com|access-date=2018-07-31|date=2008|last=Rosati Allen|first=Peggy|archive-url=|archive-date=|dead-url=|registration=|format=Login Required}}</ref>

=== Postpartum ===

In one survey, after delivery, 30% had no change in symptoms, 20% improved, and 20% got worse. Dr. Klimas reports that her patients typically do well postpartum until about 3 to 6 months after at which time there is often a severe relapse.<ref name=":0" /> Another study indicates that postpartum relapse or worsening of symptoms is likely due to the extra effort of taking care of a baby, as well as the shift away from pregnancy-related hormones and the TH2 state.<ref name=":3" />

Postpartum depression is two to three times more common in mothers with ME/CFS compared to healthy mothers.<ref name=":3" />

=== Complications ===

When comparing these women's pregnancies after illness onset to pregnancies before illness onset (but not to healthy controls), the rate of complications were similar. In pregnancies occurring after illness onset, there was a higher rate of miscarriages (30% vs. 8%) and development delays or learning disabilities (21% vs. 8%).<ref name=":1" /> However, this may be explained by maternal age (pregnancies before illness onset occurred when women were younger than pregnancies occurring after illness onset).<ref>{{Cite news|url=http://emerge.org.au/about-mecfs/diagnosis/managing-symptoms-daily-basis/pregnancy-motherhood-mecfs/#.VkpwyrSYe6w|title=Pregnancy, Motherhood, Parenthood and ME/CFS - Emerge Australia|work=Emerge Australia|access-date=2018-07-31|language=en-US}}</ref>

== Significant studies ==

===Schacterle and Komaroff (2004) ===
Schacterle and Komaroff (2004) conducted a retrospective study on women with ME/CFS who had undergone pregnancy before and/or after onset of illness. Many women with ME/CFS have to make the difficult decision of whether to have a child, and concern due to illness has resulted in lower rates of pregnancy. Of interest, "women who had children before the onset of CFS and decided to continue to have children had more pregnancies after the onset. Among the 19 patients (22%) who reported pregnancies both before and after the onset of CFS, 30 pregnancies occurred before and 46 occurred after the onset."

The study showed that during pregnancy, symptoms were unchanged or improved in 71% of women with ME/CFS. After pregnancy, symptoms were unchanged or improved in 50% of patients. Many women report concern over adverse outcomes for their children, yet there is little evidence that this occurs. Importantly, most maternal and offspring outcomes from pregnancies that occurred after illness onset were not systematically worse than pregnancies occurring prior to illness onset. These data are overall encouraging for women with ME/CFS considering pregnancy. <ref name=":1" />

== Pregnancy in other conditions ==

In general, [[Th1]] dominant immune disorders tend to improve during pregnancy while [[Th2]] dominant immune disorders tend to worsen.<ref>{{Cite journal|last=ØSTENSEN|first=MONICA|date=1999-06-01|title=Sex Hormones and Pregnancy in Rheumatoid Arthritis and Systemic Lupus Erythematosus|url=http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.1999.tb07630.x/abstract?userIsAuthenticated=false&deniedAccessCustomisedMessage=|journal=Annals of the New York Academy of Sciences|language=en|volume=876|issue=1|doi=10.1111/j.1749-6632.1999.tb07630.x/abstract|issn=1749-6632}}</ref> For example, in a study of women with [[rheumatoid arthritis]] 75% of patients experienced remission of their RA during pregnancy and 62% experienced a worsening of symptoms after delivery.<ref>{{Cite journal|last=Østensen|first=Monika|last2=Aune|first2=Berit|last3=Husby|first3=Gunnar|date=Jan 1983|title=Effect of Pregnancy and Hormonal Changes on the Activity of Rheumatoid Arthritis|url=http://www.tandfonline.com/doi/abs/10.3109/03009748309102886|journal=Scandinavian Journal of Rheumatology|language=en|volume=12|issue=2|pages=69–72|doi=10.3109/03009748309102886|issn=0300-9742}}</ref> 92% relapse within the first three months after delivery.<ref>{{Cite journal|date=2010-01-01|title=The impact of pregnancy on rheumatoid arthritis outcome: The role of maternofetal HLA class II disparity|url=https://www.sciencedirect.com/science/article/pii/S1297319X09001997|journal=Joint Bone Spine|language=en|volume=77|issue=1|pages=36–40|doi=10.1016/j.jbspin.2009.11.009|issn=1297-319X}}</ref> The course of [[Crohn's disease]] and [[ulcerative colitis]] improves during and after pregnancy.<ref>{{Cite journal|date=2013-08-01|title=Do pregnancy-related changes in the microbiome stimulate innate immunity?|url=https://www.sciencedirect.com/science/article/pii/S1471491413001093|journal=Trends in Molecular Medicine|language=en|volume=19|issue=8|pages=454–459|doi=10.1016/j.molmed.2013.06.002|issn=1471-4914}}</ref> In relapsing-remitting [[multiple sclerosis]], rates of relapse decrease during the first two trimesters and increase significantly postpartum.<ref>{{Cite journal|last=Confavreux|first=Christian|last2=Hutchinson|first2=Michael|last3=Hours|first3=Martine Marie|last4=Cortinovis-Tourniaire|first4=Patricia|last5=Moreau|first5=Thibault|date=1998-07-30|title=Rate of Pregnancy-Related Relapse in Multiple Sclerosis|url=http://www.nejm.org/doi/full/10.1056/nejm199807303390501|journal=New England Journal of Medicine|language=EN|volume=339|issue=5|pages=285–291|doi=10.1056/nejm199807303390501|issn=0028-4793}}</ref>

By contrast, pregnancy increases rates of [[lupus]] flares.<ref>{{Cite journal|last=Ruiz-Irastorza|first=G.|last2=Lima|first2=F.|last3=Alves|first3=J.|last4=Khamashta|first4=M. A.|last5=Simpson|first5=J.|last6=Hughes|first6=G. R. V.|last7=Buchanan|first7=N. M. M.|date=1996-02-01|title=INCREASED RATE OF LUPUS FLARE DURING PREGNANCY AND THE PUERPERIUM: A PROSPECTIVE STUDY OF 78 PREGNANCIES|url=https://academic.oup.com/rheumatology/article/35/2/133/1782393|journal=Rheumatology|language=en|volume=35|issue=2|pages=133–138|doi=10.1093/rheumatology/35.2.133|issn=1462-0324}}</ref> In a retrospective study of [[fibromyalgia]] patients based on personal interviews, nearly all patients surveyed experienced a worsening of symptoms during pregnancy, especially during the third trimester. Fibromyalgia did not appear to have an adverse effect on the outcome of pregnancy or the health of the baby.<ref>{{Cite journal|last=Østensen|first=Monika|last2=Rugelsjoen|first2=Anne|last3=Wigers|first3=Sigrid Horven|date=Jan 1997|title=The Effect of Reproductive Events and Alterations of Sex Hormone Levels on the Symptoms of Fibromyalgia|url=http://www.tandfonline.com/doi/abs/10.3109/03009749709065698|journal=Scandinavian Journal of Rheumatology|language=en|volume=26|issue=5|pages=355–360|doi=10.3109/03009749709065698|issn=0300-9742}}</ref>

== Related potential therapy ==

===Human Placental Extract===

HPE is used as a type of Complementary and Alternative Medicine therapy in various conditions involving chronic inflammation for its anti-inflammatory properties. In one interventional trial, injections of subcutaneous human placental extract (HPE) were found to improve symptoms in ME/CFS patients. Of note, the study did not find a difference between HPE injections and placebo. <ref>{{Cite journal|last=Park|first=Sat Byul|last2=Kim|first2=Kyu-Nam|last3=Sung|first3=Eunju|last4=Lee|first4=Suk Young|last5=Shin|first5=Ho Cheol|date=2016|title=Human Placental Extract as a Subcutaneous Injection Is Effective in Chronic Fatigue Syndrome: A Multi-Center, Double-Blind, Randomized, Placebo-Controlled Study|url=https://www.jstage.jst.go.jp/article/bpb/advpub/0/advpub_b15-00623/_article|journal=Biological & Pharmaceutical Bulletin|language=en|volume=39|issue=5|pages=674–679|doi=10.1248/bpb.b15-00623|issn=0918-6158}}</ref>
== See also ==

*[[Menstrual cycle]]
==Learn more==
*[http://emerge.org.au/about-mecfs/diagnosis/managing-symptoms-daily-basis/pregnancy-motherhood-mecfs/#.Vkp1cLSYe6x Pregnancy, Motherhood, Parenthood and ME/CFS]<ref>{{Cite news|url=http://emerge.org.au/about-mecfs/diagnosis/managing-symptoms-daily-basis/pregnancy-motherhood-mecfs/#.Vkp1cLSYe6x|title=Pregnancy, Motherhood, Parenthood and ME/CFS - Emerge Australia|work=Emerge Australia|access-date=2018-08-11|language=en-US}}</ref>
*2010, [http://www.njcfsa.org/wp-content/uploads/2010/09/Pregnancy-in-Women-with-ME-CFS.pdf Pregnancy in Women with Chronic Fatigue Syndrome (ME/CFS)]<ref name=":3">{{Cite news|url=http://www.njcfsa.org/wp-content/uploads/2010/09/Pregnancy-in-Women-with-ME-CFS.pdf|title=Pregnancy in Women with Chronic Fatigue Syndrome (ME/CFS)|last=Underhill|first=Rosemary|date=|work=NJCFSA|access-date=|archive-url=|archive-date=|dead-url=|publisher=New Jersey Chronic Fatigue Syndrome Association|format=PDF}}</ref>
*2016, [https://batemanhornecenter.org/pregnancy-and-mecfs/ Pregnancy and ME/CFS]<ref>{{Cite news|url=https://batemanhornecenter.org/pregnancy-and-mecfs/|title=Pregnancy and ME/CFS|last=Reynolds|first=Leigh|date=2016-07-06|work=Bateman Horne Center|access-date=2018-08-11|archive-url=|archive-date=|dead-url=|publisher=Bateman Horne Center|language=en-US}}</ref>
*[https://www.healthrising.org/blog/2014/03/02/pregnancy-chronic-fatigue-syndrome-four-mothers-talk-offer/ Pregnancy and Chronic Fatigue Syndrome-- Four Mothers Who've Been Through It Talk]

==References==
<references />
[[Category:Triggers and risk factors]]
[[Reproductive system‎]]

Epstein-Barr virus

2018-11-15T01:03:18Z

Paulitasofia1:/* Initial infection symptoms */

The Epstein-Barr virus (EBV) or HHV4 is a [[herpesvirus]]. It is the most common cause of infectious mononucleosis or "glandular fever," and infects 90% of adults worldwide.<ref name="Saha2016" /> It has been implicated in numerous immune diseases and chronic illnesses, including [[chronic fatigue syndrome]], [[multiple sclerosis]], [[myasthenia gravis]], and [[systemic lupus erythematosus]]. It is known to turn on "risk genes" for autoimmune disease in the cells it infects.<ref name=":0">{{Cite journal|last=Harley|first=John|date= 16 April 2018|title=Transcription factors operate across disease loci, with EBNA2 implicated in autoimmunity|url=https://www.nature.com/articles/s41588-018-0102-3|journal=Nature genetics|volume=|pages=|via=}}</ref><ref name=":1">{{Cite web|url=https://www.nih.gov/news-events/news-releases/epstein-barr-virus-protein-can-switch-risk-genes-autoimmune-diseases|title=Epstein-Barr virus protein can “switch on” risk genes for autoimmune diseases|last=|first=|date=16 April 2018|website=National Institutes of Health|archive-url=|archive-date=|dead-url=|access-date=}}</ref>

== Initial infection ==
[[File:Epstein-barr virus (ebv).jpg|thumb|A stained sample of Epstein-Barr virus.]]
Symptoms of EBV infection include:
* fatigue

* fever
* rash
* inflamed throat
* swollen lymph nodes
* enlarged spleen
* swollen liver<ref name=":2">{{Cite web|url=http://www.cdc.gov/epstein-barr/about-ebv.html|title=Epstein-barr {{!}} Mononucleosis {{!}} About Virus {{!}} Mono {{!}} CDC|date=2018-05-10|website=www.cdc.gov|language=en-us|access-date=2018-11-14}}</ref>

===Age of infection===

Most people acquire EBV in early childhood. Typically, young children who acquire EBV are either not symptomatic or have mild symptoms that are hard to distinguish from a cold or other other mild, childhood illnesses.

In adolescents and young adults, EBV can cause [[infectious mononucleosis]] (IM), also known as glandular fever.<ref name=":2" /> IM is characterized by [[fever]], [[sore throat]], swollen [[lymph nodes]], [[pain|body aches]], and [[fatigue]]. It generally resolves with rest and only rarely causes serious complications. It typically occurs in people who have not been exposed to EBV in early childhood, and in comparison, is more severe than infection in childhood (i.e., it can last for months).

Following initial infection, EBV can reactivate and has been shown to have many connections with various chronic illnesses. Relative to initial infections, reactivated EBV is much more severe.

==Transmission==

EBV is transmitted through bodily fluids, most commonly through saliva. The first time a person is infected with EBV, the person is contagious for weeks (even when not displaying symptoms). The virus then transitions to the latent or inactive form, and stays in the body. If the virus reactivates, the person will be contagious again.<ref name=":2" />

== Diagnosis ==
EBV infection is confirmed with blood tests that detect presence of antibodies. Nine out of ten adults have these antibodies, indicating that they have a current or past EBV infection.<ref name=":2" />

==Latency==

In healthy adults, the virus remains latent for life in memory [[B cell]]s. It is estimated that 1 in every one hundred thousand to one million circulating B cells carry EBV.<ref>{{Cite journal|last=Hsu|first=J. L.|last2=Glaser|first2=S. L.|date=2000-4|title=Epstein-barr virus-associated malignancies: epidemiologic patterns and etiologic implications|url=https://www.ncbi.nlm.nih.gov/pubmed/10781747/|journal=Critical Reviews in Oncology/Hematology|volume=34|issue=1|pages=27–53|issn=1040-8428|pmid=10781747}}</ref> In healthy hosts, EBV populations are kept in check by [[CD4]]<sup>+</sup> and [[CD8]]<sup>+</sup> [[T-cell]] responses.

The equilibrium can be disrupted in individuals with compromised [[immune system]]s such as patients with [[AIDS]] or transplant patients taking immune system suppressing drugs.<ref>{{Cite journal|last=Priatel|first=John J|last2=Chung|first2=Brian K|last3=Tsai|first3=Kevin|last4=Tan|first4=Rusung|date=2014-04-09|title=Natural killer T cell strategies to combat Epstein–Barr virus infection|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4063158/|journal=Oncoimmunology|volume=3|doi=10.4161/onci.28329|issn=2162-4011|pmc=PMC4063158|pmid=25050206}}</ref> It has been observed that these patients are more susceptible to EBV-related cancers, such as certain [[lymphoma]]s and [[carcinoma]]s.<ref>{{Cite journal|last=Pattle|first=Samuel B.|last2=Farrell|first2=Paul J.|date=2006-11|title=The role of Epstein-Barr virus in cancer|url=https://www.ncbi.nlm.nih.gov/pubmed/17049016|journal=Expert Opinion on Biological Therapy|volume=6|issue=11|pages=1193–1205|doi=10.1517/14712598.6.11.1193|issn=1744-7682|pmid=17049016}}</ref> In immunocompromised patients, EBV can induce lymphoproliferation, [[lymphoma]], and [[hemophagocytic lymphohistiocytosis]] (HLH).<ref>{{Cite journal|last=Tangye|first=Stuart|date=January 20, 2017|title=Human immunity against EBV—lessons from the clinic|url=http://jem.rupress.org/content/214/2/269|journal=Journal of Experimental Medicine|volume=|pages=|via=}}</ref>
===Natural killer T cells===

It is thought that [[natural killer T cell]]s (NKT) play a pivotal role in the control of EBV-infected B cells through their recognition of [[CD1d]] expressing cells.<ref>{{Cite journal|last=Priatel|first=John J|last2=Chung|first2=Brian K|last3=Tsai|first3=Kevin|last4=Tan|first4=Rusung|date=2014-04-09|title=Natural killer T cell strategies to combat Epstein–Barr virus infection|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4063158/|journal=Oncoimmunology|volume=3|doi=10.4161/onci.28329|issn=2162-4011|pmc=PMC4063158|pmid=25050206}}</ref>

==Neuronal infection==
A 2015 study<ref name="JhaHC2015" /> demonstrated that human [[neuron]]al cells could be directly and actively infected with EBV and another [[herpesvirus]], Kaposi's sarcoma-associated herpesvirus (KSHV).

Neuronal cells were infected with EBV or KSHV viruses which had been combined with a fluorescent protein so that the infection could be observed. The infection was seen to produce new virus cells (productive) and spread efficiently. Significantly, it not only infected surrounding neuronal cells but also nearby [[peripheral blood mononuclear cells]].

EBV is known to be linked to many neuronal diseases<ref name="Kleines2011" /> but this is the first evidence of how this may occur. The researchers note that this research supports the presence of EBV in neuronal diseases, but does not indicate why this is so.

==In human disease==

Epstein-Barr virus has been associated with a wide number of immune diseases including [[multiple sclerosis]], [[rheumatoid arthritis]], [[systemic lupus erythematosus]],<ref>{{Cite journal|last=Lossius|first=Andreas|date=December 2012|title=Epstein-Barr Virus in Systemic Lupus Erythematosus, Rheumatoid Arthritis and Multiple Sclerosis—Association and Causation|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3528287/|journal=Virus|volume=|pages=|via=}}</ref> [[Chronic fatigue syndrome]], and [[myasthenia gravis]]. EBV was recently discovered to turn on "risk genes" for autoimmune disease in the cells it infects. [[EBNA]]2, a protein produced by EBV-infected cells, and its related transcription factors activate half the human genes known to be associated with the risk for lupus as well as genes associated with several other autoimmune diseases including [[multiple sclerosis]], [[rheumatoid arthritis]], [[inflammatory bowel disease]], [[type 1 diabetes]], [[juvenile idiopathic arthritis]] and [[celiac disease]]. EBV activation can thus increase the risk of developing these diseases.<ref name=":0" /><ref name=":1" />

===Chronic fatigue syndrome===

A prospective study of 250 primary care patients revealed a higher prevalence of [[chronic fatigue syndrome]] after infectious [[mononucleosis]] (glandular fever) when compared to an ordinary upper respiratory tract infection.<ref>{{Cite journal|last=White|first=P. D.|last2=Thomas|first2=J. M.|last3=Amess|first3=J.|last4=Crawford|first4=D. H.|last5=Grover|first5=S. A.|last6=Kangro|first6=H. O.|last7=Clare|first7=A. W.|date=1998-12|title=Incidence, risk and prognosis of acute and chronic fatigue syndromes and psychiatric disorders after glandular fever|url=https://www.ncbi.nlm.nih.gov/pubmed/9926075|journal=The British Journal of Psychiatry: The Journal of Mental Science|volume=173|pages=475–481|issn=0007-1250|pmid=9926075}}</ref> Anti-early antigen titers to EBV were elevated in CFS patients and associated with worse symptoms.<ref>{{Cite journal|last=Schmaling|first=K. B.|last2=Jones|first2=J. F.|date=1996-1|title=MMPI profiles of patients with chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/8730646|journal=Journal of Psychosomatic Research|volume=40|issue=1|pages=67–74|issn=0022-3999|pmid=8730646}}</ref>

===Multiple sclerosis===

Infection later in life, high serum titers against EBV, and [[mononucleosis]] have all been associated with an increased risk of multiple sclerosis. MS relapses are correlated with EBV reactivation.<ref>{{Cite journal|last=Holmøy|first=Trygve|date=2008|title=Vitamin D status modulates the immune response to Epstein Barr virus: Synergistic effect of risk factors in multiple sclerosis|url=http://www.sciencedirect.com/science/article/pii/S0306987707003167|journal=Medical Hypotheses|volume=70|pages=|via=}}</ref>

Several studies by Alberto Ascherio, MD, DrPH, and his team at the Harvard School of Public Health have suggested that Epstein-Barr virus is involved in [[multiple sclerosis]], specifically in people with a certain immune-related gene and high levels of antibodies to EBV in their blood.<ref>{{Cite web|url=https://www.nationalmssociety.org/What-is-MS/What-Causes-MS/Viruses|title=Viruses|last=|first=|date=|website=National Multiple Sclerosis Society|archive-url=|archive-date=|dead-url=|access-date=11/14/18}}</ref>

=== Systemic lupus erythematosus ===
In a study of young patients with lupus, 99% had EBV as compared to 70% of healthy controls.<ref>{{Cite journal|last=James|first=JA|date=15 December 1997|title=An increased prevalence of Epstein-Barr virus infection in young patients suggests a possible etiology for systemic lupus erythematosus|url=https://www.jci.org/articles/view/119856|journal=The Journal of Clinical Investigation|volume=|pages=|via=}}</ref> Another study found that patients with SLE had an ∼40-fold increase in EBV viral loads compared with controls, likely stemming from altered [[t cell]] responses against EBV.<ref>{{Cite journal|last=Kang|first=Insoo|date=15 January 2004|title=Defective Control of Latent Epstein-Barr Virus Infection in Systemic Lupus Erythematosus|url=http://www.jimmunol.org/content/172/2/1287.short|journal=The Journal of Immunology|volume=|pages=|via=}}</ref>

===Myasthenia gravis===

[[B cell]]s from [[myasthenia gravis]] patient stimulated ''in vitro'' by Epstein-Barr virus produced [[acetylcholine]] autoantibodies.<ref>{{Cite journal|last=Brenner|first=T.|last2=Timore|first2=Y.|last3=Wirguin|first3=I.|last4=Abramsky|first4=O.|last5=Steinitz|first5=M.|date=1989-10|title=In vitro synthesis of antibodies to acetylcholine receptor by Epstein-Barr virus-stimulated B-lymphocytes derived from patients with myasthenia gravis|url=https://www.ncbi.nlm.nih.gov/pubmed/2553772|journal=Journal of Neuroimmunology|volume=24|issue=3|pages=217–222|issn=0165-5728|pmid=2553772}}</ref> Ongoing EBV infection of the [[thymus]] has been posited as a causative agent for the production of [[acetylcholine]] receptor autoantibodies in [[myasthenia gravis]].<ref>{{Cite journal|last=J.|first=Kaminski, Henry|last2=Janos|first2=Minarovits,|title=Epstein-barr virus: Trigger for autoimmunity?|url=http://www.academia.edu/20258853/Epstein-barr_virus_Trigger_for_autoimmunity/|journal=Annals of Neurology|language=en|issn=0364-5134}}</ref><ref>{{Cite web|url=http://journals.lww.com/neurologynow/_layouts/15/oaks.journals.mobile/post.aspx?blogId=2&postId=10|title=Official Brain & Life Home Page|website=journals.lww.com|language=en|access-date=2018-11-15}}</ref>

=== Gastrointestinal disease ===
One study of EBV in patients with [[gastritis]], [[Crohn's disease]], and [[ulcerative colitis]] and normal controls found essentially undetectable levels of EBV in normal gastric mucosa. However, EBV was detected in 46% of gastritis lesions, 44% of normal colonic mucosa, 55% of Crohn’s disease, and 64% of ulcerative colitis samples.<ref>{{Cite journal|last=Ryan|first=Julie|date=2013|title=Epstein-Barr Virus Infection is Common in Inflamed Gastrointestinal Mucosa|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3535492/|journal=Dig Dis Sci.|volume=|pages=|via=}}</ref>

===Lyme Disease===

Several herpesviruses including Epstein-Barr virus<ref name="Goossens1999" /> may cause false positives on Lyme Disease tests.

===X-MEN Disease===

A 2014 study found chronic Epstein-Barr infection was linked to a magnesium transporter([https://www.ncbi.nlm.nih.gov/gene/84061 MAGT-1]) mutation. Dysfunction in this transporter also resulted in decreased NK cell function, and neoplasia (sometimes-cancerous growths).<ref name="X-men_disease_1" /> This disorder, termed 'X-MEN' (for X-linked, EBV, and neoplasia) was identified as a [https://en.wikipedia.org/wiki/X-linked_recessive_inheritance recessive, X-linked disorder] that would therefore be many times more common in men.

Since chronic Epstein-Barr virus infection has been associated with chronic fatigue syndrome, this error in [[magnesium]] transport may be worth considering in male patients, especially with slow onset and history of childhood infection.<ref name="X-men_disease_1" /><ref name="X-men_disease_2" /> However, in this disorder, EBV would be seen as an indicator of the illness rather than the cause.

==Vitamin D==

Some recent research is finding links between EBV and [[Vitamin D]]

An Epstein-Barr virus protein EBNA-3 has an affinity for [[VDR]] and may actually block the activation of VDR-dependent genes by [[Vitamin D]].<ref>{{Cite journal|last=Yenamandra|first=Surya Pavan|last2=Hellman|first2=Ulf|last3=Kempkes|first3=Bettina|last4=Darekar|first4=Suhas Deoram|last5=Petermann|first5=Sabine|last6=Sculley|first6=Tom|last7=Klein|first7=George|last8=Kashuba|first8=Elena|date=2010-12|title=Epstein-Barr virus encoded EBNA-3 binds to vitamin D receptor and blocks activation of its target genes|url=https://www.ncbi.nlm.nih.gov/pubmed/20593215|journal=Cellular and molecular life sciences: CMLS|volume=67|issue=24|pages=4249–4256|doi=10.1007/s00018-010-0441-4|issn=1420-9071|pmid=20593215}}</ref>

[[Vitamin D receptor]] may be required for the normal development of [[natural killer T cell]]s that react to cells expressing [[CD1d]], as in cells infected by EBV.<ref>{{Cite journal|last=Yu|first=Sanhong|last2=Cantorna|first2=Margherita T.|date=2008-04-01|title=The vitamin D receptor is required for iNKT cell development|url=http://www.pnas.org/content/105/13/5207|journal=Proceedings of the National Academy of Sciences|language=en|volume=105|issue=13|pages=5207–5212|doi=10.1073/pnas.0711558105|issn=0027-8424|pmid=18364394}}</ref>

As low Vitamin D is also a risk factor for MS, some studies have attempt to find a link between low Vitamin D status, EBV and MS. One study of healthy individuals found no link between EBV load and Vitamin D status. However, over half the subjects were Vitamin D deficient and none had optimal levels<ref>{{Cite journal|last=Ramien|first=Caren|last2=Pachnio|first2=Annette|last3=Sisay|first3=Sofia|last4=Begum|first4=Jusnara|last5=Leese|first5=Alison|last6=Disanto|first6=Giulio|last7=Kuhle|first7=Jens|last8=Giovannoni|first8=Gavin|last9=Rickinson|first9=Alan|date=2014-5|title=Hypovitaminosis-D and EBV: no interdependence between two MS risk factors in a healthy young UK autumn cohort|url=https://www.ncbi.nlm.nih.gov/pubmed/24192216?dopt=Abstract|journal=Multiple Sclerosis (Houndmills, Basingstoke, England)|volume=20|issue=6|pages=751–753|doi=10.1177/1352458513509507|issn=1477-0970|pmid=24192216}}</ref> (i.e., above 100 nmol/l).

==Treatment==

There is no specific treatment for EBV, only treatment of symptoms, such as taking over-the-counter medications for pain and fever.<ref name=":2" /> EBV is thought to persistent harmlessly in immunocompetent individuals, but in those with compromised immune systems it has been associated with certain cancers and possibly autoimmune disease.

===Antivirals===

Several [[antiviral]]s are active against EBV including [[valganciclovir|valganciclovir,]] [[valacyclovir]]<ref>{{Cite journal|last=Hoshino|first=Yo|date=|title=Long-Term Administration of Valacyclovir Reduces the Number of Epstein-Barr Virus (EBV)-Infected B Cells but Not the Number of EBV DNA Copies per B Cell in Healthy Volunteers|url=http://jvi.asm.org/content/83/22/11857.full|journal=Journal of Virology|volume=|pages=|via=}}</ref>, [[acyclovir]]<ref>{{Cite journal|last=Rafaillidis|first=Pl|date=November 2013|title=Antiviral treatment for severe EBV infections in apparently immunocompetent patients|url=https://www.ncbi.nlm.nih.gov/pubmed/20739216|journal=Journal of Clinical Virology|volume=|pages=|via=}}</ref> and [[spironolactone]]<ref name="Verma2016" />.

[[Acyclovir]], an [[antiviral]] drug which inhibits (but does not destroy) herpesviruses, was shown to also inhibit the virus production. This suggests that EBV replicates via lytic replication.

A theoretical [[immunotherapy]] treatment proposes that inducing [[CD1d]] expression on EBV-infected B cells could prompt effective immune suppression of EBV by NKT cells.<ref>{{Cite journal|last=Priatel|first=John J|last2=Chung|first2=Brian K|last3=Tsai|first3=Kevin|last4=Tan|first4=Rusung|date=2014-04-09|title=Natural killer T cell strategies to combat Epstein–Barr virus infection|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4063158/|journal=Oncoimmunology|volume=3|doi=10.4161/onci.28329|issn=2162-4011|pmc=PMC4063158|pmid=25050206}}</ref>

===Rituximab===

[[Rituximab]] may be effective in completely eliminating Epstein-Barr virus infection from the peripheral blood.<ref>{{Cite journal|last=Diamantopoulos|first=Panagiotis T.|last2=Polonyfi|first2=Katerina|last3=Sofotasiou|first3=Maria|last4=Papadopoulou|first4=Vasiliki|last5=Kalala|first5=Fani|last6=Iliakis|first6=Theodoros|last7=Zervakis|first7=Kostantinos|last8=Tsilimidos|first8=Gerassimos|last9=Kouzis|first9=Panagiotis|date=2013-12|title=Rituximab in the treatment of EBV-positive low grade B-cell lymphoma|url=https://www.ncbi.nlm.nih.gov/pubmed/24324119|journal=Anticancer Research|volume=33|issue=12|pages=5693–5698|issn=1791-7530|pmid=24324119}}</ref> A study of seventeen patients with low-grade [[B cell]] lymphoma found that after three cycles of Rituximab, the virus had been completely eliminated from the peripheral blood in all but one patient.

===Herbs and nutraceuticals===

Herbs shown to have antiviral properties against EBV including [[licorice|licorice.]]<ref>{{Cite journal|last=Lin|first=Jung-Chung|last2=Cherng|first2=Jaw-Ming|last3=Hung|first3=Man-Shan|last4=Baltina|first4=Lidia A.|last5=Baltina|first5=Lia|last6=Kondratenko|first6=Rimma|date=2008-7|title=Inhibitory effects of some derivatives of glycyrrhizic acid against Epstein-Barr virus infection: structure-activity relationships|url=https://www.ncbi.nlm.nih.gov/pubmed/18423902|journal=Antiviral Research|volume=79|issue=1|pages=6–11|doi=10.1016/j.antiviral.2008.01.160|issn=0166-3542|pmid=18423902}}</ref> [[Vitamin C]] and Vitamin D<ref>{{Cite journal|last=Rolf|first=L|date=July 2017|title=Exploring the effect of vitamin D3 supplementation on the anti-EBV antibody response in relapsing-remitting multiple sclerosis|url=https://www.ncbi.nlm.nih.gov/pubmed/28731372|journal=Multiple Sclerosis|volume=|pages=|via=}}</ref> might also decrease duration and severity of the symptoms of EBV infection.<ref>{{Cite journal|last=Mikirova|first=N|date=May 2014|title=Effect of high dose vitamin C on Epstein-Barr viral infection|url=https://www.ncbi.nlm.nih.gov/pubmed/24793092|journal=Med Sci Monit|volume=|pages=|via=}}</ref>

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[[Category:Infectious agents]]
[[Category:Triggers and risk factors]]
[[Category:Virology]]

Epstein-Barr virus

2018-11-15T01:00:38Z

Paulitasofia1:/* Treatment */

The Epstein-Barr virus (EBV) or HHV4 is a [[herpesvirus]]. It is the most common cause of infectious mononucleosis or "glandular fever," and infects 90% of adults worldwide.<ref name="Saha2016" /> It has been implicated in numerous immune diseases and chronic illnesses, including [[chronic fatigue syndrome]], [[multiple sclerosis]], [[myasthenia gravis]], and [[systemic lupus erythematosus]]. It is known to turn on "risk genes" for autoimmune disease in the cells it infects.<ref name=":0">{{Cite journal|last=Harley|first=John|date= 16 April 2018|title=Transcription factors operate across disease loci, with EBNA2 implicated in autoimmunity|url=https://www.nature.com/articles/s41588-018-0102-3|journal=Nature genetics|volume=|pages=|via=}}</ref><ref name=":1">{{Cite web|url=https://www.nih.gov/news-events/news-releases/epstein-barr-virus-protein-can-switch-risk-genes-autoimmune-diseases|title=Epstein-Barr virus protein can “switch on” risk genes for autoimmune diseases|last=|first=|date=16 April 2018|website=National Institutes of Health|archive-url=|archive-date=|dead-url=|access-date=}}</ref>

== Initial infection symptoms ==
[[File:Epstein-barr virus (ebv).jpg|thumb|A stained sample of Epstein-Barr virus.]]
Symptoms of EBV infection include:
* fatigue

* fever
* rash
* inflamed throat
* swollen lymph nodes
* enlarged spleen
* swollen liver<ref name=":2">{{Cite web|url=http://www.cdc.gov/epstein-barr/about-ebv.html|title=Epstein-barr {{!}} Mononucleosis {{!}} About Virus {{!}} Mono {{!}} CDC|date=2018-05-10|website=www.cdc.gov|language=en-us|access-date=2018-11-14}}</ref>

===Age of infection===

Most people acquire EBV in early childhood. Typically, young children who acquire EBV are either not symptomatic or have mild symptoms that are hard to distinguish from a cold or other other mild, childhood illnesses.

In adolescents and young adults, EBV can cause [[infectious mononucleosis]] (IM), also known as glandular fever.<ref name=":2" /> IM is characterized by [[fever]], [[sore throat]], swollen [[lymph nodes]], [[pain|body aches]], and [[fatigue]]. It generally resolves with rest and only rarely causes serious complications. It typically occurs in people who have not been exposed to EBV in early childhood, and in comparison, is more severe than infection in childhood (i.e., it can last for months).

Following initial infection, EBV can reactivate and has been shown to have many connections with various chronic illnesses. Relative to initial infections, reactivated EBV is much more severe.

==Transmission==

EBV is transmitted through bodily fluids, most commonly through saliva. The first time a person is infected with EBV, the person is contagious for weeks (even when not displaying symptoms). The virus then transitions to the latent or inactive form, and stays in the body. If the virus reactivates, the person will be contagious again.<ref name=":2" />

== Diagnosis ==
EBV infection is confirmed with blood tests that detect presence of antibodies. Nine out of ten adults have these antibodies, indicating that they have a current or past EBV infection.<ref name=":2" />

==Latency==

In healthy adults, the virus remains latent for life in memory [[B cell]]s. It is estimated that 1 in every one hundred thousand to one million circulating B cells carry EBV.<ref>{{Cite journal|last=Hsu|first=J. L.|last2=Glaser|first2=S. L.|date=2000-4|title=Epstein-barr virus-associated malignancies: epidemiologic patterns and etiologic implications|url=https://www.ncbi.nlm.nih.gov/pubmed/10781747/|journal=Critical Reviews in Oncology/Hematology|volume=34|issue=1|pages=27–53|issn=1040-8428|pmid=10781747}}</ref> In healthy hosts, EBV populations are kept in check by [[CD4]]<sup>+</sup> and [[CD8]]<sup>+</sup> [[T-cell]] responses.

The equilibrium can be disrupted in individuals with compromised [[immune system]]s such as patients with [[AIDS]] or transplant patients taking immune system suppressing drugs.<ref>{{Cite journal|last=Priatel|first=John J|last2=Chung|first2=Brian K|last3=Tsai|first3=Kevin|last4=Tan|first4=Rusung|date=2014-04-09|title=Natural killer T cell strategies to combat Epstein–Barr virus infection|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4063158/|journal=Oncoimmunology|volume=3|doi=10.4161/onci.28329|issn=2162-4011|pmc=PMC4063158|pmid=25050206}}</ref> It has been observed that these patients are more susceptible to EBV-related cancers, such as certain [[lymphoma]]s and [[carcinoma]]s.<ref>{{Cite journal|last=Pattle|first=Samuel B.|last2=Farrell|first2=Paul J.|date=2006-11|title=The role of Epstein-Barr virus in cancer|url=https://www.ncbi.nlm.nih.gov/pubmed/17049016|journal=Expert Opinion on Biological Therapy|volume=6|issue=11|pages=1193–1205|doi=10.1517/14712598.6.11.1193|issn=1744-7682|pmid=17049016}}</ref> In immunocompromised patients, EBV can induce lymphoproliferation, [[lymphoma]], and [[hemophagocytic lymphohistiocytosis]] (HLH).<ref>{{Cite journal|last=Tangye|first=Stuart|date=January 20, 2017|title=Human immunity against EBV—lessons from the clinic|url=http://jem.rupress.org/content/214/2/269|journal=Journal of Experimental Medicine|volume=|pages=|via=}}</ref>
===Natural killer T cells===

It is thought that [[natural killer T cell]]s (NKT) play a pivotal role in the control of EBV-infected B cells through their recognition of [[CD1d]] expressing cells.<ref>{{Cite journal|last=Priatel|first=John J|last2=Chung|first2=Brian K|last3=Tsai|first3=Kevin|last4=Tan|first4=Rusung|date=2014-04-09|title=Natural killer T cell strategies to combat Epstein–Barr virus infection|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4063158/|journal=Oncoimmunology|volume=3|doi=10.4161/onci.28329|issn=2162-4011|pmc=PMC4063158|pmid=25050206}}</ref>

==Neuronal infection==
A 2015 study<ref name="JhaHC2015" /> demonstrated that human [[neuron]]al cells could be directly and actively infected with EBV and another [[herpesvirus]], Kaposi's sarcoma-associated herpesvirus (KSHV).

Neuronal cells were infected with EBV or KSHV viruses which had been combined with a fluorescent protein so that the infection could be observed. The infection was seen to produce new virus cells (productive) and spread efficiently. Significantly, it not only infected surrounding neuronal cells but also nearby [[peripheral blood mononuclear cells]].

EBV is known to be linked to many neuronal diseases<ref name="Kleines2011" /> but this is the first evidence of how this may occur. The researchers note that this research supports the presence of EBV in neuronal diseases, but does not indicate why this is so.

==In human disease==

Epstein-Barr virus has been associated with a wide number of immune diseases including [[multiple sclerosis]], [[rheumatoid arthritis]], [[systemic lupus erythematosus]],<ref>{{Cite journal|last=Lossius|first=Andreas|date=December 2012|title=Epstein-Barr Virus in Systemic Lupus Erythematosus, Rheumatoid Arthritis and Multiple Sclerosis—Association and Causation|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3528287/|journal=Virus|volume=|pages=|via=}}</ref> [[Chronic fatigue syndrome]], and [[myasthenia gravis]]. EBV was recently discovered to turn on "risk genes" for autoimmune disease in the cells it infects. [[EBNA]]2, a protein produced by EBV-infected cells, and its related transcription factors activate half the human genes known to be associated with the risk for lupus as well as genes associated with several other autoimmune diseases including [[multiple sclerosis]], [[rheumatoid arthritis]], [[inflammatory bowel disease]], [[type 1 diabetes]], [[juvenile idiopathic arthritis]] and [[celiac disease]]. EBV activation can thus increase the risk of developing these diseases.<ref name=":0" /><ref name=":1" />

===Chronic fatigue syndrome===

A prospective study of 250 primary care patients revealed a higher prevalence of [[chronic fatigue syndrome]] after infectious [[mononucleosis]] (glandular fever) when compared to an ordinary upper respiratory tract infection.<ref>{{Cite journal|last=White|first=P. D.|last2=Thomas|first2=J. M.|last3=Amess|first3=J.|last4=Crawford|first4=D. H.|last5=Grover|first5=S. A.|last6=Kangro|first6=H. O.|last7=Clare|first7=A. W.|date=1998-12|title=Incidence, risk and prognosis of acute and chronic fatigue syndromes and psychiatric disorders after glandular fever|url=https://www.ncbi.nlm.nih.gov/pubmed/9926075|journal=The British Journal of Psychiatry: The Journal of Mental Science|volume=173|pages=475–481|issn=0007-1250|pmid=9926075}}</ref> Anti-early antigen titers to EBV were elevated in CFS patients and associated with worse symptoms.<ref>{{Cite journal|last=Schmaling|first=K. B.|last2=Jones|first2=J. F.|date=1996-1|title=MMPI profiles of patients with chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/8730646|journal=Journal of Psychosomatic Research|volume=40|issue=1|pages=67–74|issn=0022-3999|pmid=8730646}}</ref>

===Multiple sclerosis===

Infection later in life, high serum titers against EBV, and [[mononucleosis]] have all been associated with an increased risk of multiple sclerosis. MS relapses are correlated with EBV reactivation.<ref>{{Cite journal|last=Holmøy|first=Trygve|date=2008|title=Vitamin D status modulates the immune response to Epstein Barr virus: Synergistic effect of risk factors in multiple sclerosis|url=http://www.sciencedirect.com/science/article/pii/S0306987707003167|journal=Medical Hypotheses|volume=70|pages=|via=}}</ref>

Several studies by Alberto Ascherio, MD, DrPH, and his team at the Harvard School of Public Health have suggested that Epstein-Barr virus is involved in [[multiple sclerosis]], specifically in people with a certain immune-related gene and high levels of antibodies to EBV in their blood.<ref>{{Cite web|url=https://www.nationalmssociety.org/What-is-MS/What-Causes-MS/Viruses|title=Viruses|last=|first=|date=|website=National Multiple Sclerosis Society|archive-url=|archive-date=|dead-url=|access-date=11/14/18}}</ref>

=== Systemic lupus erythematosus ===
In a study of young patients with lupus, 99% had EBV as compared to 70% of healthy controls.<ref>{{Cite journal|last=James|first=JA|date=15 December 1997|title=An increased prevalence of Epstein-Barr virus infection in young patients suggests a possible etiology for systemic lupus erythematosus|url=https://www.jci.org/articles/view/119856|journal=The Journal of Clinical Investigation|volume=|pages=|via=}}</ref> Another study found that patients with SLE had an ∼40-fold increase in EBV viral loads compared with controls, likely stemming from altered [[t cell]] responses against EBV.<ref>{{Cite journal|last=Kang|first=Insoo|date=15 January 2004|title=Defective Control of Latent Epstein-Barr Virus Infection in Systemic Lupus Erythematosus|url=http://www.jimmunol.org/content/172/2/1287.short|journal=The Journal of Immunology|volume=|pages=|via=}}</ref>

===Myasthenia gravis===

[[B cell]]s from [[myasthenia gravis]] patient stimulated ''in vitro'' by Epstein-Barr virus produced [[acetylcholine]] autoantibodies.<ref>{{Cite journal|last=Brenner|first=T.|last2=Timore|first2=Y.|last3=Wirguin|first3=I.|last4=Abramsky|first4=O.|last5=Steinitz|first5=M.|date=1989-10|title=In vitro synthesis of antibodies to acetylcholine receptor by Epstein-Barr virus-stimulated B-lymphocytes derived from patients with myasthenia gravis|url=https://www.ncbi.nlm.nih.gov/pubmed/2553772|journal=Journal of Neuroimmunology|volume=24|issue=3|pages=217–222|issn=0165-5728|pmid=2553772}}</ref> Ongoing EBV infection of the [[thymus]] has been posited as a causative agent for the production of [[acetylcholine]] receptor autoantibodies in [[myasthenia gravis]].<ref>{{Cite journal|last=J.|first=Kaminski, Henry|last2=Janos|first2=Minarovits,|title=Epstein-barr virus: Trigger for autoimmunity?|url=http://www.academia.edu/20258853/Epstein-barr_virus_Trigger_for_autoimmunity/|journal=Annals of Neurology|language=en|issn=0364-5134}}</ref><ref>{{Cite web|url=http://journals.lww.com/neurologynow/_layouts/15/oaks.journals.mobile/post.aspx?blogId=2&postId=10|title=Official Brain & Life Home Page|website=journals.lww.com|language=en|access-date=2018-11-15}}</ref>

=== Gastrointestinal disease ===
One study of EBV in patients with [[gastritis]], [[Crohn's disease]], and [[ulcerative colitis]] and normal controls found essentially undetectable levels of EBV in normal gastric mucosa. However, EBV was detected in 46% of gastritis lesions, 44% of normal colonic mucosa, 55% of Crohn’s disease, and 64% of ulcerative colitis samples.<ref>{{Cite journal|last=Ryan|first=Julie|date=2013|title=Epstein-Barr Virus Infection is Common in Inflamed Gastrointestinal Mucosa|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3535492/|journal=Dig Dis Sci.|volume=|pages=|via=}}</ref>

===Lyme Disease===

Several herpesviruses including Epstein-Barr virus<ref name="Goossens1999" /> may cause false positives on Lyme Disease tests.

===X-MEN Disease===

A 2014 study found chronic Epstein-Barr infection was linked to a magnesium transporter([https://www.ncbi.nlm.nih.gov/gene/84061 MAGT-1]) mutation. Dysfunction in this transporter also resulted in decreased NK cell function, and neoplasia (sometimes-cancerous growths).<ref name="X-men_disease_1" /> This disorder, termed 'X-MEN' (for X-linked, EBV, and neoplasia) was identified as a [https://en.wikipedia.org/wiki/X-linked_recessive_inheritance recessive, X-linked disorder] that would therefore be many times more common in men.

Since chronic Epstein-Barr virus infection has been associated with chronic fatigue syndrome, this error in [[magnesium]] transport may be worth considering in male patients, especially with slow onset and history of childhood infection.<ref name="X-men_disease_1" /><ref name="X-men_disease_2" /> However, in this disorder, EBV would be seen as an indicator of the illness rather than the cause.

==Vitamin D==

Some recent research is finding links between EBV and [[Vitamin D]]

An Epstein-Barr virus protein EBNA-3 has an affinity for [[VDR]] and may actually block the activation of VDR-dependent genes by [[Vitamin D]].<ref>{{Cite journal|last=Yenamandra|first=Surya Pavan|last2=Hellman|first2=Ulf|last3=Kempkes|first3=Bettina|last4=Darekar|first4=Suhas Deoram|last5=Petermann|first5=Sabine|last6=Sculley|first6=Tom|last7=Klein|first7=George|last8=Kashuba|first8=Elena|date=2010-12|title=Epstein-Barr virus encoded EBNA-3 binds to vitamin D receptor and blocks activation of its target genes|url=https://www.ncbi.nlm.nih.gov/pubmed/20593215|journal=Cellular and molecular life sciences: CMLS|volume=67|issue=24|pages=4249–4256|doi=10.1007/s00018-010-0441-4|issn=1420-9071|pmid=20593215}}</ref>

[[Vitamin D receptor]] may be required for the normal development of [[natural killer T cell]]s that react to cells expressing [[CD1d]], as in cells infected by EBV.<ref>{{Cite journal|last=Yu|first=Sanhong|last2=Cantorna|first2=Margherita T.|date=2008-04-01|title=The vitamin D receptor is required for iNKT cell development|url=http://www.pnas.org/content/105/13/5207|journal=Proceedings of the National Academy of Sciences|language=en|volume=105|issue=13|pages=5207–5212|doi=10.1073/pnas.0711558105|issn=0027-8424|pmid=18364394}}</ref>

As low Vitamin D is also a risk factor for MS, some studies have attempt to find a link between low Vitamin D status, EBV and MS. One study of healthy individuals found no link between EBV load and Vitamin D status. However, over half the subjects were Vitamin D deficient and none had optimal levels<ref>{{Cite journal|last=Ramien|first=Caren|last2=Pachnio|first2=Annette|last3=Sisay|first3=Sofia|last4=Begum|first4=Jusnara|last5=Leese|first5=Alison|last6=Disanto|first6=Giulio|last7=Kuhle|first7=Jens|last8=Giovannoni|first8=Gavin|last9=Rickinson|first9=Alan|date=2014-5|title=Hypovitaminosis-D and EBV: no interdependence between two MS risk factors in a healthy young UK autumn cohort|url=https://www.ncbi.nlm.nih.gov/pubmed/24192216?dopt=Abstract|journal=Multiple Sclerosis (Houndmills, Basingstoke, England)|volume=20|issue=6|pages=751–753|doi=10.1177/1352458513509507|issn=1477-0970|pmid=24192216}}</ref> (i.e., above 100 nmol/l).

==Treatment==

There is no specific treatment for EBV, only treatment of symptoms, such as taking over-the-counter medications for pain and fever.<ref name=":2" /> EBV is thought to persistent harmlessly in immunocompetent individuals, but in those with compromised immune systems it has been associated with certain cancers and possibly autoimmune disease.

===Antivirals===

Several [[antiviral]]s are active against EBV including [[valganciclovir|valganciclovir,]] [[valacyclovir]]<ref>{{Cite journal|last=Hoshino|first=Yo|date=|title=Long-Term Administration of Valacyclovir Reduces the Number of Epstein-Barr Virus (EBV)-Infected B Cells but Not the Number of EBV DNA Copies per B Cell in Healthy Volunteers|url=http://jvi.asm.org/content/83/22/11857.full|journal=Journal of Virology|volume=|pages=|via=}}</ref>, [[acyclovir]]<ref>{{Cite journal|last=Rafaillidis|first=Pl|date=November 2013|title=Antiviral treatment for severe EBV infections in apparently immunocompetent patients|url=https://www.ncbi.nlm.nih.gov/pubmed/20739216|journal=Journal of Clinical Virology|volume=|pages=|via=}}</ref> and [[spironolactone]]<ref name="Verma2016" />.

[[Acyclovir]], an [[antiviral]] drug which inhibits (but does not destroy) herpesviruses, was shown to also inhibit the virus production. This suggests that EBV replicates via lytic replication.

A theoretical [[immunotherapy]] treatment proposes that inducing [[CD1d]] expression on EBV-infected B cells could prompt effective immune suppression of EBV by NKT cells.<ref>{{Cite journal|last=Priatel|first=John J|last2=Chung|first2=Brian K|last3=Tsai|first3=Kevin|last4=Tan|first4=Rusung|date=2014-04-09|title=Natural killer T cell strategies to combat Epstein–Barr virus infection|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4063158/|journal=Oncoimmunology|volume=3|doi=10.4161/onci.28329|issn=2162-4011|pmc=PMC4063158|pmid=25050206}}</ref>

===Rituximab===

[[Rituximab]] may be effective in completely eliminating Epstein-Barr virus infection from the peripheral blood.<ref>{{Cite journal|last=Diamantopoulos|first=Panagiotis T.|last2=Polonyfi|first2=Katerina|last3=Sofotasiou|first3=Maria|last4=Papadopoulou|first4=Vasiliki|last5=Kalala|first5=Fani|last6=Iliakis|first6=Theodoros|last7=Zervakis|first7=Kostantinos|last8=Tsilimidos|first8=Gerassimos|last9=Kouzis|first9=Panagiotis|date=2013-12|title=Rituximab in the treatment of EBV-positive low grade B-cell lymphoma|url=https://www.ncbi.nlm.nih.gov/pubmed/24324119|journal=Anticancer Research|volume=33|issue=12|pages=5693–5698|issn=1791-7530|pmid=24324119}}</ref> A study of seventeen patients with low-grade [[B cell]] lymphoma found that after three cycles of Rituximab, the virus had been completely eliminated from the peripheral blood in all but one patient.

===Herbs and nutraceuticals===

Herbs shown to have antiviral properties against EBV including [[licorice|licorice.]]<ref>{{Cite journal|last=Lin|first=Jung-Chung|last2=Cherng|first2=Jaw-Ming|last3=Hung|first3=Man-Shan|last4=Baltina|first4=Lidia A.|last5=Baltina|first5=Lia|last6=Kondratenko|first6=Rimma|date=2008-7|title=Inhibitory effects of some derivatives of glycyrrhizic acid against Epstein-Barr virus infection: structure-activity relationships|url=https://www.ncbi.nlm.nih.gov/pubmed/18423902|journal=Antiviral Research|volume=79|issue=1|pages=6–11|doi=10.1016/j.antiviral.2008.01.160|issn=0166-3542|pmid=18423902}}</ref> [[Vitamin C]] and Vitamin D<ref>{{Cite journal|last=Rolf|first=L|date=July 2017|title=Exploring the effect of vitamin D3 supplementation on the anti-EBV antibody response in relapsing-remitting multiple sclerosis|url=https://www.ncbi.nlm.nih.gov/pubmed/28731372|journal=Multiple Sclerosis|volume=|pages=|via=}}</ref> might also decrease duration and severity of the symptoms of EBV infection.<ref>{{Cite journal|last=Mikirova|first=N|date=May 2014|title=Effect of high dose vitamin C on Epstein-Barr viral infection|url=https://www.ncbi.nlm.nih.gov/pubmed/24793092|journal=Med Sci Monit|volume=|pages=|via=}}</ref>

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[[Category:Infectious agents]]
[[Category:Triggers and risk factors]]
[[Category:Virology]]

Epstein-Barr virus

2018-11-15T00:46:01Z

Paulitasofia1:reference cleanup

[[File:Epstein-barr virus (ebv).jpg|thumb|A stained sample of Epstein-Barr virus.]]
The Epstein-Barr virus (EBV) or HHV4 is a [[herpesvirus]]. It is the most common cause of infectious mononucleosis or "glandular fever," and infects 90% of adults worldwide.<ref name="Saha2016" /> It has been implicated in numerous immune diseases including [[chronic fatigue syndrome]], [[multiple sclerosis]], [[myasthenia gravis]], and [[systemic lupus erythematosus]]. It is known to turn on "risk genes" for autoimmune disease in the cells it infects.<ref name=":0">{{Cite journal|last=Harley|first=John|date= 16 April 2018|title=Transcription factors operate across disease loci, with EBNA2 implicated in autoimmunity|url=https://www.nature.com/articles/s41588-018-0102-3|journal=Nature genetics|volume=|pages=|via=}}</ref><ref name=":1">{{Cite web|url=https://www.nih.gov/news-events/news-releases/epstein-barr-virus-protein-can-switch-risk-genes-autoimmune-diseases|title=Epstein-Barr virus protein can “switch on” risk genes for autoimmune diseases|last=|first=|date=16 April 2018|website=National Institutes of Health|archive-url=|archive-date=|dead-url=|access-date=}}</ref>

== Symptoms ==
Symptoms of EBV infection include:
* fatigue

* fever
* rash
* inflamed throat
* swollen lymph nodes
* enlarged spleen
* swollen liver<ref name=":2">{{Cite web|url=http://www.cdc.gov/epstein-barr/about-ebv.html|title=Epstein-barr {{!}} Mononucleosis {{!}} About Virus {{!}} Mono {{!}} CDC|date=2018-05-10|website=www.cdc.gov|language=en-us|access-date=2018-11-14}}</ref>

==Initial infection==

===Age of infection===

Most people acquire EBV in early childhood. Typically, young children who acquire EBV are either not symptomatic or have mild symptoms that are hard to distinguish from a cold or other other mild, childhood illnesses.

In adolescents and young adults, EBV can cause [[infectious mononucleosis]] (IM), also known as glandular fever.<ref name=":2" /> IM is characterized by [[fever]], [[sore throat]], swollen [[lymph nodes]], [[pain|body aches]], and [[fatigue]]. It generally resolves with rest and only rarely causes serious complications.

==Transmission==

EBV is transmitted through bodily fluids, most commonly through saliva. The first time a person is infected with EBV, the person is contagious for weeks (even when not displaying symptoms). The virus then transitions to the latent or inactive form, and stays in the body. If the virus reactivates, the person will be contagious again.<ref name=":2" />

== Diagnosis ==
EBV infection is confirmed with blood tests that detect presence of antibodies. Nine out of ten adults have these antibodies, indicating that they have a current or past EBV infection.<ref name=":2" />

==Latency==

In healthy adults, the virus remains latent for life in memory [[B cell]]s. It is estimated that 1 in every one hundred thousand to one million circulating B cells carry EBV.<ref>{{Cite journal|last=Hsu|first=J. L.|last2=Glaser|first2=S. L.|date=2000-4|title=Epstein-barr virus-associated malignancies: epidemiologic patterns and etiologic implications|url=https://www.ncbi.nlm.nih.gov/pubmed/10781747/|journal=Critical Reviews in Oncology/Hematology|volume=34|issue=1|pages=27–53|issn=1040-8428|pmid=10781747}}</ref> In healthy hosts, EBV populations are kept in check by [[CD4]]<sup>+</sup> and [[CD8]]<sup>+</sup> [[T-cell]] responses.

The equilibrium can be disrupted in individuals with compromised [[immune system]]s such as patients with [[AIDS]] or transplant patients taking immune system suppressing drugs.<ref>{{Cite journal|last=Priatel|first=John J|last2=Chung|first2=Brian K|last3=Tsai|first3=Kevin|last4=Tan|first4=Rusung|date=2014-04-09|title=Natural killer T cell strategies to combat Epstein–Barr virus infection|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4063158/|journal=Oncoimmunology|volume=3|doi=10.4161/onci.28329|issn=2162-4011|pmc=PMC4063158|pmid=25050206}}</ref> It has been observed that these patients are more susceptible to EBV-related cancers, such as certain [[lymphoma]]s and [[carcinoma]]s.<ref>{{Cite journal|last=Pattle|first=Samuel B.|last2=Farrell|first2=Paul J.|date=2006-11|title=The role of Epstein-Barr virus in cancer|url=https://www.ncbi.nlm.nih.gov/pubmed/17049016|journal=Expert Opinion on Biological Therapy|volume=6|issue=11|pages=1193–1205|doi=10.1517/14712598.6.11.1193|issn=1744-7682|pmid=17049016}}</ref> In immunocompromised patients, EBV can induce lymphoproliferation, [[lymphoma]], and [[hemophagocytic lymphohistiocytosis]] (HLH).<ref>{{Cite journal|last=Tangye|first=Stuart|date=January 20, 2017|title=Human immunity against EBV—lessons from the clinic|url=http://jem.rupress.org/content/214/2/269|journal=Journal of Experimental Medicine|volume=|pages=|via=}}</ref>
===Natural killer T cells===

It is thought that [[natural killer T cell]]s (NKT) play a pivotal role in the control of EBV-infected B cells through their recognition of [[CD1d]] expressing cells.<ref>{{Cite journal|last=Priatel|first=John J|last2=Chung|first2=Brian K|last3=Tsai|first3=Kevin|last4=Tan|first4=Rusung|date=2014-04-09|title=Natural killer T cell strategies to combat Epstein–Barr virus infection|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4063158/|journal=Oncoimmunology|volume=3|doi=10.4161/onci.28329|issn=2162-4011|pmc=PMC4063158|pmid=25050206}}</ref>

==Neuronal infection==
A 2015 study<ref name="JhaHC2015" /> demonstrated that human [[neuron]]al cells could be directly and actively infected with EBV and another [[herpesvirus]], Kaposi's sarcoma-associated herpesvirus (KSHV).

Neuronal cells were infected with EBV or KSHV viruses which had been combined with a fluorescent protein so that the infection could be observed. The infection was seen to produce new virus cells (productive) and spread efficiently. Significantly, it not only infected surrounding neuronal cells but also nearby [[peripheral blood mononuclear cells]].

EBV is known to be linked to many neuronal diseases<ref name="Kleines2011" /> but this is the first evidence of how this may occur. The researchers note that this research supports the presence of EBV in neuronal diseases, but does not indicate why this is so.

==In human disease==

Epstein-Barr virus has been associated with a wide number of immune diseases including [[multiple sclerosis]], [[rheumatoid arthritis]], [[systemic lupus erythematosus]],<ref>{{Cite journal|last=Lossius|first=Andreas|date=December 2012|title=Epstein-Barr Virus in Systemic Lupus Erythematosus, Rheumatoid Arthritis and Multiple Sclerosis—Association and Causation|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3528287/|journal=Virus|volume=|pages=|via=}}</ref> [[Chronic fatigue syndrome]], and [[myasthenia gravis]]. EBV was recently discovered to turn on "risk genes" for autoimmune disease in the cells it infects. [[EBNA]]2, a protein produced by EBV-infected cells, and its related transcription factors activate half the human genes known to be associated with the risk for lupus as well as genes associated with several other autoimmune diseases including [[multiple sclerosis]], [[rheumatoid arthritis]], [[inflammatory bowel disease]], [[type 1 diabetes]], [[juvenile idiopathic arthritis]] and [[celiac disease]]. EBV activation can thus increase the risk of developing these diseases.<ref name=":0" /><ref name=":1" />

===Chronic fatigue syndrome===

A prospective study of 250 primary care patients revealed a higher prevalence of [[chronic fatigue syndrome]] after infectious [[mononucleosis]] (glandular fever) when compared to an ordinary upper respiratory tract infection.<ref>{{Cite journal|last=White|first=P. D.|last2=Thomas|first2=J. M.|last3=Amess|first3=J.|last4=Crawford|first4=D. H.|last5=Grover|first5=S. A.|last6=Kangro|first6=H. O.|last7=Clare|first7=A. W.|date=1998-12|title=Incidence, risk and prognosis of acute and chronic fatigue syndromes and psychiatric disorders after glandular fever|url=https://www.ncbi.nlm.nih.gov/pubmed/9926075|journal=The British Journal of Psychiatry: The Journal of Mental Science|volume=173|pages=475–481|issn=0007-1250|pmid=9926075}}</ref> Anti-early antigen titers to EBV were elevated in CFS patients and associated with worse symptoms.<ref>{{Cite journal|last=Schmaling|first=K. B.|last2=Jones|first2=J. F.|date=1996-1|title=MMPI profiles of patients with chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/8730646|journal=Journal of Psychosomatic Research|volume=40|issue=1|pages=67–74|issn=0022-3999|pmid=8730646}}</ref>

===Multiple sclerosis===

Infection later in life, high serum titers against EBV, and [[mononucleosis]] have all been associated with an increased risk of multiple sclerosis. MS relapses are correlated with EBV reactivation.<ref>{{Cite journal|last=Holmøy|first=Trygve|date=2008|title=Vitamin D status modulates the immune response to Epstein Barr virus: Synergistic effect of risk factors in multiple sclerosis|url=http://www.sciencedirect.com/science/article/pii/S0306987707003167|journal=Medical Hypotheses|volume=70|pages=|via=}}</ref>

Several studies by Alberto Ascherio, MD, DrPH, and his team at the Harvard School of Public Health have suggested that Epstein-Barr virus is involved in [[multiple sclerosis]], specifically in people with a certain immune-related gene and high levels of antibodies to EBV in their blood.<ref>{{Cite web|url=https://www.nationalmssociety.org/What-is-MS/What-Causes-MS/Viruses|title=Viruses|last=|first=|date=|website=National Multiple Sclerosis Society|archive-url=|archive-date=|dead-url=|access-date=11/14/18}}</ref>

=== Systemic lupus erythematosus ===
In a study of young patients with lupus, 99% had EBV as compared to 70% of healthy controls.<ref>{{Cite journal|last=James|first=JA|date=15 December 1997|title=An increased prevalence of Epstein-Barr virus infection in young patients suggests a possible etiology for systemic lupus erythematosus|url=https://www.jci.org/articles/view/119856|journal=The Journal of Clinical Investigation|volume=|pages=|via=}}</ref> Another study found that patients with SLE had an ∼40-fold increase in EBV viral loads compared with controls, likely stemming from altered [[t cell]] responses against EBV.<ref>{{Cite journal|last=Kang|first=Insoo|date=15 January 2004|title=Defective Control of Latent Epstein-Barr Virus Infection in Systemic Lupus Erythematosus|url=http://www.jimmunol.org/content/172/2/1287.short|journal=The Journal of Immunology|volume=|pages=|via=}}</ref>

===Myasthenia gravis===

[[B cell]]s from [[myasthenia gravis]] patient stimulated ''in vitro'' by Epstein-Barr virus produced [[acetylcholine]] autoantibodies.<ref>{{Cite journal|last=Brenner|first=T.|last2=Timore|first2=Y.|last3=Wirguin|first3=I.|last4=Abramsky|first4=O.|last5=Steinitz|first5=M.|date=1989-10|title=In vitro synthesis of antibodies to acetylcholine receptor by Epstein-Barr virus-stimulated B-lymphocytes derived from patients with myasthenia gravis|url=https://www.ncbi.nlm.nih.gov/pubmed/2553772|journal=Journal of Neuroimmunology|volume=24|issue=3|pages=217–222|issn=0165-5728|pmid=2553772}}</ref> Ongoing EBV infection of the [[thymus]] has been posited as a causative agent for the production of [[acetylcholine]] receptor autoantibodies in [[myasthenia gravis]].<ref>{{Cite journal|last=J.|first=Kaminski, Henry|last2=Janos|first2=Minarovits,|title=Epstein-barr virus: Trigger for autoimmunity?|url=http://www.academia.edu/20258853/Epstein-barr_virus_Trigger_for_autoimmunity/|journal=Annals of Neurology|language=en|issn=0364-5134}}</ref><ref>{{Cite web|url=http://journals.lww.com/neurologynow/_layouts/15/oaks.journals.mobile/post.aspx?blogId=2&postId=10|title=Official Brain & Life Home Page|website=journals.lww.com|language=en|access-date=2018-11-15}}</ref>

=== Gastrointestinal disease ===
One study of EBV in patients with [[gastritis]], [[Crohn's disease]], and [[ulcerative colitis]] and normal controls found essentially undetectable levels of EBV in normal gastric mucosa. However, EBV was detected in 46% of gastritis lesions, 44% of normal colonic mucosa, 55% of Crohn’s disease, and 64% of ulcerative colitis samples.<ref>{{Cite journal|last=Ryan|first=Julie|date=2013|title=Epstein-Barr Virus Infection is Common in Inflamed Gastrointestinal Mucosa|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3535492/|journal=Dig Dis Sci.|volume=|pages=|via=}}</ref>

===Lyme Disease===

Several herpesviruses including Epstein-Barr virus<ref name="Goossens1999" /> may cause false positives on Lyme Disease tests.

===X-MEN Disease===

A 2014 study found chronic Epstein-Barr infection was linked to a magnesium transporter([https://www.ncbi.nlm.nih.gov/gene/84061 MAGT-1]) mutation. Dysfunction in this transporter also resulted in decreased NK cell function, and neoplasia (sometimes-cancerous growths).<ref name="X-men_disease_1" /> This disorder, termed 'X-MEN' (for X-linked, EBV, and neoplasia) was identified as a [https://en.wikipedia.org/wiki/X-linked_recessive_inheritance recessive, X-linked disorder] that would therefore be many times more common in men.

Since chronic Epstein-Barr virus infection has been associated with chronic fatigue syndrome, this error in [[magnesium]] transport may be worth considering in male patients, especially with slow onset and history of childhood infection.<ref name="X-men_disease_1" /><ref name="X-men_disease_2" /> However, in this disorder, EBV would be seen as an indicator of the illness rather than the cause.

==Vitamin D==

Some recent research is finding links between EBV and [[Vitamin D]]

An Epstein-Barr virus protein EBNA-3 has an affinity for [[VDR]] and may actually block the activation of VDR-dependent genes by [[Vitamin D]].<ref>{{Cite journal|last=Yenamandra|first=Surya Pavan|last2=Hellman|first2=Ulf|last3=Kempkes|first3=Bettina|last4=Darekar|first4=Suhas Deoram|last5=Petermann|first5=Sabine|last6=Sculley|first6=Tom|last7=Klein|first7=George|last8=Kashuba|first8=Elena|date=2010-12|title=Epstein-Barr virus encoded EBNA-3 binds to vitamin D receptor and blocks activation of its target genes|url=https://www.ncbi.nlm.nih.gov/pubmed/20593215|journal=Cellular and molecular life sciences: CMLS|volume=67|issue=24|pages=4249–4256|doi=10.1007/s00018-010-0441-4|issn=1420-9071|pmid=20593215}}</ref>

[[Vitamin D receptor]] may be required for the normal development of [[natural killer T cell]]s that react to cells expressing [[CD1d]], as in cells infected by EBV.<ref>{{Cite journal|last=Yu|first=Sanhong|last2=Cantorna|first2=Margherita T.|date=2008-04-01|title=The vitamin D receptor is required for iNKT cell development|url=http://www.pnas.org/content/105/13/5207|journal=Proceedings of the National Academy of Sciences|language=en|volume=105|issue=13|pages=5207–5212|doi=10.1073/pnas.0711558105|issn=0027-8424|pmid=18364394}}</ref>

As low Vitamin D is also a risk factor for MS, some studies have attempt to find a link between low Vitamin D status, EBV and MS. One study of healthy individuals found no link between EBV load and Vitamin D status. However, over half the subjects were Vitamin D deficient and none had optimal levels<ref>{{Cite journal|last=Ramien|first=Caren|last2=Pachnio|first2=Annette|last3=Sisay|first3=Sofia|last4=Begum|first4=Jusnara|last5=Leese|first5=Alison|last6=Disanto|first6=Giulio|last7=Kuhle|first7=Jens|last8=Giovannoni|first8=Gavin|last9=Rickinson|first9=Alan|date=2014-5|title=Hypovitaminosis-D and EBV: no interdependence between two MS risk factors in a healthy young UK autumn cohort|url=https://www.ncbi.nlm.nih.gov/pubmed/24192216?dopt=Abstract|journal=Multiple Sclerosis (Houndmills, Basingstoke, England)|volume=20|issue=6|pages=751–753|doi=10.1177/1352458513509507|issn=1477-0970|pmid=24192216}}</ref> (i.e., above 100 nmol/l).

==Treatment==

EBV is thought to persistent harmlessly in immunocompetent individuals, but in those with compromised immune systems it has been associated with certain cancers and possibly autoimmune disease.

===Antivirals===

Several [[antiviral]]s are active against EBV including [[valganciclovir|valganciclovir,]] [[valacyclovir]]<ref>{{Cite journal|last=Hoshino|first=Yo|date=|title=Long-Term Administration of Valacyclovir Reduces the Number of Epstein-Barr Virus (EBV)-Infected B Cells but Not the Number of EBV DNA Copies per B Cell in Healthy Volunteers|url=http://jvi.asm.org/content/83/22/11857.full|journal=Journal of Virology|volume=|pages=|via=}}</ref>, [[acyclovir]]<ref>{{Cite journal|last=Rafaillidis|first=Pl|date=November 2013|title=Antiviral treatment for severe EBV infections in apparently immunocompetent patients|url=https://www.ncbi.nlm.nih.gov/pubmed/20739216|journal=Journal of Clinical Virology|volume=|pages=|via=}}</ref> and [[spironolactone]]<ref name="Verma2016" />.

[[Acyclovir]], an [[antiviral]] drug which inhibits (but does not destroy) herpesviruses, was shown to also inhibit the virus production. This suggests that EBV replicates via lytic replication.

A theoretical [[immunotherapy]] treatment proposes that inducing [[CD1d]] expression on EBV-infected B cells could prompt effective immune suppression of EBV by NKT cells.<ref>{{Cite journal|last=Priatel|first=John J|last2=Chung|first2=Brian K|last3=Tsai|first3=Kevin|last4=Tan|first4=Rusung|date=2014-04-09|title=Natural killer T cell strategies to combat Epstein–Barr virus infection|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4063158/|journal=Oncoimmunology|volume=3|doi=10.4161/onci.28329|issn=2162-4011|pmc=PMC4063158|pmid=25050206}}</ref>

===Rituximab===

[[Rituximab]] may be effective in completely eliminating Epstein-Barr virus infection from the peripheral blood.<ref>{{Cite journal|last=Diamantopoulos|first=Panagiotis T.|last2=Polonyfi|first2=Katerina|last3=Sofotasiou|first3=Maria|last4=Papadopoulou|first4=Vasiliki|last5=Kalala|first5=Fani|last6=Iliakis|first6=Theodoros|last7=Zervakis|first7=Kostantinos|last8=Tsilimidos|first8=Gerassimos|last9=Kouzis|first9=Panagiotis|date=2013-12|title=Rituximab in the treatment of EBV-positive low grade B-cell lymphoma|url=https://www.ncbi.nlm.nih.gov/pubmed/24324119|journal=Anticancer Research|volume=33|issue=12|pages=5693–5698|issn=1791-7530|pmid=24324119}}</ref> A study of seventeen patients with low-grade [[B cell]] lymphoma found that after three cycles of Rituximab, the virus had been completely eliminated from the peripheral blood in all but one patient.

===Herbs and nutraceuticals===

Herbs shown to have antiviral properties against EBV including [[licorice|licorice.]]<ref>{{Cite journal|last=Lin|first=Jung-Chung|last2=Cherng|first2=Jaw-Ming|last3=Hung|first3=Man-Shan|last4=Baltina|first4=Lidia A.|last5=Baltina|first5=Lia|last6=Kondratenko|first6=Rimma|date=2008-7|title=Inhibitory effects of some derivatives of glycyrrhizic acid against Epstein-Barr virus infection: structure-activity relationships|url=https://www.ncbi.nlm.nih.gov/pubmed/18423902|journal=Antiviral Research|volume=79|issue=1|pages=6–11|doi=10.1016/j.antiviral.2008.01.160|issn=0166-3542|pmid=18423902}}</ref> [[Vitamin C]] and Vitamin D<ref>{{Cite journal|last=Rolf|first=L|date=July 2017|title=Exploring the effect of vitamin D3 supplementation on the anti-EBV antibody response in relapsing-remitting multiple sclerosis|url=https://www.ncbi.nlm.nih.gov/pubmed/28731372|journal=Multiple Sclerosis|volume=|pages=|via=}}</ref> might also decrease duration and severity of the symptoms of EBV infection.<ref>{{Cite journal|last=Mikirova|first=N|date=May 2014|title=Effect of high dose vitamin C on Epstein-Barr viral infection|url=https://www.ncbi.nlm.nih.gov/pubmed/24793092|journal=Med Sci Monit|volume=|pages=|via=}}</ref>

==References==

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| title = Gammaherpesvirus Infection of Human Neuronal Cells
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| date = 2016-12-01
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| title = Epstein-Barr Virus–Associated B-cell Lymphomas: Pathogenesis and Clinical Outcomes
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[[Category:Infectious agents]]
[[Category:Triggers and risk factors]]
[[Category:Virology]]

Pregnancy

2018-11-14T21:24:31Z

Paulitasofia1:minor edits

Research on outcomes of pregnancy for women with [[chronic fatigue syndrome]] is limited.

There is some evidence of symptom improvement or remission in various inflammatory and autoimmune diseases during pregnancy. This may be due to hormonal or immune changes.<ref>{{Cite journal|date=2013-08-01|title=Do pregnancy-related changes in the microbiome stimulate innate immunity?|url=https://www.sciencedirect.com/science/article/pii/S1471491413001093|journal=Trends in Molecular Medicine|language=en|volume=19|issue=8|pages=454–459|doi=10.1016/j.molmed.2013.06.002|issn=1471-4914}}</ref>

== Biological changes during pregnancy ==

===Development of the placenta===

The placenta is a vascular organ that develops during pregnancy, attaching to the wall of the uterus. The umbilical cord connects the placenta to the developing fetus, allowing for blood to pass from the mother. The placenta allows for nutrient supply, thermoregulation, waste elimination, and gas exchange for the developing fetus, as well as production of hormones that support pregnancy for the mother. Towards the end of the pregnancy, the placenta provides antibodies to the fetus for postpartum protection.<ref name=":4">{{Cite web|url=https://www.pregnancybirthbaby.org.au/what-is-the-placenta|title=What is the placenta?|last=|first=|date=July 2017|website=Pregnancy, Birth & Baby|archive-url=|archive-date=|dead-url=|access-date=11/14/2018}}</ref>

The fetus and the placenta may be detected as foreign allograft by the mother's immune system. To prevent this from happening, the placenta secretes molecules containing Neurokinin-B. This is the same mechanism that parasitic nematodes use to evade detection by the host immune system. Additionally, there is a presence of lymphocytic suppressor cells in the fetus, which can inhibit maternal cytotoxic T cells.<ref name=":4" /><ref>{{Cite journal|date=2018-05-16|title=Immune tolerance in pregnancy|url=https://en.wikipedia.org/w/index.php?title=Immune_tolerance_in_pregnancy&oldid=841525208|journal=Wikipedia|language=en}}</ref><ref>{{Cite journal|last=Sakamoto|first=Rie|last2=Osada|first2=Hisao|last3=Iitsuka|first3=Yoshinori|last4=Masuda|first4=Kentarou|last5=Kaku|first5=Kenshi|last6=Seki|first6=Katsuyoshi|last7=Sekiya|first7=Souei|date=2003-5|title=Profile of neurokinin B concentrations in maternal and cord blood in normal pregnancy|url=https://www.ncbi.nlm.nih.gov/pubmed/12699441|journal=Clinical Endocrinology|volume=58|issue=5|pages=597–600|issn=0300-0664|pmid=12699441}}</ref> [[File:Pregnant non pregnant histamine ascorbic acid.jpg|right]]

===Immune system===

As a prerequisite for a successful pregnancy, the [[immune system]] undergoes changes so that the mother's body will not reject the fetus.<ref name=":2">{{Cite journal|last=Reinhard|first=G.|last2=Noll|first2=A.|last3=Schlebusch|first3=H.|last4=Mallmann|first4=P.|last5=Ruecker|first5=A. V.|date=1998-04-28|title=Shifts in the TH1/TH2 balance during human pregnancy correlate with apoptotic changes|url=https://www.ncbi.nlm.nih.gov/pubmed/9588218|journal=Biochemical and Biophysical Research Communications|volume=245|issue=3|pages=933–938|doi=10.1006/bbrc.1998.8549|issn=0006-291X|pmid=9588218}}</ref> One study has shown that T cells from pregnant women produce less TH1 cytokines and more TH2 cytokines, indicating a general shift toward the TH2 anti-inflammatory state. In contrast, the T cells in women with recurrent spontaneous abortions produce normal, non-pregnancy levels of TH1 and TH2 cytokines, indicating a shift towards the TH1 pro-inflammatory state in unsuccessful pregnancies.<ref name=":2" /> (Many spontaneous abortions are similar to organ transplant rejections.) Additionally, levels of [[Treg]]s, progesterone, and estrogen increase during pregnancy, which have anti-inflammatory properties.<ref>{{Cite journal|last=Munoz-Suano|first=Alba|last2=Hamilton|first2=Alexander B.|last3=Betz|first3=Alexander G.|date=May 2011|title=Gimme shelter: the immune system during pregnancy|url=http://www.ncbi.nlm.nih.gov/pubmed/21488887|journal=Immunological Reviews|volume=241|issue=1|pages=20–38|doi=10.1111/j.1600-065X.2011.01002.x|issn=1600-065X|pmid=21488887}}</ref>

==Pregnancy and ME/CFS ==

=== Fertility ===

Women with [[chronic fatigue syndrome]] report higher rates of [[polycystic ovarian syndrome]] (PCOS) and anovulatory cycles, higher rates of [[dysmenorrhea]] and higher rates of [[endometriosis]].<ref name=":0" />

=== Symptoms during pregnancy ===

There has been very little research on pregnancy and ME/CFS. One retrospective survey found that 41% of respondents reported no change in symptoms during pregnancy, 30% improved and 39% got worse.<ref name=":1">{{Cite journal|last=Schacterle|first=Richard S.|last2=Komaroff|first2=Anthony L.|date=2004-02-23|title=A Comparison of Pregnancies That Occur Before and After the Onset of Chronic Fatigue Syndrome|url=http://archinte.jamanetwork.com/article.aspx?articleid=216675|journal=Archives of Internal Medicine|language=en|volume=164|issue=4|pages=401|doi=10.1001/archinte.164.4.401|issn=0003-9926}}</ref>

In clinical practice, Dr. [[Nancy Klimas]], Dr. [[Lucinda Bateman]], and Dr. [[Charles Lapp]] report higher rates of improvement or remission during pregnancy. Klimas reports that in the 20 women she has followed through pregnancy, improvement in symptoms during pregnancy was "almost universal" and in some cases resulted in total temporary remission. Dr. Lapp reported that 25 out of 27 patients in his practice felt better during pregnancy. Dr. Klimas suggests that improvement may be due to increased blood volume during pregnancy or hormonal changes.<ref name=":0">{{Cite web|url=http://www.medscape.com/viewarticle/576986_6|title=Chronic Fatigue Syndrome: Implications for Women and Their Health Care Providers During the Childbearing Years|website=www.medscape.com|access-date=2018-07-31|date=2008|last=Rosati Allen|first=Peggy|archive-url=|archive-date=|dead-url=|registration=|format=Login Required}}</ref>

=== Postpartum ===

In one survey, after delivery, 30% had no change in symptoms, 20% improved, and 20% got worse. Dr. Klimas reports that her patients typically do well postpartum until about 3 to 6 months after at which time there is often a severe relapse.<ref name=":0" /> Another study indicates that postpartum relapse or worsening of symptoms is likely due to the extra effort of taking care of a baby, as well as the shift away from pregnancy-related hormones and the TH2 state.<ref name=":3" />

Postpartum depression is two to three times more common in mothers with ME/CFS compared to healthy mothers.<ref name=":3" />

=== Complications ===

When comparing these women's pregnancies after illness onset to pregnancies before illness onset (but not to healthy controls), the rate of complications were similar. In pregnancies occurring after illness onset, there was a higher rate of miscarriages (30% vs. 8%) and development delays or learning disabilities (21% vs. 8%).<ref name=":1" /> However, this may be explained by maternal age (pregnancies before illness onset occurred when women were younger than pregnancies occurring after illness onset).<ref>{{Cite news|url=http://emerge.org.au/about-mecfs/diagnosis/managing-symptoms-daily-basis/pregnancy-motherhood-mecfs/#.VkpwyrSYe6w|title=Pregnancy, Motherhood, Parenthood and ME/CFS - Emerge Australia|work=Emerge Australia|access-date=2018-07-31|language=en-US}}</ref>

===Schacterle and Komaroff (2004) ===
Schacterle and Komaroff (2004) conducted a retrospective study on women with ME/CFS who had undergone pregnancy before and/or after onset of illness. Many women with ME/CFS have to make the difficult decision of whether to have a child, and concern due to illness has resulted in lower rates of pregnancy. Of interest, "women who had children before the onset of CFS and decided to continue to have children had more pregnancies after the onset. Among the 19 patients (22%) who reported pregnancies both before and after the onset of CFS, 30 pregnancies occurred before and 46 occurred after the onset."

The study showed that during pregnancy, symptoms were unchanged or improved in 71% of women with ME/CFS. After pregnancy, symptoms were unchanged or improved in 50% of patients. Many women report concern over adverse outcomes for their children, yet there is little evidence that this occurs. Importantly, most maternal and offspring outcomes from pregnancies that occurred after illness onset were not systematically worse than pregnancies occurring prior to illness onset. These data are overall encouraging for women with ME/CFS considering pregnancy. <ref name=":1" />

== Pregnancy in other conditions ==

In general, [[Th1]] dominant immune disorders tend to improve during pregnancy while [[Th2]] dominant immune disorders tend to worsen.<ref>{{Cite journal|last=ØSTENSEN|first=MONICA|date=1999-06-01|title=Sex Hormones and Pregnancy in Rheumatoid Arthritis and Systemic Lupus Erythematosus|url=http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.1999.tb07630.x/abstract?userIsAuthenticated=false&deniedAccessCustomisedMessage=|journal=Annals of the New York Academy of Sciences|language=en|volume=876|issue=1|doi=10.1111/j.1749-6632.1999.tb07630.x/abstract|issn=1749-6632}}</ref> For example, in a study of women with [[rheumatoid arthritis]] 75% of patients experienced remission of their RA during pregnancy and 62% experienced a worsening of symptoms after delivery.<ref>{{Cite journal|last=Østensen|first=Monika|last2=Aune|first2=Berit|last3=Husby|first3=Gunnar|date=Jan 1983|title=Effect of Pregnancy and Hormonal Changes on the Activity of Rheumatoid Arthritis|url=http://www.tandfonline.com/doi/abs/10.3109/03009748309102886|journal=Scandinavian Journal of Rheumatology|language=en|volume=12|issue=2|pages=69–72|doi=10.3109/03009748309102886|issn=0300-9742}}</ref> 92% relapse within the first three months after delivery.<ref>{{Cite journal|date=2010-01-01|title=The impact of pregnancy on rheumatoid arthritis outcome: The role of maternofetal HLA class II disparity|url=https://www.sciencedirect.com/science/article/pii/S1297319X09001997|journal=Joint Bone Spine|language=en|volume=77|issue=1|pages=36–40|doi=10.1016/j.jbspin.2009.11.009|issn=1297-319X}}</ref> The course of [[Crohn's disease]] and [[ulcerative colitis]] improves during and after pregnancy.<ref>{{Cite journal|date=2013-08-01|title=Do pregnancy-related changes in the microbiome stimulate innate immunity?|url=https://www.sciencedirect.com/science/article/pii/S1471491413001093|journal=Trends in Molecular Medicine|language=en|volume=19|issue=8|pages=454–459|doi=10.1016/j.molmed.2013.06.002|issn=1471-4914}}</ref> In relapsing-remitting [[multiple sclerosis]], rates of relapse decrease during the first two trimesters and increase significantly postpartum.<ref>{{Cite journal|last=Confavreux|first=Christian|last2=Hutchinson|first2=Michael|last3=Hours|first3=Martine Marie|last4=Cortinovis-Tourniaire|first4=Patricia|last5=Moreau|first5=Thibault|date=1998-07-30|title=Rate of Pregnancy-Related Relapse in Multiple Sclerosis|url=http://www.nejm.org/doi/full/10.1056/nejm199807303390501|journal=New England Journal of Medicine|language=EN|volume=339|issue=5|pages=285–291|doi=10.1056/nejm199807303390501|issn=0028-4793}}</ref>

By contrast, pregnancy increases rates of [[lupus]] flares.<ref>{{Cite journal|last=Ruiz-Irastorza|first=G.|last2=Lima|first2=F.|last3=Alves|first3=J.|last4=Khamashta|first4=M. A.|last5=Simpson|first5=J.|last6=Hughes|first6=G. R. V.|last7=Buchanan|first7=N. M. M.|date=1996-02-01|title=INCREASED RATE OF LUPUS FLARE DURING PREGNANCY AND THE PUERPERIUM: A PROSPECTIVE STUDY OF 78 PREGNANCIES|url=https://academic.oup.com/rheumatology/article/35/2/133/1782393|journal=Rheumatology|language=en|volume=35|issue=2|pages=133–138|doi=10.1093/rheumatology/35.2.133|issn=1462-0324}}</ref> In a retrospective study of [[fibromyalgia]] patients based on personal interviews, nearly all patients surveyed experienced a worsening of symptoms during pregnancy, especially during the third trimester. Fibromyalgia did not appear to have an adverse effect on the outcome of pregnancy or the health of the baby.<ref>{{Cite journal|last=Østensen|first=Monika|last2=Rugelsjoen|first2=Anne|last3=Wigers|first3=Sigrid Horven|date=Jan 1997|title=The Effect of Reproductive Events and Alterations of Sex Hormone Levels on the Symptoms of Fibromyalgia|url=http://www.tandfonline.com/doi/abs/10.3109/03009749709065698|journal=Scandinavian Journal of Rheumatology|language=en|volume=26|issue=5|pages=355–360|doi=10.3109/03009749709065698|issn=0300-9742}}</ref>

== Related potential therapy ==

===Human Placental Extract===

HPE is used as a type of Complementary and Alternative Medicine therapy in various conditions involving chronic inflammation for its anti-inflammatory properties. In one interventional trial, injections of subcutaneous human placental extract (HPE) were found to improve symptoms in ME/CFS patients. Of note, the study did not find a difference between HPE injections and placebo. <ref>{{Cite journal|last=Park|first=Sat Byul|last2=Kim|first2=Kyu-Nam|last3=Sung|first3=Eunju|last4=Lee|first4=Suk Young|last5=Shin|first5=Ho Cheol|date=2016|title=Human Placental Extract as a Subcutaneous Injection Is Effective in Chronic Fatigue Syndrome: A Multi-Center, Double-Blind, Randomized, Placebo-Controlled Study|url=https://www.jstage.jst.go.jp/article/bpb/advpub/0/advpub_b15-00623/_article|journal=Biological & Pharmaceutical Bulletin|language=en|volume=39|issue=5|pages=674–679|doi=10.1248/bpb.b15-00623|issn=0918-6158}}</ref>
== See also ==

*[[Menstrual cycle]]
==Learn more==
*[http://emerge.org.au/about-mecfs/diagnosis/managing-symptoms-daily-basis/pregnancy-motherhood-mecfs/#.Vkp1cLSYe6x Pregnancy, Motherhood, Parenthood and ME/CFS]<ref>{{Cite news|url=http://emerge.org.au/about-mecfs/diagnosis/managing-symptoms-daily-basis/pregnancy-motherhood-mecfs/#.Vkp1cLSYe6x|title=Pregnancy, Motherhood, Parenthood and ME/CFS - Emerge Australia|work=Emerge Australia|access-date=2018-08-11|language=en-US}}</ref>
*2010, [http://www.njcfsa.org/wp-content/uploads/2010/09/Pregnancy-in-Women-with-ME-CFS.pdf Pregnancy in Women with Chronic Fatigue Syndrome (ME/CFS)]<ref name=":3">{{Cite news|url=http://www.njcfsa.org/wp-content/uploads/2010/09/Pregnancy-in-Women-with-ME-CFS.pdf|title=Pregnancy in Women with Chronic Fatigue Syndrome (ME/CFS)|last=Underhill|first=Rosemary|date=|work=NJCFSA|access-date=|archive-url=|archive-date=|dead-url=|publisher=New Jersey Chronic Fatigue Syndrome Association|format=PDF}}</ref>
*2016, [https://batemanhornecenter.org/pregnancy-and-mecfs/ Pregnancy and ME/CFS]<ref>{{Cite news|url=https://batemanhornecenter.org/pregnancy-and-mecfs/|title=Pregnancy and ME/CFS|last=Reynolds|first=Leigh|date=2016-07-06|work=Bateman Horne Center|access-date=2018-08-11|archive-url=|archive-date=|dead-url=|publisher=Bateman Horne Center|language=en-US}}</ref>
*[https://www.healthrising.org/blog/2014/03/02/pregnancy-chronic-fatigue-syndrome-four-mothers-talk-offer/ Pregnancy and Chronic Fatigue Syndrome-- Four Mothers Who've Been Through It Talk]

==References==
<references />
[[Category:Triggers and risk factors]]
[[Reproductive system‎]]

Pregnancy

2018-11-14T19:26:53Z

Paulitasofia1:additional information

Research on outcomes of pregnancy for women with [[chronic fatigue syndrome]] is limited.

There is some evidence of symptom improvement or remission in various inflammatory and autoimmune diseases during pregnancy. This may be due to hormonal or immune changes.<ref>{{Cite journal|date=2013-08-01|title=Do pregnancy-related changes in the microbiome stimulate innate immunity?|url=https://www.sciencedirect.com/science/article/pii/S1471491413001093|journal=Trends in Molecular Medicine|language=en|volume=19|issue=8|pages=454–459|doi=10.1016/j.molmed.2013.06.002|issn=1471-4914}}</ref>

== Changes during pregnancy ==

===Development of the placenta===

The placenta is a vascular organ that develops during pregnancy, attaching to the wall of the uterus. The umbilical cord connects the placenta to the developing fetus, allowing for blood to pass from the mother. The placenta allows for nutrient supply, thermoregulation, waste elimination, and gas exchange for the developing fetus, as well as production of hormones that support pregnancy for the mother. Towards the end of the pregnancy, the placenta provides antibodies to the fetus for postpartum protection.

The fetus and the placenta may be detected as foreign allograft by the mother's immune system. To prevent this from happening, the placenta secretes molecules containing Neurokinin-B. This is the same mechanism that parasitic nematodes use to evade detection by the host immune system. Additionally, there is a presence of lymphocytic suppressor cells in the fetus, which can inhibit maternal cytotoxic T cells. [[File:Pregnant non pregnant histamine ascorbic acid.jpg|right]]

===Immune system===

As a prerequisite for a successful pregnancy, the [[immune system]] undergoes changes so that the mother's body will not reject the fetus.<ref name=":2">{{Cite journal|last=Reinhard|first=G.|last2=Noll|first2=A.|last3=Schlebusch|first3=H.|last4=Mallmann|first4=P.|last5=Ruecker|first5=A. V.|date=1998-04-28|title=Shifts in the TH1/TH2 balance during human pregnancy correlate with apoptotic changes|url=https://www.ncbi.nlm.nih.gov/pubmed/9588218|journal=Biochemical and Biophysical Research Communications|volume=245|issue=3|pages=933–938|doi=10.1006/bbrc.1998.8549|issn=0006-291X|pmid=9588218}}</ref> One study has shown that T cells from pregnant women produce less TH1 cytokines and more TH2 cytokines, indicating a general shift toward the TH2 anti-inflammatory state. In contrast, the T cells in women with recurrent spontaneous abortions produce normal, non-pregnancy levels of TH1 and TH2 cytokines, indicating a shift towards the TH1 pro-inflammatory state in unsuccessful pregnancies.<ref name=":2" /> (Many spontaneous abortions are similar to organ transplant rejections.) Additionally, levels of [[Treg]]s, progesterone, and estrogen increase during pregnancy, which have anti-inflammatory properties.<ref>{{Cite journal|last=Munoz-Suano|first=Alba|last2=Hamilton|first2=Alexander B.|last3=Betz|first3=Alexander G.|date=May 2011|title=Gimme shelter: the immune system during pregnancy|url=http://www.ncbi.nlm.nih.gov/pubmed/21488887|journal=Immunological Reviews|volume=241|issue=1|pages=20–38|doi=10.1111/j.1600-065X.2011.01002.x|issn=1600-065X|pmid=21488887}}</ref>

==Pregnancy and ME/CFS ==

=== Fertility ===

Women with [[chronic fatigue syndrome]] report higher rates of [[polycystic ovarian syndrome]] (PCOS) and anovulatory cycles, higher rates of [[dysmenorrhea]] and higher rates of [[endometriosis]].<ref name=":0" />

=== Symptoms during pregnancy ===

There has been very little research on pregnancy and ME/CFS. One retrospective survey found that 41% of respondents reported no change in symptoms during pregnancy, 30% improved and 39% got worse.<ref name=":1">{{Cite journal|last=Schacterle|first=Richard S.|last2=Komaroff|first2=Anthony L.|date=2004-02-23|title=A Comparison of Pregnancies That Occur Before and After the Onset of Chronic Fatigue Syndrome|url=http://archinte.jamanetwork.com/article.aspx?articleid=216675|journal=Archives of Internal Medicine|language=en|volume=164|issue=4|pages=401|doi=10.1001/archinte.164.4.401|issn=0003-9926}}</ref>

In clinical practice, Dr. [[Nancy Klimas]], Dr. [[Lucinda Bateman]], and Dr. [[Charles Lapp]] report higher rates of improvement or remission during pregnancy. Klimas reports that in the 20 women she has followed through pregnancy, improvement in symptoms during pregnancy was "almost universal" and in some cases resulted in total temporary remission. Dr. Lapp reported that 25 out of 27 patients in his practice felt better during pregnancy. Dr. Klimas suggests that improvement may be due to increased blood volume during pregnancy or hormonal changes.<ref name=":0">{{Cite web|url=http://www.medscape.com/viewarticle/576986_6|title=Chronic Fatigue Syndrome: Implications for Women and Their Health Care Providers During the Childbearing Years|website=www.medscape.com|access-date=2018-07-31|date=2008|last=Rosati Allen|first=Peggy|archive-url=|archive-date=|dead-url=|registration=|format=Login Required}}</ref>

=== Postpartum ===

In one survey, after delivery, 30% had no change in symptoms, 20% improved, and 20% got worse. Dr. Klimas reports that her patients typically do well postpartum until about 3 to 6 months after at which time there is often a severe relapse.<ref name=":0" /> Another study indicates that postpartum relapse or worsening of symptoms is likely due to the extra effort of taking care of a baby, as well as the shift away from pregnancy-related hormones and the TH2 state.<ref name=":3" />

Postpartum depression is two to three times more common in mothers with ME/CFS compared to healthy mothers.

=== Complications ===

When comparing these women's pregnancies after illness onset to pregnancies before illness onset (but not to healthy controls), the rate of complications were similar. In pregnancies occurring after illness onset, there was a higher rate of miscarriages (30% vs. 8%) and development delays or learning disabilities (21% vs. 8%).<ref name=":1" /> However, this may be explained by maternal age (pregnancies before illness onset occurred when women were younger than pregnancies occurring after illness onset).<ref>{{Cite news|url=http://emerge.org.au/about-mecfs/diagnosis/managing-symptoms-daily-basis/pregnancy-motherhood-mecfs/#.VkpwyrSYe6w|title=Pregnancy, Motherhood, Parenthood and ME/CFS - Emerge Australia|work=Emerge Australia|access-date=2018-07-31|language=en-US}}</ref>

=== Schacterle and Komaroff (2004) ===
Schacterle and Komaroff (2004) conducted a retrospective study on women with ME/CFS who had undergone pregnancy before and/or after onset of illness. Many women with ME/CFS have to make the difficult decision of whether to have a child, and concern due to illness has resulted in lower rates of pregnancy. Of interest, "women who had children before the onset of CFS and decided to continue to have children had more pregnancies after the onset. Among the 19 patients (22%) who reported pregnancies both before and after the onset of CFS, 30 pregnancies occurred before and 46 occurred after the onset."

The study showed that during pregnancy, symptoms were unchanged or improved in 71% of women with ME/CFS. After pregnancy, symptoms were unchanged or improved in 50% of patients. Many women report concern over adverse outcomes for their children, yet there is little evidence that this occurs. Importantly, most maternal and offspring outcomes from pregnancies that occurred after illness onset were not systematically worse than pregnancies occurring prior to illness onset. These data are overall encouraging for women with ME/CFS considering pregnancy. <ref name=":1" />

== Pregnancy in other conditions ==

In general, [[Th1]] dominant immune disorders tend to improve during pregnancy while [[Th2]] dominant immune disorders tend to worsen.<ref>{{Cite journal|last=ØSTENSEN|first=MONICA|date=1999-06-01|title=Sex Hormones and Pregnancy in Rheumatoid Arthritis and Systemic Lupus Erythematosus|url=http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.1999.tb07630.x/abstract?userIsAuthenticated=false&deniedAccessCustomisedMessage=|journal=Annals of the New York Academy of Sciences|language=en|volume=876|issue=1|doi=10.1111/j.1749-6632.1999.tb07630.x/abstract|issn=1749-6632}}</ref> For example, in a study of women with [[rheumatoid arthritis]] 75% of patients experienced remission of their RA during pregnancy and 62% experienced a worsening of symptoms after delivery.<ref>{{Cite journal|last=Østensen|first=Monika|last2=Aune|first2=Berit|last3=Husby|first3=Gunnar|date=Jan 1983|title=Effect of Pregnancy and Hormonal Changes on the Activity of Rheumatoid Arthritis|url=http://www.tandfonline.com/doi/abs/10.3109/03009748309102886|journal=Scandinavian Journal of Rheumatology|language=en|volume=12|issue=2|pages=69–72|doi=10.3109/03009748309102886|issn=0300-9742}}</ref> 92% relapse within the first three months after delivery.<ref>{{Cite journal|date=2010-01-01|title=The impact of pregnancy on rheumatoid arthritis outcome: The role of maternofetal HLA class II disparity|url=https://www.sciencedirect.com/science/article/pii/S1297319X09001997|journal=Joint Bone Spine|language=en|volume=77|issue=1|pages=36–40|doi=10.1016/j.jbspin.2009.11.009|issn=1297-319X}}</ref> The course of [[Crohn's disease]] and [[ulcerative colitis]] improves during and after pregnancy.<ref>{{Cite journal|date=2013-08-01|title=Do pregnancy-related changes in the microbiome stimulate innate immunity?|url=https://www.sciencedirect.com/science/article/pii/S1471491413001093|journal=Trends in Molecular Medicine|language=en|volume=19|issue=8|pages=454–459|doi=10.1016/j.molmed.2013.06.002|issn=1471-4914}}</ref> In relapsing-remitting [[multiple sclerosis]], rates of relapse decrease during the first two trimesters and increase significantly postpartum.<ref>{{Cite journal|last=Confavreux|first=Christian|last2=Hutchinson|first2=Michael|last3=Hours|first3=Martine Marie|last4=Cortinovis-Tourniaire|first4=Patricia|last5=Moreau|first5=Thibault|date=1998-07-30|title=Rate of Pregnancy-Related Relapse in Multiple Sclerosis|url=http://www.nejm.org/doi/full/10.1056/nejm199807303390501|journal=New England Journal of Medicine|language=EN|volume=339|issue=5|pages=285–291|doi=10.1056/nejm199807303390501|issn=0028-4793}}</ref>

By contrast, pregnancy increases rates of [[lupus]] flares.<ref>{{Cite journal|last=Ruiz-Irastorza|first=G.|last2=Lima|first2=F.|last3=Alves|first3=J.|last4=Khamashta|first4=M. A.|last5=Simpson|first5=J.|last6=Hughes|first6=G. R. V.|last7=Buchanan|first7=N. M. M.|date=1996-02-01|title=INCREASED RATE OF LUPUS FLARE DURING PREGNANCY AND THE PUERPERIUM: A PROSPECTIVE STUDY OF 78 PREGNANCIES|url=https://academic.oup.com/rheumatology/article/35/2/133/1782393|journal=Rheumatology|language=en|volume=35|issue=2|pages=133–138|doi=10.1093/rheumatology/35.2.133|issn=1462-0324}}</ref> In a retrospective study of [[fibromyalgia]] patients based on personal interviews, nearly all patients surveyed experienced a worsening of symptoms during pregnancy, especially during the third trimester. Fibromyalgia did not appear to have an adverse effect on the outcome of pregnancy or the health of the baby.<ref>{{Cite journal|last=Østensen|first=Monika|last2=Rugelsjoen|first2=Anne|last3=Wigers|first3=Sigrid Horven|date=Jan 1997|title=The Effect of Reproductive Events and Alterations of Sex Hormone Levels on the Symptoms of Fibromyalgia|url=http://www.tandfonline.com/doi/abs/10.3109/03009749709065698|journal=Scandinavian Journal of Rheumatology|language=en|volume=26|issue=5|pages=355–360|doi=10.3109/03009749709065698|issn=0300-9742}}</ref>

== Related potential therapy ==

===Human Placental Extract===

HPE is used as a type of Complementary and Alternative Medicine therapy in various conditions involving chronic inflammation for its anti-inflammatory properties. In one interventional trial, injections of subcutaneous human placental extract (HPE) were found to improve symptoms in ME/CFS patients. Of note, the study did not find a difference between HPE injections and placebo. <ref>{{Cite journal|last=Park|first=Sat Byul|last2=Kim|first2=Kyu-Nam|last3=Sung|first3=Eunju|last4=Lee|first4=Suk Young|last5=Shin|first5=Ho Cheol|date=2016|title=Human Placental Extract as a Subcutaneous Injection Is Effective in Chronic Fatigue Syndrome: A Multi-Center, Double-Blind, Randomized, Placebo-Controlled Study|url=https://www.jstage.jst.go.jp/article/bpb/advpub/0/advpub_b15-00623/_article|journal=Biological & Pharmaceutical Bulletin|language=en|volume=39|issue=5|pages=674–679|doi=10.1248/bpb.b15-00623|issn=0918-6158}}</ref>
== See also ==

*[[Menstrual cycle]]
==Learn more==
*[http://emerge.org.au/about-mecfs/diagnosis/managing-symptoms-daily-basis/pregnancy-motherhood-mecfs/#.Vkp1cLSYe6x Pregnancy, Motherhood, Parenthood and ME/CFS]<ref>{{Cite news|url=http://emerge.org.au/about-mecfs/diagnosis/managing-symptoms-daily-basis/pregnancy-motherhood-mecfs/#.Vkp1cLSYe6x|title=Pregnancy, Motherhood, Parenthood and ME/CFS - Emerge Australia|work=Emerge Australia|access-date=2018-08-11|language=en-US}}</ref>
*2010, [http://www.njcfsa.org/wp-content/uploads/2010/09/Pregnancy-in-Women-with-ME-CFS.pdf Pregnancy in Women with Chronic Fatigue Syndrome (ME/CFS)]<ref name=":3">{{Cite news|url=http://www.njcfsa.org/wp-content/uploads/2010/09/Pregnancy-in-Women-with-ME-CFS.pdf|title=Pregnancy in Women with Chronic Fatigue Syndrome (ME/CFS)|last=Underhill|first=Rosemary|date=|work=NJCFSA|access-date=|archive-url=|archive-date=|dead-url=|publisher=New Jersey Chronic Fatigue Syndrome Association|format=PDF}}</ref>
*2016, [https://batemanhornecenter.org/pregnancy-and-mecfs/ Pregnancy and ME/CFS]<ref>{{Cite news|url=https://batemanhornecenter.org/pregnancy-and-mecfs/|title=Pregnancy and ME/CFS|last=Reynolds|first=Leigh|date=2016-07-06|work=Bateman Horne Center|access-date=2018-08-11|archive-url=|archive-date=|dead-url=|publisher=Bateman Horne Center|language=en-US}}</ref>
*[https://www.healthrising.org/blog/2014/03/02/pregnancy-chronic-fatigue-syndrome-four-mothers-talk-offer/ Pregnancy and Chronic Fatigue Syndrome-- Four Mothers Who've Been Through It Talk]

==References==
<references />
[[Category:Triggers and risk factors]]
[[Reproductive system‎]]

Pregnancy

2018-11-07T21:33:28Z

Paulitasofia1:/* References */

Research on outcomes of pregnancy for women with [[chronic fatigue syndrome]] is limited.

There is evidence of symptom improvement or remission in many inflammatory and autoimmune diseases during pregnancy. This may be due to hormonal or immune changes.<ref>{{Cite journal|date=2013-08-01|title=Do pregnancy-related changes in the microbiome stimulate innate immunity?|url=https://www.sciencedirect.com/science/article/pii/S1471491413001093|journal=Trends in Molecular Medicine|language=en|volume=19|issue=8|pages=454–459|doi=10.1016/j.molmed.2013.06.002|issn=1471-4914}}</ref>

== Changes during pregnancy ==

===Placenta===

The [[placenta]] secretes [[progesterone]] and high levels of [[estrogen]] . It also contains high concentrations of [[diamine oxidase]], an [[enzyme]] that breaks down [[histamine]]. [[File:Pregnant non pregnant histamine ascorbic acid.jpg|right]]

===Immune system===

The [[mucosal immune system]] undergoes profound changes so that the mother's body won't reject the fetus. [[Treg]]s increase. TGF-beta increases. [[Progesterone]] and [[estrogen]], which both have anti-inflammatory properties, increase.<ref>{{Cite journal|last=Munoz-Suano|first=Alba|last2=Hamilton|first2=Alexander B.|last3=Betz|first3=Alexander G.|date=May 2011|title=Gimme shelter: the immune system during pregnancy|url=http://www.ncbi.nlm.nih.gov/pubmed/21488887|journal=Immunological Reviews|volume=241|issue=1|pages=20–38|doi=10.1111/j.1600-065X.2011.01002.x|issn=1600-065X|pmid=21488887}}</ref> The immune skews to a [[Th2]] response.

== Pregnancy and ME/CFS ==

=== Fertility ===

Women with [[chronic fatigue syndrome]] report higher rates of [[polycystic ovarian syndrome]] (PCOS) and anovulatory cycles, higher rates of [[dysmenorrhea]] and higher rates of [[endometriosis]].<ref name=":0" />

=== Symptoms during pregnancy ===

There has been very little research on pregnancy and ME or CFS. One retrospective survey found that 41% of respondents reported no change in symptoms during pregnancy, 30% improved and 39% got worse.<ref name=":1">{{Cite journal|last=Schacterle|first=Richard S.|last2=Komaroff|first2=Anthony L.|date=2004-02-23|title=A Comparison of Pregnancies That Occur Before and After the Onset of Chronic Fatigue Syndrome|url=http://archinte.jamanetwork.com/article.aspx?articleid=216675|journal=Archives of Internal Medicine|language=en|volume=164|issue=4|pages=401|doi=10.1001/archinte.164.4.401|issn=0003-9926}}</ref>

In clinical practice, Dr. [[Nancy Klimas]], Dr. [[Lucinda Bateman]], and Dr. [[Charles Lapp]] report higher rates of improvement or remission during pregnancy. Klimas reports that in the 20 women she has followed through pregnancy, improvement in symptoms during pregnancy was "almost universal" and in some cases resulted in total temporary remission. Dr. Lapp reported that 25 out of 27 patients in his practice felt better during pregnancy. Dr. Klimas suggests that improvement may be due to increased blood volume during pregnancy or hormonal changes.<ref name=":0">{{Cite web|url=http://www.medscape.com/viewarticle/576986_6|title=Chronic Fatigue Syndrome: Implications for Women and Their Health Care Providers During the Childbearing Years|website=www.medscape.com|access-date=2018-07-31|date=2008|last=Rosati Allen|first=Peggy|archive-url=|archive-date=|dead-url=|registration=|format=Login Required}}</ref>

=== Postpartum ===

In one survey, after delivery, 30% had no change in symptoms, 20% improved, and 20% got worse. Dr. Klimas reports that her patients typically do well postpartum until about 3 to 6 months after at which time there is often a severe relapse.<ref name=":0" />

=== Complications ===

When comparing these women's pregnancies after illness onset to pregnancy before illness onset (but not to healthy controls), the rate of complications were similar but in pregnancies occurring after illness onset, there was a higher rate of miscarriages (30% v. 8%) and development delays or learning disabilities (21% v. 8%).<ref name=":1" /> However, this may have been due in whole are part to maternal age (pregnancies before illness onset occurred when women were younger than pregnancies occurring after illness onset).<ref>{{Cite news|url=http://emerge.org.au/about-mecfs/diagnosis/managing-symptoms-daily-basis/pregnancy-motherhood-mecfs/#.VkpwyrSYe6w|title=Pregnancy, Motherhood, Parenthood and ME/CFS - Emerge Australia|work=Emerge Australia|access-date=2018-07-31|language=en-US}}</ref>

===Placenta===

In a randomized, double blind, controlled trial, injections of subcutaneous human placental extract were found to improve symptoms in [[Chronic fatigue syndrome]] patients.<ref>{{Cite journal|last=Park|first=Sat Byul|last2=Kim|first2=Kyu-Nam|last3=Sung|first3=Eunju|last4=Lee|first4=Suk Young|last5=Shin|first5=Ho Cheol|date=2016|title=Human Placental Extract as a Subcutaneous Injection Is Effective in Chronic Fatigue Syndrome: A Multi-Center, Double-Blind, Randomized, Placebo-Controlled Study|url=https://www.jstage.jst.go.jp/article/bpb/advpub/0/advpub_b15-00623/_article|journal=Biological & Pharmaceutical Bulletin|language=en|volume=39|issue=5|pages=674–679|doi=10.1248/bpb.b15-00623|issn=0918-6158}}</ref>

== Pregnancy in other conditions ==

In general, [[Th1]] dominant immune disorders tend to improve during pregnancy while [[Th2]] dominant immune disorders tend to worsen.<ref>{{Cite journal|last=ØSTENSEN|first=MONICA|date=1999-06-01|title=Sex Hormones and Pregnancy in Rheumatoid Arthritis and Systemic Lupus Erythematosus|url=http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.1999.tb07630.x/abstract?userIsAuthenticated=false&deniedAccessCustomisedMessage=|journal=Annals of the New York Academy of Sciences|language=en|volume=876|issue=1|doi=10.1111/j.1749-6632.1999.tb07630.x/abstract|issn=1749-6632}}</ref> For example, in a study of women with [[rheumatoid arthritis]] 75% of patients experienced remission of their RA during pregnancy and 62% experienced a worsening of symptoms after delivery.<ref>{{Cite journal|last=Østensen|first=Monika|last2=Aune|first2=Berit|last3=Husby|first3=Gunnar|date=Jan 1983|title=Effect of Pregnancy and Hormonal Changes on the Activity of Rheumatoid Arthritis|url=http://www.tandfonline.com/doi/abs/10.3109/03009748309102886|journal=Scandinavian Journal of Rheumatology|language=en|volume=12|issue=2|pages=69–72|doi=10.3109/03009748309102886|issn=0300-9742}}</ref> 92% relapse within the first three months after delivery.<ref>{{Cite journal|date=2010-01-01|title=The impact of pregnancy on rheumatoid arthritis outcome: The role of maternofetal HLA class II disparity|url=https://www.sciencedirect.com/science/article/pii/S1297319X09001997|journal=Joint Bone Spine|language=en|volume=77|issue=1|pages=36–40|doi=10.1016/j.jbspin.2009.11.009|issn=1297-319X}}</ref> The course of [[Crohn's disease]] and [[ulcerative colitis]] improves during and after pregnancy.<ref>{{Cite journal|date=2013-08-01|title=Do pregnancy-related changes in the microbiome stimulate innate immunity?|url=https://www.sciencedirect.com/science/article/pii/S1471491413001093|journal=Trends in Molecular Medicine|language=en|volume=19|issue=8|pages=454–459|doi=10.1016/j.molmed.2013.06.002|issn=1471-4914}}</ref> In relapsing-remitting [[multiple sclerosis]], rates of relapse decrease during the first two trimesters and increase significantly postpartum.<ref>{{Cite journal|last=Confavreux|first=Christian|last2=Hutchinson|first2=Michael|last3=Hours|first3=Martine Marie|last4=Cortinovis-Tourniaire|first4=Patricia|last5=Moreau|first5=Thibault|date=1998-07-30|title=Rate of Pregnancy-Related Relapse in Multiple Sclerosis|url=http://www.nejm.org/doi/full/10.1056/nejm199807303390501|journal=New England Journal of Medicine|language=EN|volume=339|issue=5|pages=285–291|doi=10.1056/nejm199807303390501|issn=0028-4793}}</ref>

By contrast, pregnancy increases rates of [[lupus]] flares.<ref>{{Cite journal|last=Ruiz-Irastorza|first=G.|last2=Lima|first2=F.|last3=Alves|first3=J.|last4=Khamashta|first4=M. A.|last5=Simpson|first5=J.|last6=Hughes|first6=G. R. V.|last7=Buchanan|first7=N. M. M.|date=1996-02-01|title=INCREASED RATE OF LUPUS FLARE DURING PREGNANCY AND THE PUERPERIUM: A PROSPECTIVE STUDY OF 78 PREGNANCIES|url=https://academic.oup.com/rheumatology/article/35/2/133/1782393|journal=Rheumatology|language=en|volume=35|issue=2|pages=133–138|doi=10.1093/rheumatology/35.2.133|issn=1462-0324}}</ref> In a retrospective study of [[fibromyalgia]] patients based on personal interviews, nearly all patients surveyed experienced a worsening of symptoms during pregnancy, especially during the third trimester. Fibromyalgia did not appear to have an adverse effect on the outcome of pregnancy or the health of the baby.<ref>{{Cite journal|last=Østensen|first=Monika|last2=Rugelsjoen|first2=Anne|last3=Wigers|first3=Sigrid Horven|date=Jan 1997|title=The Effect of Reproductive Events and Alterations of Sex Hormone Levels on the Symptoms of Fibromyalgia|url=http://www.tandfonline.com/doi/abs/10.3109/03009749709065698|journal=Scandinavian Journal of Rheumatology|language=en|volume=26|issue=5|pages=355–360|doi=10.3109/03009749709065698|issn=0300-9742}}</ref>

== See also ==

*[[Menstrual cycle]]
==Learn more==
*[http://emerge.org.au/about-mecfs/diagnosis/managing-symptoms-daily-basis/pregnancy-motherhood-mecfs/#.Vkp1cLSYe6x Pregnancy, Motherhood, Parenthood and ME/CFS]<ref>{{Cite news|url=http://emerge.org.au/about-mecfs/diagnosis/managing-symptoms-daily-basis/pregnancy-motherhood-mecfs/#.Vkp1cLSYe6x|title=Pregnancy, Motherhood, Parenthood and ME/CFS - Emerge Australia|work=Emerge Australia|access-date=2018-08-11|language=en-US}}</ref>
*2010, [http://www.njcfsa.org/wp-content/uploads/2010/09/Pregnancy-in-Women-with-ME-CFS.pdf Pregnancy in Women with Chronic Fatigue Syndrome (ME/CFS)]<ref>{{Cite news|url=http://www.njcfsa.org/wp-content/uploads/2010/09/Pregnancy-in-Women-with-ME-CFS.pdf|title=Pregnancy in Women with Chronic Fatigue Syndrome (ME/CFS)|last=Underhill|first=Rosemary|date=|work=NJCFSA|access-date=|archive-url=|archive-date=|dead-url=|publisher=New Jersey Chronic Fatigue Syndrome Association|format=PDF}}</ref>
*2016, [https://batemanhornecenter.org/pregnancy-and-mecfs/ Pregnancy and ME/CFS]<ref>{{Cite news|url=https://batemanhornecenter.org/pregnancy-and-mecfs/|title=Pregnancy and ME/CFS|last=Reynolds|first=Leigh|date=2016-07-06|work=Bateman Horne Center|access-date=2018-08-11|archive-url=|archive-date=|dead-url=|publisher=Bateman Horne Center|language=en-US}}</ref>

==References==
<references />
[[Category:Triggers and risk factors]]
[[Reproductive system‎]]

Ehlers-Danlos syndrome

2018-10-30T22:05:54Z

Paulitasofia1:minor edits

'''Ehlers-Danlos syndromes''' (EDS) is a group of inherited disorders that affects [[Connective tissue|connective tissues]] — primarily skin, joints, and [https://www.lecturio.com/magazine/wall_structure_of_arteries_and_veins/ blood vessel walls].<ref>{{Cite news|url=http://www.mayoclinic.org/diseases-conditions/ehlers-danlos-syndrome/basics/definition/con-20033656|title=Ehlers-Danlos syndrome - Symptoms and causes|work=Mayo Clinic|access-date=2018-08-17|language=en}}</ref> It is a genetic disease that causes a defect in the production of [[collagen]].<ref name=":2" /> It is characterized by joint hypermobility, skin hyperextensibility, and tissue fragility, and ranges widely in severity.<ref>{{Cite news|url=https://www.ehlers-danlos.com/what-is-eds/|title=What are the Ehlers-Danlos Syndromes? {{!}} The Ehlers Danlos Society|work=The Ehlers Danlos Society|access-date=2018-10-07|language=en-US}}</ref>

== Symptoms and presentation ==
[[File:Hypermobile (double jointed) phalangeal joints.JPG|300px|thumb|right|An 18 years old patient with EDS can extend his fingers back to almost touching the forearm due to hypermobile [[wikipedia:Phalanx_bone|phalangeal]] joints]]Symptoms vary widely between individuals, based on the sub-type of EDS they have. EDS affects connective tissues, which results in symptoms that range from mild joint effects to life-threatening complications.<ref>{{Cite journal|date=2018-10-17|title=Ehlers–Danlos syndromes|url=https://en.wikipedia.org/w/index.php?title=Ehlers%E2%80%93Danlos_syndromes&oldid=864500626|journal=Wikipedia|language=en}}</ref>
* joint hypermobility (stretch further than normal)
* loose/unstable joints, prone to subluxations/dislocations
* joint pain
* joints that move beyond the normal range (hyperextensibility)
* early onset of arthritis
* soft, velvety-like skin
* fragile skin that tears or bruises easily
* severe scarring
* slow and poor wound healing
* development of molluscoid psuedo tumors
* musculoskeletal pain
* poor muscle tone (less common)
== Sub-types ==
<div style="max-width:270px;float:right;margin:0;padding-bottom: 3em;clear:both">
<gallery style="font-size:1.em;margin:0;padding:0;" widths="350" mode="slideshow">
File:Beighton Score - Thumb Reaches Forearm.JPG|Hypermobile EDS, cEDS, and clEDS can be diagnosed using [https://www.ehlers-danlos.com/assessing-joint-hypermobility/ The Beighton Scoring System] along with [https://www.ehlers-danlos.com/eds-types/ EDS Types] criteria. Here, thumb reaches forearm in one of its measurements|alt=
File:PMC3504533 1471-2415-12-47-2 (cropped).png|Hyperelastic skin in a person with cEDS|alt=
File:PMC3567970 1752-1947-7-35-1 (cropped).png|Translucent skin in Vascular EDS (VEDS)|alt=
File:751768.fig.002a.jpg|Atrophic scar found in cEDS, clEDS, Dermatosparaxis, and some other types|alt=
File:Marfan.JPG|"Marfanoid habitus" (resembling Marfans Syndrome) long slender fingers of Kyphoscoliosis Type EDS|alt=
File:Ehlers-danlos.png|4 y/o diagnosed by swelling of eyelids, corneas protruded anteriorly, blue sclerae, high myopia, and keratoconus. EDS, Rare Types: Brittle Cornea Syndrome (BCS)|alt=
</gallery>
</div>
There are currently thirteen sub-types of EDS. These include six distinct types of EDS and sub-types, as well as five presentations that fit into an 'other' category.<ref name=":1">{{Cite web|url=https://rarediseases.info.nih.gov/diseases/6322/ehlers-danlos-syndromes|title=Ehlers-Danlos syndromes {{!}} Genetic and Rare Diseases Information Center (GARD) – an NCATS Program|website=rarediseases.info.nih.gov|language=en|access-date=2018-10-06}}</ref><ref name=":0">{{Cite news|url=http://ehlers-danlos.com/eds-types/|title=The Types of EDS|work=The Ehlers Danlos Society|access-date=2018-08-17|language=en-US}}</ref><ref name=":2" /> They are:
* [https://rarediseases.info.nih.gov/diseases/2081/ehlers-danlos-syndrome-hypermobility-type Hypermobile EDS] - the most dominant clinical manifestation; presents with joint hypermobility, resulting into dislocations, bruising and [[chronic pain]] often out of proportion to physical and radiological findings.

*[https://rarediseases.info.nih.gov/diseases/2088/ehlers-danlos-syndrome-classic-type Classical (cEDS)] and [https://www.ehlers-danlos.com/eds-types/#clEDS Classical-like (clEDS)] presents with marked skin hyperextensibility, joint hypermobility, and in clEDS easy bruising.
*[https://rarediseases.info.nih.gov/diseases/2082/ehlers-danlos-syndrome-vascular-type Vascular EDS (VEDS)] and [https://www.ehlers-danlos.com/eds-types/#cvEDS Cardiac-valvular EDS (cvEDS)] - presents with arterial/intestinal/uterine fragility with possibility of arterial or organ rupture; often presents with thin or translucent skin with veins being visible thru the skin and in cvEDS severe progressive cardiac-valvular problems.
*[https://rarediseases.info.nih.gov/diseases/2083/ehlers-danlos-syndrome-kyphoscoliosis-type Kyphoscoliosis Type] - presents with scoliosis, joint laxity, and severe muscle hypotonia at birth; scoliosis is progressive and may result in the loss of the ability to walk in one's 20's or 30's. Other common features include a "marfanoid habitus" characterized by long, slender fingers; unusually long limbs; and a sunken chest or protruding chest.
*[https://rarediseases.info.nih.gov/diseases/2084/ehlers-danlos-syndrome-arthrochalasia-type Arthrochalasia Type] - presents with congenital hip dislocation and generalized joint hypermobility; may also have skin hyperextensibility, tissue fragility, kyphoscoliosis, and muscle hypotonia.
*[https://rarediseases.info.nih.gov/diseases/2089/ehlers-danlos-syndrome-dermatosparaxis-type Dermatosparaxis Type] - presents with severe skin fragility and substantial bruising.
*Other Types - [https://www.ehlers-danlos.com/eds-types/#BCS Brittle Cornea Syndrome (BCS)]; [https://www.ehlers-danlos.com/eds-types/#spEDS Spondylodysplastic EDS (spEDS)],[https://www.ehlers-danlos.com/eds-types/#mcEDS Musculocontractural EDS (mcEDS)], [https://www.ehlers-danlos.com/eds-types/#mEDS Myopathic EDS (mEDS)], [https://www.ehlers-danlos.com/eds-types/#pEDS Periodontal EDS (pEDS)] - this category groups the rarest genetic presentations sometimes only seen in one family.<ref name=":1" /><ref name=":0" />

== Prevalence ==
Ehlers-Danlos syndrome affects both males and females.<ref name=":0" />

1 in 5,000 have all types of EDS worldwide. Hypermobile and classical forms are most common. Hypermobile may affect as many as 1 in 5,000 to 20,000 people, while the classical type probably occurs in 1 in 20,000 to 40,000 people. Other forms are rare, often with only a few cases or affected families in the world.<ref>{{Cite web|url=https://ghr.nlm.nih.gov/condition/ehlers-danlos-syndrome#statistics|title=Ehlers-Danlos syndrome|last=Reference|first=Genetics Home|website=Genetics Home Reference|language=en|access-date=2018-10-07}}</ref>

== Risk factors ==
Ehlers-Danlos syndrome is a hereditary disease cause by a genetic mutation in one or more of the genes involved in the synthesis of collagen,<ref name=":2" /> an important protein found in muscle, skin, ligaments, tendons, cartilage, bones, blood vessels, and other other body tissue.<ref>{{Cite journal|date=2018-08-09|title=Collagen|url=https://en.wikipedia.org/w/index.php?title=Collagen&oldid=854113611|journal=Wikipedia|language=en}}</ref><ref name=":2" />

== Diagnosis ==
Diagnosis is made through physical examination which includes a test for hypermobility, such as the Beighton Scoring System<ref>{{Cite news|url=http://ehlers-danlos.com/assessing-joint-hypermobility/|title=Assessing Joint Hypermobility {{!}} The Ehlers Danlos Society|work=The Ehlers Danlos Society|access-date=2018-08-17|language=en-US}}</ref> or the Brighton Criteria.<ref>{{Cite web|url=http://hypermobility.org/help-advice/hypermobility-syndromes/the-brighton-score/|title=Hypermobility Syndromes Association » The Brighton Criteria for JHS|website=hypermobility.org|access-date=2018-08-17}}</ref>

== Pathophysiology ==
EDS is a diverse group of inherited connective-tissue disorders. Joint hypermobility, skin fragility, and hyperextensibility characterize the disorders. Collagen defect has been identified in at least six types.<ref name=":2">{{Cite journal|last=|first=|date=Jan 11, 2018|title=Ehlers-Danlos Syndrome: Background, Pathophysiology, Etiology|url=https://emedicine.medscape.com/article/1114004-overview#a5|format=Login Needed|journal=Medscape|volume=|pages=|at=Pathophysiology|via=}}</ref>

The vascular form is characterized by a decreased amount of type III collagen. It is [https://medlineplus.gov/ency/article/002049.htm autosomal dominant] (AD), one parent with a defective gene are needed to pass on this form of EDS and is caused by mutations in COL3A1. This results in increased fragility of connective tissue with arterial, intestinal, and uterine ruptures and premature death.<ref>{{Cite web|url=https://reference.medscape.com/medline/abstract/23489429|title=A new COL3A1 mutation in Ehlers-Danlos syndrome type IV.|last=Eder|first=J|last2=Laccone|first2=F|date=|website=reference.medscape.com|publisher=Medscape|format=Login Needed|issn=|archive-url=|archive-date=|dead-url=|access-date=2018-10-06|last3=Rohrbach|first3=M|last4=Guinta|first4=C|last5=Aumayr|first5=K|last6=Reichel|first6=C|last7=Trautinger|first7=F}}</ref>

In EDS types I and II, cEDS and clEDS, causative mutations may involved the ''COL5A1, COL5A2,'' and ''tenascin-X'' genes and are implied to be in the ''COL1A2'' gene. "Although half of the mutations that cause Ehlers-Danlos syndrome types I and II are likely to affect the ''COL5A1'' gene, a significant portion of the mutations result in low levels of mRNA from the mutant allele as a consequence of nonsense-mediated mRNA decay."<ref name=":2" /> <ref>{{Cite web|url=https://reference.medscape.com/medline/abstract/10796876|title=Null alleles of the COL5A1 gene of type V collagen are a cause of the classical forms of Ehlers-Danlos syndrome (types I and II).|last=Schwarze|first=U|last2=Atkinson|first2=M|date=|website=reference.medscape.com|publisher=Medscape|format=Login Needed|issn=|archive-url=|archive-date=|dead-url=|access-date=2018-10-06|last3=Hoffman|first3=GG|last4=Greenspan|first4=DS|last5=Byers|first5=PH}}</ref>

Kyphoscoliotic (type VI) is characterized by generalized joint laxity, skin fragility, and severe muscle hypotonia at birth. It is [https://medlineplus.gov/ency/article/002052.htm autosomal recessive] (AR), both parents with defective genes are needed to pass on this form of EDS. More than 20 mutations are identified in the LH1 gene that contributes to LH deficiency and clinical EDS type VI.<ref name=":2" /><ref>{{Cite web|url=https://reference.medscape.com/medline/abstract/11001813|title=Mutations in the lysyl hydroxylase 1 gene that result in enzyme deficiency and the clinical phenotype of Ehlers-Danlos syndrome type VI.|last=Yeowell|first=HN|last2=Walker|first2=LC|date=|website=reference.medscape.com|publisher=Medscape|format=Login Needed|issn=1096-7192|archive-url=|archive-date=|dead-url=|access-date=2018-10-06}}</ref>

Impaired wound healing is a typical feature of EDS.<ref name=":2" />

Pediatric patients have deficiencies in three genes of glutathione S-transferase family (''GSTM1, GSTT1, GSTP1'').<ref name=":2" /><ref>{{Cite web|url=https://reference.medscape.com/medline/abstract/18683505|title=Polymorphism of detoxification genes and cell resistance to mutagens in patients with Ehlers-Danlos syndrome.|last=Kuz'mina|first=NS|last2=Shipaeva|first2=EV|date=|website=reference.medscape.com|publisher=Medscape|format=Login Needed|issn=0007-4888|archive-url=|archive-date=|dead-url=|access-date=2018-10-06|last3=Semyachkina|first3=AN|last4=Vasil'eva|first4=IM|last5=Kovalenko|first5=LP|last6=Durnev|first6=LP|last7=Zasukhina|first7=GD}}</ref>

Reduced activity of beta4GalT-7 is associated with the progeriform (causing children to age rapidly) EDS.<ref name=":2" />

"Biallelic mutations in ''FKBP14'' may result in a recessive form of Ehlers-Danlos syndrome with progressive kyphoscoliosis, myopathy, hearing loss, and, possibly, an increased risk for vascular complications."<ref name=":2" /><ref>{{Cite web|url=https://reference.medscape.com/medline/abstract/24677762|title=FKBP14-related Ehlers-Danlos syndrome: expansion of the phenotype to include vascular complications.|last=Murray|first=ML|last2=Yang|first2=M|date=|website=reference.medscape.com|publisher=Medscape|format=Login Needed|issn=|archive-url=|archive-date=|dead-url=|access-date=2018-10-06|last3=Frauth|first3=C|last4=Byers|first4=PH}}</ref>

An ''[https://www.ehlers-danlos.com/eds-types/#chart EDS Types Chart]''<ref>{{Cite news|url=https://www.ehlers-danlos.com/eds-types/#chart|title=The Types of EDS|last=|first=|date=|work=The Ehlers Danlos Society|access-date=2018-10-06|archive-url=|archive-date=|dead-url=|at=EDS Types Chart|language=en-US}}</ref> with AD/AR inheritance pattern (IP), genetic basis, and protein involved are provided by [https://www.ehlers-danlos.com/ The Ehlers Danlos Society].

== Health complications ==
Health complications of EDS include:
* [[anxiety]] disorders and [[depression]]
* bladder
* bleeding
* [[brain]] and spine
* circulatory system, [[Cardiovascular system|cardiovascular]]
* dental, oral, and voice problems
* [[Digestive problems|digestive disorders]]
* diverticulitis
* heart and valve leakage
* hernia
* joint, [[Musculoskeletal system|musculoskeletal]]
* ocular
* [[Postural orthostatic tachycardia syndrome|Postural tachycardia syndrome]] (POTS)
* reproductive
* skin
* subluxations and dislocations<ref>{{Cite web|url=https://www.ehlers-danlos.org/what-is-eds/information-on-eds/mental-health/|title=Mental health – The Ehlers-Danlos Support UK|website=www.ehlers-danlos.org|language=en|access-date=2018-10-06}}</ref><ref>{{Cite web|url=https://www.ehlers-danlos.org/what-is-eds/information-on-eds/brain-and-spine/|title=Brain and spine – The Ehlers-Danlos Support UK|website=www.ehlers-danlos.org|language=en|access-date=2018-10-07}}</ref><ref>{{Cite web|url=https://www.ehlers-danlos.org/what-is-eds/information-on-eds/dental-oral-and-voice-problems/|title=Dental, oral and voice problems – The Ehlers-Danlos Support UK|website=www.ehlers-danlos.org|language=en|access-date=2018-10-07}}</ref><ref>{{Cite web|url=https://www.ehlers-danlos.org/what-is-eds/information-on-eds/digestive-disorders/|title=Digestive disorders – The Ehlers-Danlos Support UK|website=www.ehlers-danlos.org|language=en|access-date=2018-10-07}}</ref><ref>{{Cite web|url=https://www.chronicpainpartners.com/ehlers-danlos-syndrome-common-associated-health-problems/|title=Ehlers-Danlos Syndrome Commonly Associated Health Problems {{!}} EDSAwareness.com|website=www.chronicpainpartners.com|language=en|access-date=2018-10-06}}</ref><ref>{{Cite web|url=https://www.ehlers-danlos.org/what-is-eds/information-on-eds/joint-problems/|title=Joint problems – The Ehlers-Danlos Support UK|website=www.ehlers-danlos.org|language=en|access-date=2018-10-07}}</ref><ref>{{Cite news|url=https://totaleyecare.com/ocular-complications-ehlers-danlos-syndrome/|title=Ocular Complications of Ehlers Danlos Syndrome - Total Eye Care|work=Total Eye Care|access-date=2018-10-06|language=en-US}}</ref><ref>{{Cite news|url=https://www.msdmanuals.com/home/children-s-health-issues/connective-tissue-disorders-in-children/ehlers-danlos-syndrome|title=Ehlers-Danlos Syndrome - Children's Health Issues - MSD Manual Consumer Version|work=MSD Manual Consumer Version|access-date=2018-10-07|language=en}}</ref><ref>{{Cite web|url=https://www.ehlers-danlos.org/what-is-eds/information-on-eds/postural-tachycardia-syndrome-pots/|title=Postural tachycardia syndrome (PoTS) – The Ehlers-Danlos Support UK|website=www.ehlers-danlos.org|language=en|access-date=2018-10-07}}</ref><ref>{{Cite news|url=https://www.healthline.com/health/erectile-dysfunction|title=Erectile Dysfunction (ED): Causes, Treatment, and More|work=Healthline|access-date=2018-10-07|language=en}}</ref><ref>{{Cite journal|last=Hurst|first=B.S.|last2=Lang|first2=M.B.|last3=Kullstam|first3=S.M.|last4=Usadi|first4=R.S.|last5=Matthews|first5=M.L.|last6=Marshburn|first6=P.B.|date=2012|title=Reproductive challenges in women with Ehlers-Danlos syndrome: survey results from over 1350 respondents from the Ehlers-Danlos National Foundation|url=https://www.fertstert.org/article/S0015-0282(12)01145-4/fulltext|journal=Fertility and Sterility|language=English|volume=98|issue=3|pages=S112|doi=10.1016/j.fertnstert.2012.07.411|issn=0015-0282|via=}}</ref><ref>{{Cite web|url=https://www.ehlers-danlos.org/what-is-eds/information-on-eds/skin/|title=Skin – The Ehlers-Danlos Support UK|website=www.ehlers-danlos.org|language=en|access-date=2018-10-07}}</ref><ref>{{Cite news|url=https://www.ehlers-danlos.com/dislocation-subluxation-management/|title=Dislocation/Subluxation Management|work=The Ehlers Danlos Society|access-date=2018-10-07|language=en-US}}</ref>

== Comorbidities ==
* [[Chiari malformation]]
* [[Craniocervical instability]]
* [[Dysautonomia]]
* [[Mast cell activation syndrome]]

* [[Postural orthostatic tachycardia syndrome]]<ref>{{Cite web|url=https://www.inspire.com/groups/ehlers-danlos-syndromes-and-related-disorders/discussion/the-ehlers-danlos-society-is-forming-a-comorbid-condition-coalition/|title=The Ehlers-Danlos Society is forming a Comorbid Condition Coalition! - Inspire|last=|first=|date=Nov 8, 2017|website=www.inspire.com|archive-url=|archive-date=|dead-url=|access-date=2018-10-07}}</ref><ref>{{Cite news|url=http://www.thepainrelieffoundation.com/craniocervical-instability/|title=What is Craniocervical Instability? - The Pain Relief Foundation|work=The Pain Relief Foundation|access-date=2018-10-07|language=en-US}}</ref><ref>{{Cite news|url=https://www.ehlers-danlos.com/2017-eds-classification-non-experts/neurological-spinal-manifestations-ehlers-danlos-syndromes/|title=Neurological and Spinal Manifestations of the Ehlers-Danlos Syndromes (for Non-experts) {{!}} The Ehlers Danlos Society|work=The Ehlers Danlos Society|access-date=2018-10-07|language=en-US}}</ref>

== Treatment ==

'''Medications'''

There is no cure for EDS and treatments are limited to over-the-counter pain relievers such as acetaminophen (Tylenol and others) ibuprofen (Advil, Motrin IB, others), and naproxen sodium (Aleve). Prescription medications are used for acute injuries. Blood pressure medications are sometimes used to keep pressure low to relieve stress on vessels.<ref name=":3">{{Cite web|url=https://www.mayoclinic.org/diseases-conditions/ehlers-danlos-syndrome/diagnosis-treatment/drc-20362149|title=Ehlers-Danlos syndrome - Diagnosis and treatment - Mayo Clinic|website=www.mayoclinic.org|language=en|access-date=2018-10-07}}</ref>

'''Physical therapy'''

Because dislocations occur in EDS, exercise to strengthen the muscles and stabilize joints are the primary treatment. Braces help prevent joint dislocations.<ref name=":3" />

'''Surgical and other procedures'''

Surgery may be recommended to repair joints damaged by dislocations but connective tissue may not heal properly. Ruptured blood vessels or organs for patients with VEDS may also be necessary.<ref name=":3" />

== See also ==
* [[Collagen]]

==Learn more==
* [http://www.rcgp.org.uk/clinical-and-research/resources/toolkits/ehlers-danlos-syndromes-toolkit.aspx Ehlers-Danlos Syndrome Toolkit]<ref>{{Cite web|url=http://www.rcgp.org.uk/clinical-and-research/resources/toolkits/ehlers-danlos-syndromes-toolkit.aspx|title=Ehlers Danlos Syndromes Toolkit|last=|first=|date=|website=www.rcgp.org.uk|publisher=Royal College of General Practitioners|language=en|archive-url=|archive-date=|dead-url=|access-date=2018-10-29}}</ref>
* [https://www.ehlers-danlos.org/information/pregnancy-birth-feeding-and-hypermobile-ehlers-danlos-syndrome-hypermobility-spectrum-disorders/ Pregnancy, birth, feeding and hypermobile Ehlers-Danlos syndrome / hypermobility spectrum disorders]<ref>{{Cite web|url=https://www.ehlers-danlos.org/information/pregnancy-birth-feeding-and-hypermobile-ehlers-danlos-syndrome-hypermobility-spectrum-disorders/|title=Pregnancy, birth, feeding and hypermobile Ehlers-Danlos syndrome / hypermobility spectrum disorders – The Ehlers-Danlos Support UK|website=www.ehlers-danlos.org|language=en|access-date=2018-10-07}}</ref>

*2016, [http://www.healthrising.org/blog/2016/07/01/chronic-fatigue-fibromyalgia-ehlers-danlos-syndrome-diagnosis/ Another Piece of the Puzzle: An ME/CFS/FM Patient Gets an Ehlers Danlos Syndrome Diagnosis]<ref>{{Cite news|url=http://www.healthrising.org/blog/2016/07/01/chronic-fatigue-fibromyalgia-ehlers-danlos-syndrome-diagnosis/|title=Another Piece of the Puzzle: An ME/CFS/FM Patient Gets an Ehlers Danlos Syndrome Diagnosis - Health Rising|last=Burns|first=Darden|date=2016-07-01|work=Health Rising|access-date=2018-08-17|archive-url=|archive-date=|dead-url=|language=en-US}}</ref>

== References==
<references />

[[Category:Diagnoses]]
[[Category:Comorbidities]]

Ehlers-Danlos syndrome

2018-10-30T21:48:17Z

Paulitasofia1:edits and additions

'''Ehlers-Danlos syndromes''' (EDS) is a group of inherited disorders that affects [[Connective tissue|connective tissues]] — primarily skin, joints, and [https://www.lecturio.com/magazine/wall_structure_of_arteries_and_veins/ blood vessel walls].<ref>{{Cite news|url=http://www.mayoclinic.org/diseases-conditions/ehlers-danlos-syndrome/basics/definition/con-20033656|title=Ehlers-Danlos syndrome - Symptoms and causes|work=Mayo Clinic|access-date=2018-08-17|language=en}}</ref> It is a genetic disease that causes a defect in the production of [[collagen]].<ref name=":2" /> It is characterized by joint hypermobility, skin hyperextensibility, and tissue fragility.<ref>{{Cite news|url=https://www.ehlers-danlos.com/what-is-eds/|title=What are the Ehlers-Danlos Syndromes? {{!}} The Ehlers Danlos Society|work=The Ehlers Danlos Society|access-date=2018-10-07|language=en-US}}</ref>

== Symptoms and presentation ==
* joint hypermobility (stretch further than normal)
* loose/unstable joints, prone to subluxations/dislocations
* joint pain
* joints that move beyond the normal range (hyperextensibility)
* early onset of arthritis
* soft, velvety-like skin
* fragile skin that tears or bruises easily
* severe scarring
* slow and poor wound healing
* development of molluscoid psuedo tumors
* musculoskeletal pain
* poor muscle tone (less common)
[[File:Hypermobile (double jointed) phalangeal joints.JPG|300px|thumb|right|An 18 years old patient with EDS can extend his fingers back to almost touching the forearm due to hypermobile [[wikipedia:Phalanx_bone|phalangeal]] joints]]

== Sub-types ==
<div style="max-width:270px;float:right;margin:0;padding-bottom: 3em;clear:both">
<gallery style="font-size:1.em;margin:0;padding:0;" widths="350px" mode="slideshow">
File:Beighton Score - Thumb Reaches Forearm.JPG|Hypermobile EDS, cEDS, and clEDS can be diagnosed using [https://www.ehlers-danlos.com/assessing-joint-hypermobility/ The Beighton Scoring System] along with [https://www.ehlers-danlos.com/eds-types/ EDS Types] criteria. Here, thumb reaches forearm in one of its measurements|alt=
File:PMC3504533 1471-2415-12-47-2 (cropped).png|Hyperelastic skin in a person with cEDS|alt=
File:PMC3567970 1752-1947-7-35-1 (cropped).png|Translucent skin in Vascular EDS (VEDS)|alt=
File:751768.fig.002a.jpg|Atrophic scar found in cEDS, clEDS, Dermatosparaxis, and some other types|alt=
File:Marfan.JPG|"Marfanoid habitus" (resembling Marfans Syndrome) long slender fingers of Kyphoscoliosis Type EDS|alt=
File:Ehlers-danlos.png|4 y/o diagnosed by swelling of eyelids, corneas protruded anteriorly, blue sclerae, high myopia, and keratoconus. Parents happen to be first cousins. EDS, Rare Types: Brittle Cornea Syndrome (BCS)|alt=
</gallery>
</div>
There are currently thirteen sub-types of EDS. These include six distinct types of EDS and sub-types, as well as five presentations that fit into an 'other' category.<ref name=":1">{{Cite web|url=https://rarediseases.info.nih.gov/diseases/6322/ehlers-danlos-syndromes|title=Ehlers-Danlos syndromes {{!}} Genetic and Rare Diseases Information Center (GARD) – an NCATS Program|website=rarediseases.info.nih.gov|language=en|access-date=2018-10-06}}</ref><ref name=":0">{{Cite news|url=http://ehlers-danlos.com/eds-types/|title=The Types of EDS|work=The Ehlers Danlos Society|access-date=2018-08-17|language=en-US}}</ref><ref name=":2" /> They are:
* [https://rarediseases.info.nih.gov/diseases/2081/ehlers-danlos-syndrome-hypermobility-type Hypermobile EDS] - the most dominant clinical manifestation; presents with joint hypermobility, resulting into dislocations, bruising and [[chronic pain]] often out of proportion to physical and radiological findings.

*[https://rarediseases.info.nih.gov/diseases/2088/ehlers-danlos-syndrome-classic-type Classical (cEDS)] and [https://www.ehlers-danlos.com/eds-types/#clEDS Classical-like (clEDS)] presents with marked skin hyperextensibility, joint hypermobility, and in clEDS easy bruising.
*[https://rarediseases.info.nih.gov/diseases/2082/ehlers-danlos-syndrome-vascular-type Vascular EDS (VEDS)] and [https://www.ehlers-danlos.com/eds-types/#cvEDS Cardiac-valvular EDS (cvEDS)] - presents with arterial/intestinal/uterine fragility with possibility of arterial or organ rupture; often presents with thin or translucent skin with veins being visible thru the skin and in cvEDS severe progressive cardiac-valvular problems.
*[https://rarediseases.info.nih.gov/diseases/2083/ehlers-danlos-syndrome-kyphoscoliosis-type Kyphoscoliosis Type] - presents with scoliosis, joint laxity, and severe muscle hypotonia at birth; scoliosis is progressive and may result in the loss of the ability to walk in one's 20's or 30's. Other common features include a "marfanoid habitus" characterized by long, slender fingers; unusually long limbs; and a sunken chest or protruding chest.
*[https://rarediseases.info.nih.gov/diseases/2084/ehlers-danlos-syndrome-arthrochalasia-type Arthrochalasia Type] - presents with congenital hip dislocation and generalized joint hypermobility; may also have skin hyperextensibility, tissue fragility, kyphoscoliosis, and muscle hypotonia.
*[https://rarediseases.info.nih.gov/diseases/2089/ehlers-danlos-syndrome-dermatosparaxis-type Dermatosparaxis Type] - presents with severe skin fragility and substantial bruising.
*Other Types - [https://www.ehlers-danlos.com/eds-types/#BCS Brittle Cornea Syndrome (BCS)]; [https://www.ehlers-danlos.com/eds-types/#spEDS Spondylodysplastic EDS (spEDS)],[https://www.ehlers-danlos.com/eds-types/#mcEDS Musculocontractural EDS (mcEDS)], [https://www.ehlers-danlos.com/eds-types/#mEDS Myopathic EDS (mEDS)], [https://www.ehlers-danlos.com/eds-types/#pEDS Periodontal EDS (pEDS)] - this category groups the rarest genetic presentations sometimes only seen in one family.<ref name=":1" /><ref name=":0" />

== Prevalence ==
Ehlers-Danlos syndrome affects both males and females.<ref name=":0" />

1 in 5,000 have all types of EDS worldwide. Hypermobile and classical forms are most common. Hypermobile may affect as many as 1 in 5,000 to 20,000 people, while the classical type probably occurs in 1 in 20,000 to 40,000 people. Other forms are rare, often with only a few cases or affected families in the world.<ref>{{Cite web|url=https://ghr.nlm.nih.gov/condition/ehlers-danlos-syndrome#statistics|title=Ehlers-Danlos syndrome|last=Reference|first=Genetics Home|website=Genetics Home Reference|language=en|access-date=2018-10-07}}</ref>

== Risk factors ==
Ehlers-Danlos syndrome is a hereditary disease cause by a genetic mutation in one or more of the genes involved in the synthesis of collagen,<ref name=":2" /> an important protein found in muscle, skin, ligaments, tendons, cartilage, bones, blood vessels, and other other body tissue.<ref>{{Cite journal|date=2018-08-09|title=Collagen|url=https://en.wikipedia.org/w/index.php?title=Collagen&oldid=854113611|journal=Wikipedia|language=en}}</ref><ref name=":2" />

== Diagnosis ==
Diagnosis is made through physical examination which includes a test for hypermobility, such as the Beighton Scoring System<ref>{{Cite news|url=http://ehlers-danlos.com/assessing-joint-hypermobility/|title=Assessing Joint Hypermobility {{!}} The Ehlers Danlos Society|work=The Ehlers Danlos Society|access-date=2018-08-17|language=en-US}}</ref> or the Brighton Criteria.<ref>{{Cite web|url=http://hypermobility.org/help-advice/hypermobility-syndromes/the-brighton-score/|title=Hypermobility Syndromes Association » The Brighton Criteria for JHS|website=hypermobility.org|access-date=2018-08-17}}</ref>

== Pathophysiology ==
EDS is a diverse group of inherited connective-tissue disorders. Joint hypermobility, skin fragility, and hyperextensibility characterize the disorders. Collagen defect has been identified in at least six types.<ref name=":2">{{Cite journal|last=|first=|date=Jan 11, 2018|title=Ehlers-Danlos Syndrome: Background, Pathophysiology, Etiology|url=https://emedicine.medscape.com/article/1114004-overview#a5|format=Login Needed|journal=Medscape|volume=|pages=|at=Pathophysiology|via=}}</ref>

The vascular form is characterized by a decreased amount of type III collagen. It is [https://medlineplus.gov/ency/article/002049.htm autosomal dominant] (AD), one parent with a defective gene are needed to pass on this form of EDS and is caused by mutations in COL3A1. This results in increased fragility of connective tissue with arterial, intestinal, and uterine ruptures and premature death.<ref>{{Cite web|url=https://reference.medscape.com/medline/abstract/23489429|title=A new COL3A1 mutation in Ehlers-Danlos syndrome type IV.|last=Eder|first=J|last2=Laccone|first2=F|date=|website=reference.medscape.com|publisher=Medscape|format=Login Needed|issn=|archive-url=|archive-date=|dead-url=|access-date=2018-10-06|last3=Rohrbach|first3=M|last4=Guinta|first4=C|last5=Aumayr|first5=K|last6=Reichel|first6=C|last7=Trautinger|first7=F}}</ref>

In EDS types I and II, cEDS and clEDS, causative mutations may involved the ''COL5A1, COL5A2,'' and ''tenascin-X'' genes and are implied to be in the ''COL1A2'' gene. "Although half of the mutations that cause Ehlers-Danlos syndrome types I and II are likely to affect the ''COL5A1'' gene, a significant portion of the mutations result in low levels of mRNA from the mutant allele as a consequence of nonsense-mediated mRNA decay."<ref name=":2" /> <ref>{{Cite web|url=https://reference.medscape.com/medline/abstract/10796876|title=Null alleles of the COL5A1 gene of type V collagen are a cause of the classical forms of Ehlers-Danlos syndrome (types I and II).|last=Schwarze|first=U|last2=Atkinson|first2=M|date=|website=reference.medscape.com|publisher=Medscape|format=Login Needed|issn=|archive-url=|archive-date=|dead-url=|access-date=2018-10-06|last3=Hoffman|first3=GG|last4=Greenspan|first4=DS|last5=Byers|first5=PH}}</ref>

Kyphoscoliotic (type VI) is characterized by generalized joint laxity, skin fragility, and severe muscle hypotonia at birth. It is [https://medlineplus.gov/ency/article/002052.htm autosomal recessive] (AR), both parents with defective genes are needed to pass on this form of EDS. More than 20 mutations are identified in the LH1 gene that contributes to LH deficiency and clinical EDS type VI.<ref name=":2" /><ref>{{Cite web|url=https://reference.medscape.com/medline/abstract/11001813|title=Mutations in the lysyl hydroxylase 1 gene that result in enzyme deficiency and the clinical phenotype of Ehlers-Danlos syndrome type VI.|last=Yeowell|first=HN|last2=Walker|first2=LC|date=|website=reference.medscape.com|publisher=Medscape|format=Login Needed|issn=1096-7192|archive-url=|archive-date=|dead-url=|access-date=2018-10-06}}</ref>

Impaired wound healing is a typical feature of EDS.<ref name=":2" />

Pediatric patients have deficiencies in three genes of glutathione S-transferase family (''GSTM1, GSTT1, GSTP1'').<ref name=":2" /><ref>{{Cite web|url=https://reference.medscape.com/medline/abstract/18683505|title=Polymorphism of detoxification genes and cell resistance to mutagens in patients with Ehlers-Danlos syndrome.|last=Kuz'mina|first=NS|last2=Shipaeva|first2=EV|date=|website=reference.medscape.com|publisher=Medscape|format=Login Needed|issn=0007-4888|archive-url=|archive-date=|dead-url=|access-date=2018-10-06|last3=Semyachkina|first3=AN|last4=Vasil'eva|first4=IM|last5=Kovalenko|first5=LP|last6=Durnev|first6=LP|last7=Zasukhina|first7=GD}}</ref>

Reduced activity of beta4GalT-7 is associated with the progeriform (causing children to age rapidly) EDS.<ref name=":2" />

"Biallelic mutations in ''FKBP14'' may result in a recessive form of Ehlers-Danlos syndrome with progressive kyphoscoliosis, myopathy, hearing loss, and, possibly, an increased risk for vascular complications."<ref name=":2" /><ref>{{Cite web|url=https://reference.medscape.com/medline/abstract/24677762|title=FKBP14-related Ehlers-Danlos syndrome: expansion of the phenotype to include vascular complications.|last=Murray|first=ML|last2=Yang|first2=M|date=|website=reference.medscape.com|publisher=Medscape|format=Login Needed|issn=|archive-url=|archive-date=|dead-url=|access-date=2018-10-06|last3=Frauth|first3=C|last4=Byers|first4=PH}}</ref>

An ''[https://www.ehlers-danlos.com/eds-types/#chart EDS Types Chart]''<ref>{{Cite news|url=https://www.ehlers-danlos.com/eds-types/#chart|title=The Types of EDS|last=|first=|date=|work=The Ehlers Danlos Society|access-date=2018-10-06|archive-url=|archive-date=|dead-url=|at=EDS Types Chart|language=en-US}}</ref> with AD/AR inheritance pattern (IP), genetic basis, and protein involved are provided by [https://www.ehlers-danlos.com/ The Ehlers Danlos Society].

== Health complications ==
Health complications of EDS include:
<div style="column-count:2;-moz-column-count:2;-webkit-column-count:2">
* [[anxiety]] disorders and [[depression]]
* bladder
* bleeding
* [[brain]] and spine
* circulatory system, [[Cardiovascular system|cardiovascular]]
* dental, oral, and voice problems
* [[Digestive problems|digestive disorders]]
* diverticulitis
* heart and valve leakage
* hernia
* joint, [[Musculoskeletal system|musculoskeletal]]
* ocular
* [[Postural orthostatic tachycardia syndrome|Postural tachycardia syndrome]] (PoTS)
* reproductive
* skin
* subluxations and dislocations<ref>{{Cite web|url=https://www.ehlers-danlos.org/what-is-eds/information-on-eds/mental-health/|title=Mental health – The Ehlers-Danlos Support UK|website=www.ehlers-danlos.org|language=en|access-date=2018-10-06}}</ref><ref>{{Cite web|url=https://www.ehlers-danlos.org/what-is-eds/information-on-eds/brain-and-spine/|title=Brain and spine – The Ehlers-Danlos Support UK|website=www.ehlers-danlos.org|language=en|access-date=2018-10-07}}</ref><ref>{{Cite web|url=https://www.ehlers-danlos.org/what-is-eds/information-on-eds/dental-oral-and-voice-problems/|title=Dental, oral and voice problems – The Ehlers-Danlos Support UK|website=www.ehlers-danlos.org|language=en|access-date=2018-10-07}}</ref><ref>{{Cite web|url=https://www.ehlers-danlos.org/what-is-eds/information-on-eds/digestive-disorders/|title=Digestive disorders – The Ehlers-Danlos Support UK|website=www.ehlers-danlos.org|language=en|access-date=2018-10-07}}</ref><ref>{{Cite web|url=https://www.chronicpainpartners.com/ehlers-danlos-syndrome-common-associated-health-problems/|title=Ehlers-Danlos Syndrome Commonly Associated Health Problems {{!}} EDSAwareness.com|website=www.chronicpainpartners.com|language=en|access-date=2018-10-06}}</ref><ref>{{Cite web|url=https://www.ehlers-danlos.org/what-is-eds/information-on-eds/joint-problems/|title=Joint problems – The Ehlers-Danlos Support UK|website=www.ehlers-danlos.org|language=en|access-date=2018-10-07}}</ref><ref>{{Cite news|url=https://totaleyecare.com/ocular-complications-ehlers-danlos-syndrome/|title=Ocular Complications of Ehlers Danlos Syndrome - Total Eye Care|work=Total Eye Care|access-date=2018-10-06|language=en-US}}</ref><ref>{{Cite news|url=https://www.msdmanuals.com/home/children-s-health-issues/connective-tissue-disorders-in-children/ehlers-danlos-syndrome|title=Ehlers-Danlos Syndrome - Children's Health Issues - MSD Manual Consumer Version|work=MSD Manual Consumer Version|access-date=2018-10-07|language=en}}</ref><ref>{{Cite web|url=https://www.ehlers-danlos.org/what-is-eds/information-on-eds/postural-tachycardia-syndrome-pots/|title=Postural tachycardia syndrome (PoTS) – The Ehlers-Danlos Support UK|website=www.ehlers-danlos.org|language=en|access-date=2018-10-07}}</ref><ref>{{Cite news|url=https://www.healthline.com/health/erectile-dysfunction|title=Erectile Dysfunction (ED): Causes, Treatment, and More|work=Healthline|access-date=2018-10-07|language=en}}</ref><ref>{{Cite journal|last=Hurst|first=B.S.|last2=Lang|first2=M.B.|last3=Kullstam|first3=S.M.|last4=Usadi|first4=R.S.|last5=Matthews|first5=M.L.|last6=Marshburn|first6=P.B.|date=2012|title=Reproductive challenges in women with Ehlers-Danlos syndrome: survey results from over 1350 respondents from the Ehlers-Danlos National Foundation|url=https://www.fertstert.org/article/S0015-0282(12)01145-4/fulltext|journal=Fertility and Sterility|language=English|volume=98|issue=3|pages=S112|doi=10.1016/j.fertnstert.2012.07.411|issn=0015-0282|via=}}</ref><ref>{{Cite web|url=https://www.ehlers-danlos.org/what-is-eds/information-on-eds/skin/|title=Skin – The Ehlers-Danlos Support UK|website=www.ehlers-danlos.org|language=en|access-date=2018-10-07}}</ref><ref>{{Cite news|url=https://www.ehlers-danlos.com/dislocation-subluxation-management/|title=Dislocation/Subluxation Management|work=The Ehlers Danlos Society|access-date=2018-10-07|language=en-US}}</ref>
</div>

== Comorbidities ==
* [[Chiari malformation]]
* [[Craniocervical instability]]
* [[Dysautonomia]]
* [[Mast cell activation syndrome]]

* [[Postural orthostatic tachycardia syndrome]]<ref>{{Cite web|url=https://www.inspire.com/groups/ehlers-danlos-syndromes-and-related-disorders/discussion/the-ehlers-danlos-society-is-forming-a-comorbid-condition-coalition/|title=The Ehlers-Danlos Society is forming a Comorbid Condition Coalition! - Inspire|last=|first=|date=Nov 8, 2017|website=www.inspire.com|archive-url=|archive-date=|dead-url=|access-date=2018-10-07}}</ref><ref>{{Cite news|url=http://www.thepainrelieffoundation.com/craniocervical-instability/|title=What is Craniocervical Instability? - The Pain Relief Foundation|work=The Pain Relief Foundation|access-date=2018-10-07|language=en-US}}</ref><ref>{{Cite news|url=https://www.ehlers-danlos.com/2017-eds-classification-non-experts/neurological-spinal-manifestations-ehlers-danlos-syndromes/|title=Neurological and Spinal Manifestations of the Ehlers-Danlos Syndromes (for Non-experts) {{!}} The Ehlers Danlos Society|work=The Ehlers Danlos Society|access-date=2018-10-07|language=en-US}}</ref>

== Treatment ==

'''Medications'''

There is no cure for EDS and treatments are limited to over-the-counter pain relievers such as acetaminophen (Tylenol and others) ibuprofen (Advil, Motrin IB, others), and naproxen sodium (Aleve). Prescription medications are used for acute injuries. Blood pressure medications are sometimes used to keep pressure low to relieve stress on vessels.<ref name=":3">{{Cite web|url=https://www.mayoclinic.org/diseases-conditions/ehlers-danlos-syndrome/diagnosis-treatment/drc-20362149|title=Ehlers-Danlos syndrome - Diagnosis and treatment - Mayo Clinic|website=www.mayoclinic.org|language=en|access-date=2018-10-07}}</ref>

'''Physical therapy'''

Because dislocations occur in EDS, exercise to strengthen the muscles and stabilize joints are the primary treatment. Braces help prevent joint dislocations.<ref name=":3" />

'''Surgical and other procedures'''

Surgery may be recommended to repair joints damaged by dislocations but connective tissue may not heal properly. Ruptured blood vessels or organs for patients with VEDS may also be necessary.<ref name=":3" />

== See also ==
* [[Collagen]]

==Learn more==
* [http://www.rcgp.org.uk/clinical-and-research/resources/toolkits/ehlers-danlos-syndromes-toolkit.aspx Ehlers-Danlos Syndrome Toolkit]<ref>{{Cite web|url=http://www.rcgp.org.uk/clinical-and-research/resources/toolkits/ehlers-danlos-syndromes-toolkit.aspx|title=Ehlers Danlos Syndromes Toolkit|last=|first=|date=|website=www.rcgp.org.uk|publisher=Royal College of General Practitioners|language=en|archive-url=|archive-date=|dead-url=|access-date=2018-10-29}}</ref>
* [https://www.ehlers-danlos.org/information/pregnancy-birth-feeding-and-hypermobile-ehlers-danlos-syndrome-hypermobility-spectrum-disorders/ Pregnancy, birth, feeding and hypermobile Ehlers-Danlos syndrome / hypermobility spectrum disorders]<ref>{{Cite web|url=https://www.ehlers-danlos.org/information/pregnancy-birth-feeding-and-hypermobile-ehlers-danlos-syndrome-hypermobility-spectrum-disorders/|title=Pregnancy, birth, feeding and hypermobile Ehlers-Danlos syndrome / hypermobility spectrum disorders – The Ehlers-Danlos Support UK|website=www.ehlers-danlos.org|language=en|access-date=2018-10-07}}</ref>

*2016, [http://www.healthrising.org/blog/2016/07/01/chronic-fatigue-fibromyalgia-ehlers-danlos-syndrome-diagnosis/ Another Piece of the Puzzle: An ME/CFS/FM Patient Gets an Ehlers Danlos Syndrome Diagnosis]<ref>{{Cite news|url=http://www.healthrising.org/blog/2016/07/01/chronic-fatigue-fibromyalgia-ehlers-danlos-syndrome-diagnosis/|title=Another Piece of the Puzzle: An ME/CFS/FM Patient Gets an Ehlers Danlos Syndrome Diagnosis - Health Rising|last=Burns|first=Darden|date=2016-07-01|work=Health Rising|access-date=2018-08-17|archive-url=|archive-date=|dead-url=|language=en-US}}</ref>

== References==
<references />

[[Category:Diagnoses]]
[[Category:Comorbidities]]

Adenocorticotropic hormone

2018-10-30T21:21:35Z

Paulitasofia1:minor additions

'''Adrenocorticotropic hormone''' ('''ACTH''', also known as corticotropin) is a tropic [[Hormones|hormone]] and an important player in the [[Hypothalamic-pituitary-adrenal axis|HPA axis]]. It is produced and released by the anterior [[pituitary gland]]. ACTH acts on its target organ, the [[adrenal glands]], by stimulating the release of [[cortisol]].

== Structure and Function ==
There is a two-step process for the release of ACTH. First, the [[hypothalamus]] releases [[corticotropin-releasing hormone]] (CRH) through the [[hypophyseal portal system]] to stimulate the anterior pituitary gland. Corticotropin-releasing hormone is normally released in response to [[biological stress]], and is a part of the general [[stress response]].<ref>{{Cite web|url=http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/hypopit/acth.html|title=Adrenocorticotropic Hormone|website=www.vivo.colostate.edu|language=en|access-date=2018-10-25}}</ref> The anterior pituitary gland responds by releasing ACTH, targeting the adrenal glands (specifically the adrenal cortex). ACTH stimulates the production and secretion of [[glucocorticoid]] [[steroid]] hormones from the [[adrenal cortex]]. Cortisol is one of the principal hormones secreted, and is released into the bloodstream where it helps convert [[fats]] and [[proteins]] into [[glucose]], and has an anti-inflammatory effect. ACTH also affects the production of aldosterone in the adrenal cortex. Aldosterone facilitates sodium reabsorption and potassium secretion in the kidneys. Thus, ACTH is important in glucose, fat, and protein [[metabolism]], the [[Immune system|immune system’s]] response, and maintenance of [[blood pressure]].<ref>{{Cite web|url=https://labtestsonline.org/tests/adrenocorticotropic-hormone-acth|title=ACTH|website=labtestsonline.org|language=en|access-date=2018-10-25}}</ref>

== Dysfunction ==
Pathophysiology of ACTH arises from dysfunction of the pituitary, the adrenal glands, or [[ectopic secretion]]. If the pituitary is hypo- or hyper-functioning, there will be a respective decrease or increase in ACTH secretion. If the adrenal glands are hypo- or hyper-functioning, the response to ACTH may be muted or exaggerated. Ectopic secretion describes the secretion of ACTH from an abnormal source, such as a [[tumor]], such that normal regulatory pathways do not control such levels.

Pathophysiologies associated with ACTH dysregulation include<ref>{{Cite journal|last=Allen|first=Mary J.|last2=Sharma|first2=Sandeep|date=2018|title=Physiology, Adrenocorticotropic Hormone (ACTH)|url=http://www.ncbi.nlm.nih.gov/books/NBK500031/|location=Treasure Island (FL)|publisher=StatPearls Publishing|pmid=29763207}}</ref>:
* [[Hypopituitarism]]
* [[Pituitary adenoma]]
* [[Sheehan syndrome]]
* [[Cushing’s disease]] and syndrome

* [[Addison’s disease]]

* [[Hypercortisolism]]
* [[Small cell carcinoma]]

=== ME ===
As ACTH is a major hormone in the HPA axis, ACTH may be related to [[myalgic encephalomyelitis]] (ME) because HPA axis dysregulation has been associated with ME. However, studies in this area have found a wide range in results; a 2007 review of HPA function in ME found that about half of all studies indicated HPA hypofunction in ME, whereas the other half of the studies did not find differences in ACTH within HPA function between ME and controls.<ref>{{Cite journal|last=Van Den Eede|first=Filip|last2=Moorkens|first2=Greta|last3=Van Houdenhove|first3=Boudewijn|last4=Cosyns|first4=Paul|last5=Claes|first5=Stephan J.|date=2007|title=Hypothalamic-Pituitary-Adrenal Axis Function in Chronic Fatigue Syndrome|url=https://www.karger.com/Article/Abstract/104468|journal=Neuropsychobiology|language=english|volume=55|issue=2|pages=112–120|doi=10.1159/000104468|issn=0302-282X}}</ref> This could be partly explained by how some patients report higher levels of ACTH and cortisol early in the disease, with depleted/lower levels as the disease progresses.

== See also ==
* [[Cortisol]]

== Learn more ==
* Anatomy and Physiology | [https://www.youtube.com/watch?v=4m7XflJzm2w ACTH]

== References ==
<references />

Adenocorticotropic hormone

2018-10-25T20:25:38Z

Paulitasofia1:citation

'''Adrenocorticotropic hormone''' ('''ACTH''', also known as corticotropin) is a tropic hormone and an important player in the HPA axis. It is produced and released by the anterior pituitary gland. ACTH acts on its target organ, the adrenal glands, by stimulating the release of cortisol.

== Structure and Function ==
There is a two-step process for the release of ACTH. First, the hypothalamus releases corticotropin-releasing hormone (CRH) through the hypophyseal portal system to stimulate the anterior pituitary gland. Corticotropin-releasing hormone is normally released in response to biological stress, and is a part of the general stress response.<ref>{{Cite web|url=http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/hypopit/acth.html|title=Adrenocorticotropic Hormone|website=www.vivo.colostate.edu|language=en|access-date=2018-10-25}}</ref> The anterior pituitary gland responds by releasing ACTH, targeting the adrenal glands (specifically the adrenal cortex). ACTH stimulates the production and secretion of glucocorticoid steroid hormones from the adrenal cortex. Cortisol is one of the principal hormones secreted, and is released into the bloodstream where it helps convert fats and proteins into glucose, and has an anti-inflammatory effect. Thus, ACTH is important in glucose, fat, and protein metabolism, the immune system’s response, and maintenance of blood pressure.<ref>{{Cite web|url=https://labtestsonline.org/tests/adrenocorticotropic-hormone-acth|title=ACTH|website=labtestsonline.org|language=en|access-date=2018-10-25}}</ref>

== Dysfunction ==
Pathophysiology of ACTH arises from dysfunction of the pituitary, the adrenal glands, or ectopic secretion. If the pituitary is hypo- or hyper-functioning, there will be a respective decrease or increase in ACTH secretion. If the adrenal glands are hypo- or hyper-functioning, the response to ACTH may be muted or exaggerated. Ectopic secretion describes the secretion of ACTH from an abnormal source, such as a tumor, such that normal regulatory pathways do not control such levels.

Pathophysiologies associated with ACTH dysregulation include<ref>{{Cite journal|last=Allen|first=Mary J.|last2=Sharma|first2=Sandeep|date=2018|title=Physiology, Adrenocorticotropic Hormone (ACTH)|url=http://www.ncbi.nlm.nih.gov/books/NBK500031/|location=Treasure Island (FL)|publisher=StatPearls Publishing|pmid=29763207}}</ref>:
* Hypopituitarism
* Pituitary adenoma
* Sheehan syndrome
* Cushing’s disease and syndrome

* Addison’s disease

* Hypercortisolism
* Small cell carcinoma

=== ME ===
As ACTH is a major hormone in the HPA axis, ACTH may be related to ME because HPA axis dysregulation has been associated with ME. However, studies in this area have found a wide range in results.<ref>{{Cite journal|last=Van Den Eede|first=Filip|last2=Moorkens|first2=Greta|last3=Van Houdenhove|first3=Boudewijn|last4=Cosyns|first4=Paul|last5=Claes|first5=Stephan J.|date=2007|title=Hypothalamic-Pituitary-Adrenal Axis Function in Chronic Fatigue Syndrome|url=https://www.karger.com/Article/Abstract/104468|journal=Neuropsychobiology|language=english|volume=55|issue=2|pages=112–120|doi=10.1159/000104468|issn=0302-282X}}</ref> This could be partly explained by how some patients report higher levels of ACTH and cortisol early in the disease, with depleted/lower levels as the disease progresses.

== See more ==
Anatomy and Physiology | [https://www.youtube.com/watch?v=4m7XflJzm2w ACTH]

== References ==
<references />

Adenocorticotropic hormone

2018-10-25T20:22:55Z

Paulitasofia1:New page

'''Adrenocorticotropic hormone''' ('''ACTH''', also known as corticotropin) is a tropic hormone and an important player in the HPA axis. It is produced and released by the anterior pituitary gland. ACTH acts on its target organ, the adrenal glands, by stimulating the release of cortisol.

== Structure and Function ==
There is a two-step process for the release of ACTH. First, the hypothalamus releases corticotropin-releasing hormone (CRH) through the hypophyseal portal system to stimulate the anterior pituitary gland. Corticotropin-releasing hormone is normally released in response to biological stress, and is a part of the general stress response.<ref>{{Cite web|url=http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/hypopit/acth.html|title=Adrenocorticotropic Hormone|website=www.vivo.colostate.edu|language=en|access-date=2018-10-25}}</ref> The anterior pituitary gland responds by releasing ACTH, targeting the adrenal glands (specifically the adrenal cortex). ACTH stimulates the production and secretion of glucocorticoid steroid hormones from the adrenal cortex. Cortisol is one of the principal hormones secreted, and is released into the bloodstream where it helps convert fats and proteins into glucose, and has an anti-inflammatory effect. Thus, ACTH is important in glucose, fat, and protein metabolism, the immune system’s response, and maintenance of blood pressure.<ref>{{Cite web|url=https://labtestsonline.org/tests/adrenocorticotropic-hormone-acth|title=ACTH|website=labtestsonline.org|language=en|access-date=2018-10-25}}</ref>

== Dysfunction ==
Pathophysiology of ACTH arises from dysfunction of the pituitary, the adrenal glands, or ectopic secretion. If the pituitary is hypo- or hyper-functioning, there will be a respective decrease or increase in ACTH secretion. If the adrenal glands are hypo- or hyper-functioning, the response to ACTH may be muted or exaggerated. Ectopic secretion describes the secretion of ACTH from an abnormal source, such as a tumor, such that normal regulatory pathways do not control such levels.

Pathophysiologies associated with ACTH dysregulation include:
* Hypopituitarism
* Pituitary adenoma
* Sheehan syndrome
* Cushing’s disease and syndrome

* Addison’s disease

* Hypercortisolism
* Small cell carcinoma

=== ME ===
As ACTH is a major hormone in the HPA axis, ACTH may be related to ME because HPA axis dysregulation has been associated with ME. However, studies in this area have found a wide range in results.<ref>{{Cite journal|last=Van Den Eede|first=Filip|last2=Moorkens|first2=Greta|last3=Van Houdenhove|first3=Boudewijn|last4=Cosyns|first4=Paul|last5=Claes|first5=Stephan J.|date=2007|title=Hypothalamic-Pituitary-Adrenal Axis Function in Chronic Fatigue Syndrome|url=https://www.karger.com/Article/Abstract/104468|journal=Neuropsychobiology|language=english|volume=55|issue=2|pages=112–120|doi=10.1159/000104468|issn=0302-282X}}</ref> This could be partly explained by how some patients report higher levels of ACTH and cortisol early in the disease, with depleted/lower levels as the disease progresses.

== See more ==
Anatomy and Physiology | [https://www.youtube.com/watch?v=4m7XflJzm2w ACTH]

== References ==

Pituitary gland

2018-10-25T16:13:25Z

Paulitasofia1:added links

The '''pituitary gland''', or hypophysis, is a pea-sized gland of the [[endocrine system]], situated at the base of the brain. As part of the [[Hypothalamic-pituitary-adrenal axis|HPA axis]], it is regulated by the [[hypothalamus]] to produce, store, and secrete various [[hormones]], which target other endocrine glands. The pituitary gland is sometimes referred to as the “master gland” as it regulates the function of the other endocrine glands.<ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>

== Structure and Function ==
[[File:Pituitary lobes.jpg|thumb|Anatomical diagram of the pituitary gland, depicting the posterior, anterior, and intermediate lobes.<ref>{{Cite web|url=http://www.daviddarling.info/encyclopedia/P/pituitary_gland.html|title=pituitary gland|last=Darling|first=David|website=www.daviddarling.info|access-date=2018-10-25}}</ref>]]
The pituitary gland sits at the base of the brain, underneath the hypothalamus. It is surrounded by a protective bony cavity called the [[sella turcica]]. The pituitary is divided into three distinct lobes: posterior, anterior, and intermediate.<ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>
=== Posterior ===
The posterior pituitary develops as an extension of the [[hypothalamus]] (distinct from the anterior pituitary). The posterior pituitary is largely made up of the terminals of nerve cells of the hypothalamus, as neurons in the hypothalamus project directly to the posterior pituitary. Hormones produced by the hypothalamus are stored in the terminals of hypothalamic neurons in the posterior pituitary, and are released by nerve excitation. The two major hormones stored and secreted by the posterior pituitary include:
* [[Antidiuretic hormone]] (ADH, also known as vasopressin)
* [[Oxytocin]] <ref>{{Cite book|url=https://www.ncbi.nlm.nih.gov/books/NBK27/|title=The pituitary gland|last=Nussey|first=Stephen|last2=Whitehead|first2=Saffron|date=2001|publisher=BIOS Scientific Publishers|language=en}}</ref>

=== Anterior ===
The anterior pituitary is structurally distinct from the posterior pituitary. It makes up 80% of the pituitary gland, and is made up of different types of endocrine cells. These cells are classified by the hormones they synthesize and release, and are regulated by the hypothalamus via releasing and inhibiting hormones. The six major hormones of the anterior pituitary are:
* [[Growth hormone]] (GH)
* [[Adrenocorticotropic hormone]] (ACTH)
* [[Thyroid-stimulating hormone]] (TSH)
* [[Follicular-stimulating hormone]] (FSH)
* [[Luteinizing hormone]] (LH)
* [[Prolactin]] <ref>{{Cite book|url=https://www.ncbi.nlm.nih.gov/books/NBK27/|title=The pituitary gland|last=Nussey|first=Stephen|last2=Whitehead|first2=Saffron|date=2001|publisher=BIOS Scientific Publishers|language=en}}</ref><ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>

=== Intermediate ===
The intermediate lobe is present in many lower vertebrates, but is almost absent in humans. The intermediate pituitary synthesizes and secretes:
* [[Melanocyte-stimulating hormone]] (MSH)

== Function of Pituitary Hormones ==
{| class="wikitable"
|'''Hormone'''
|'''Target Organ'''
|'''Role'''
|-
|Growth hormone (GH)
|Muscular, skeletal, and fat tissue
|Regulates growth and physical development by stimulating muscle growth and reducing fat tissue
|-
|Adrenocorticotropic hormone (ACTH)
|Adrenal glands
|Stimulates the adrenal glands to produce cortisol and other hormones
|-
|Thyroid-stimulating hormone (TSH)
|Thyroid gland
|Stimulates the thyroid to produce thyroid hormone
|-
|Follicular-stimulating hormone (FSH)
|Ovaries or testes
|Stimulates the ovaries to produce eggs/the testes to produce sperm, and the sex organs to produce sex hormones
|-
|Luteinizing hormone (LH)
|Ovaries or testes
|Stimulates the ovaries to produce eggs/the testes to produce sperm, and the sex organs to produce sex hormones
|-
|Prolactin
|Mammary glands
|Stimulates the mammary glands to produce milk
|-
|Antidiuretic hormone (ADH, also known as vasopressin)
|Kidneys
|Regulates amount of water absorbed and excreted by the kidneys
|-
|Oxytocin
|Uterus and mammary glands
|Causes uterus contraction during childbirth, stimulates contractions of the milk ducts in breast for breastfeeding
|-
|Melanocyte-stimulating hormone (MSH)
|Skin and hair
|Stimulates the production of melanin in skin and hair, suppresses appetite, contributes to sexual arousal
|}
<ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>
[[File:Pituitary diagram.jpg|none|thumb|602x602px|Diagram of the pituitary gland, the hormones it releases, and its target organs.<ref>{{Cite web|url=https://www.earthslab.com/physiology/pituitary-gland-control-hormones-anterior-posterior-lobe/|title=Pituitary Gland – Control And Hormones of Anterior And Posterior Lobe|website=www.earthslab.com|language=en-US|access-date=2018-10-25}}</ref>]]

== Dysfunction and Disease ==
Dysfunction of the pituitary gland can result in overproduction or underproduction of pituitary hormones, thus having major consequences in bodily function. Conditions of pituitary malfunction include:
* [[Acromegaly]] -- overproduction of GH
* [[Cushing’s disease]] -- overproduction of ACTH
* [[GH deficiency]] -- underproduction of GH
* Syndrome of inappropriate antidiuretic hormone -- overproduction of antidiuretic hormone
* [[Diabetes insipidus]] -- underproduction of antidiuretic hormone
* [[Sheehan syndrome]] -- underproduction of any pituitary hormone
* [[Pickardt-Falhbusch Syndrome]] -- underproduction of any pituitary hormone aside from prolactin
* [[Hyperpituitarism]] (usually pituitary adenoma) -- overproduction of any pituitary hormone
* [[Hypopituitarism]] -- underproduction of any pituitary hormone
* [[Hypophysitis]] -- inflammation of the pituitary gland
* Autoimmune hypophysitis -- inflammation of the pituitary gland due to autoimmunity
* [[Pituitary adenoma]] -- noncancerous tumor of the pituitary gland <ref>{{Cite journal|date=2018-08-11|title=Pituitary disease|url=https://en.wikipedia.org/w/index.php?title=Pituitary_disease&oldid=854490027|journal=Wikipedia|language=en}}</ref>

=== ME ===
Dysfunction of the endocrine system, with a focus on HPA axis hypofunction, has been reported in individuals with ME.<ref>{{Cite journal|last=Nijhof|first=Sanne L.|last2=Rutten|first2=Juliette M. T. M.|last3=Uiterwaal|first3=Cuno S. P. M.|last4=Bleijenberg|first4=Gijs|last5=Kimpen|first5=Jan L. L.|last6=Putte|first6=Elise M. van de|date=2014-4|title=The role of hypocortisolism in chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/24636516|journal=Psychoneuroendocrinology|volume=42|pages=199–206|doi=10.1016/j.psyneuen.2014.01.017|issn=1873-3360|pmid=24636516}}</ref><ref>{{Cite journal|last=Papadopoulos|first=Andrew S.|last2=Cleare|first2=Anthony J.|date=2011-09-27|title=Hypothalamic-pituitary-adrenal axis dysfunction in chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/21946893|journal=Nature Reviews. Endocrinology|volume=8|issue=1|pages=22–32|doi=10.1038/nrendo.2011.153|issn=1759-5037|pmid=21946893}}</ref><ref>{{Cite journal|last=Heim|first=Christine|last2=Nater|first2=Urs M.|last3=Maloney|first3=Elizabeth|last4=Boneva|first4=Roumiana|last5=Jones|first5=James F.|last6=Reeves|first6=William C.|date=2009-1|title=Childhood trauma and risk for chronic fatigue syndrome: association with neuroendocrine dysfunction|url=https://www.ncbi.nlm.nih.gov/pubmed/19124690|journal=Archives of General Psychiatry|volume=66|issue=1|pages=72–80|doi=10.1001/archgenpsychiatry.2008.508|issn=1538-3636|pmid=19124690}}</ref><ref name=":0">{{Cite journal|last=Morris|first=Gerwyn|last2=Anderson|first2=George|last3=Maes|first3=Michael|date=2016-10-20|title=Hypothalamic-Pituitary-Adrenal Hypofunction in Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS) as a Consequence of Activated Immune-Inflammatory and Oxidative and Nitrosative Pathways|url=https://link.springer.com/article/10.1007/s12035-016-0170-2|journal=Molecular Neurobiology|language=en|volume=54|issue=9|pages=6806–6819|doi=10.1007/s12035-016-0170-2|issn=0893-7648}}</ref>. It has been suggested that HPA axis hypofunction in ME is caused by chronic activation of the inflammatory and oxidative and nitrosative stress pathways<ref name=":0" />. However, this area of research continues to lack studies with direct measures of pituitary function.

Some patients report that there seems to be a period of pituitary/HPA axis hyperfunction in the earlier stage of ME, whereas later in disease progression there's a switch to hypofunction. This could perhaps explain some of the wide variation across studies (e.g.,<ref>{{Cite journal|last=DEMITRACK|first=MARK A.|last2=DALE|first2=JANET K.|last3=STRAUS|first3=STEPHEN E.|last4=LAUE|first4=LOUISA|last5=LISTWAK|first5=SAM J.|last6=KRUESI|first6=MARKUS J. P.|last7=CHROUSOS|first7=GEORGE P.|last8=GOLD|first8=PHILIP W.|date=1991-12|title=Evidence for Impaired Activation of the Hypothalamic-Pituitary-Adrenal Axis in Patients with Chronic Fatigue Syndrome|url=https://academic.oup.com/jcem/article-abstract/73/6/1224/2653522|journal=The Journal of Clinical Endocrinology & Metabolism|language=en|volume=73|issue=6|pages=1224–1234|doi=10.1210/jcem-73-6-1224|issn=0021-972X}}</ref><ref>{{Cite journal|last=Di Giorgio|first=Annabella|last2=Hudson|first2=Marina|last3=Jerjes|first3=Walid|last4=Cleare|first4=Anthony J.|date=2005-5|title=24-hour pituitary and adrenal hormone profiles in chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/15911907|journal=Psychosomatic Medicine|volume=67|issue=3|pages=433–440|doi=10.1097/01.psy.0000161206.55324.8a|issn=1534-7796|pmid=15911907}}</ref><ref>{{Cite journal|date=2004-07-01|title=Basal circadian and pulsatile ACTH and cortisol secretion in patients with fibromyalgia and/or chronic fatigue syndrome|url=https://www.sciencedirect.com/science/article/pii/S0889159104000212|journal=Brain, Behavior, and Immunity|language=en|volume=18|issue=4|pages=314–325|doi=10.1016/j.bbi.2003.12.011|issn=0889-1591}}</ref>).

Patients with ME have also reported other problems with the pituitary, such as [[Empty Sella Syndrome]] and [[pituitary adenoma]]. These may be of note to guide future research.

== Learn more ==
Khan Academy | [https://www.sciencedirect.com/science/article/pii/S0889159104000212 The hypothalamus and pituitary gland]

== References ==
<references />

Pituitary gland

2018-10-25T16:11:34Z

Paulitasofia1:structural edits

The '''pituitary gland''', or hypophysis, is a pea-sized gland of the [[endocrine system]], situated at the base of the brain. As part of the [[Hypothalamic-pituitary-adrenal axis|HPA axis]], it is regulated by the [[hypothalamus]] to produce, store, and secrete various [[hormones]], which target other endocrine glands. The pituitary gland is sometimes referred to as the “master gland” as it regulates the function of the other endocrine glands.<ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>

== Structure and Function ==
[[File:Pituitary lobes.jpg|thumb|Anatomical diagram of the pituitary gland, depicting the posterior, anterior, and intermediate lobes.<ref>{{Cite web|url=http://www.daviddarling.info/encyclopedia/P/pituitary_gland.html|title=pituitary gland|last=Darling|first=David|website=www.daviddarling.info|access-date=2018-10-25}}</ref>]]
The pituitary gland sits at the base of the brain, underneath the hypothalamus. It is surrounded by a protective bony cavity called the [[sella turcica]]. The pituitary is divided into three distinct lobes: posterior, anterior, and intermediate.<ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>
=== Posterior ===
The posterior pituitary develops as an extension of the [[hypothalamus]] (distinct from the anterior pituitary). The posterior pituitary is largely made up of the terminals of nerve cells of the hypothalamus, as neurons in the hypothalamus project directly to the posterior pituitary. Hormones produced by the hypothalamus are stored in the terminals of hypothalamic neurons in the posterior pituitary, and are released by nerve excitation. The two major hormones stored and secreted by the posterior pituitary include:
* [[Antidiuretic hormone]] (ADH, also known as vasopressin)
* [[Oxytocin]] <ref>{{Cite book|url=https://www.ncbi.nlm.nih.gov/books/NBK27/|title=The pituitary gland|last=Nussey|first=Stephen|last2=Whitehead|first2=Saffron|date=2001|publisher=BIOS Scientific Publishers|language=en}}</ref>

=== Anterior ===
The anterior pituitary is structurally distinct from the posterior pituitary. It makes up 80% of the pituitary gland, and is made up of different types of endocrine cells. These cells are classified by the hormones they synthesize and release, and are regulated by the hypothalamus via releasing and inhibiting hormones. The six major hormones of the anterior pituitary are:
* [[Growth hormone]] (GH)
* [[Adrenocorticotropic hormone]] (ACTH)
* [[Thyroid-stimulating hormone]] (TSH)
* [[Follicular-stimulating hormone]] (FSH)
* [[Luteinizing hormone]] (LH)
* [[Prolactin]] <ref>{{Cite book|url=https://www.ncbi.nlm.nih.gov/books/NBK27/|title=The pituitary gland|last=Nussey|first=Stephen|last2=Whitehead|first2=Saffron|date=2001|publisher=BIOS Scientific Publishers|language=en}}</ref><ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>

=== Intermediate ===
The intermediate lobe is present in many lower vertebrates, but is almost absent in humans. The intermediate pituitary synthesizes and secretes:
* [[Melanocyte-stimulating hormone]] (MSH)

== Function of Pituitary Hormones ==
{| class="wikitable"
|'''Hormone'''
|'''Target Organ'''
|'''Role'''
|-
|Growth hormone (GH)
|Muscular, skeletal, and fat tissue
|Regulates growth and physical development by stimulating muscle growth and reducing fat tissue
|-
|Adrenocorticotropic hormone (ACTH)
|Adrenal glands
|Stimulates the adrenal glands to produce cortisol and other hormones
|-
|Thyroid-stimulating hormone (TSH)
|Thyroid gland
|Stimulates the thyroid to produce thyroid hormone
|-
|Follicular-stimulating hormone (FSH)
|Ovaries or testes
|Stimulates the ovaries to produce eggs/the testes to produce sperm, and the sex organs to produce sex hormones
|-
|Luteinizing hormone (LH)
|Ovaries or testes
|Stimulates the ovaries to produce eggs/the testes to produce sperm, and the sex organs to produce sex hormones
|-
|Prolactin
|Mammary glands
|Stimulates the mammary glands to produce milk
|-
|Antidiuretic hormone (ADH, also known as vasopressin)
|Kidneys
|Regulates amount of water absorbed and excreted by the kidneys
|-
|Oxytocin
|Uterus and mammary glands
|Causes uterus contraction during childbirth, stimulates contractions of the milk ducts in breast for breastfeeding
|-
|Melanocyte-stimulating hormone (MSH)
|Skin and hair
|Stimulates the production of melanin in skin and hair, suppresses appetite, contributes to sexual arousal
|}
<ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>
[[File:Pituitary diagram.jpg|none|thumb|602x602px|Diagram of the pituitary gland, the hormones it releases, and its target organs.<ref>{{Cite web|url=https://www.earthslab.com/physiology/pituitary-gland-control-hormones-anterior-posterior-lobe/|title=Pituitary Gland – Control And Hormones of Anterior And Posterior Lobe|website=www.earthslab.com|language=en-US|access-date=2018-10-25}}</ref>]]

== Dysfunction and Disease ==
Dysfunction of the pituitary gland can result in overproduction or underproduction of pituitary hormones, thus having major consequences in bodily function. Conditions of pituitary malfunction include:
* [[Acromegaly]] -- overproduction of GH
* [[Cushing’s disease]] -- overproduction of ACTH
* GH deficiency -- underproduction of GH
* Syndrome of inappropriate antidiuretic hormone -- overproduction of antidiuretic hormone
* [[Diabetes insipidus]] -- underproduction of antidiuretic hormone
* [[Sheehan syndrome]] -- underproduction of any pituitary hormone
* Pickardt-Falhbusch Syndrome -- underproduction of any pituitary hormone aside from prolactin
* Hyperpituitarism (usually pituitary adenoma) -- overproduction of any pituitary hormone
* Hypopituitarism -- underproduction of any pituitary hormone
* Hypophysitis -- inflammation of the pituitary gland
* Autoimmune hypophysitis -- inflammation of the pituitary gland due to autoimmunity
* [[Pituitary adenoma]] -- noncancerous tumor of the pituitary gland <ref>{{Cite journal|date=2018-08-11|title=Pituitary disease|url=https://en.wikipedia.org/w/index.php?title=Pituitary_disease&oldid=854490027|journal=Wikipedia|language=en}}</ref>

=== ME ===
Dysfunction of the endocrine system, with a focus on HPA axis hypofunction, has been reported in individuals with ME.<ref>{{Cite journal|last=Nijhof|first=Sanne L.|last2=Rutten|first2=Juliette M. T. M.|last3=Uiterwaal|first3=Cuno S. P. M.|last4=Bleijenberg|first4=Gijs|last5=Kimpen|first5=Jan L. L.|last6=Putte|first6=Elise M. van de|date=2014-4|title=The role of hypocortisolism in chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/24636516|journal=Psychoneuroendocrinology|volume=42|pages=199–206|doi=10.1016/j.psyneuen.2014.01.017|issn=1873-3360|pmid=24636516}}</ref><ref>{{Cite journal|last=Papadopoulos|first=Andrew S.|last2=Cleare|first2=Anthony J.|date=2011-09-27|title=Hypothalamic-pituitary-adrenal axis dysfunction in chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/21946893|journal=Nature Reviews. Endocrinology|volume=8|issue=1|pages=22–32|doi=10.1038/nrendo.2011.153|issn=1759-5037|pmid=21946893}}</ref><ref>{{Cite journal|last=Heim|first=Christine|last2=Nater|first2=Urs M.|last3=Maloney|first3=Elizabeth|last4=Boneva|first4=Roumiana|last5=Jones|first5=James F.|last6=Reeves|first6=William C.|date=2009-1|title=Childhood trauma and risk for chronic fatigue syndrome: association with neuroendocrine dysfunction|url=https://www.ncbi.nlm.nih.gov/pubmed/19124690|journal=Archives of General Psychiatry|volume=66|issue=1|pages=72–80|doi=10.1001/archgenpsychiatry.2008.508|issn=1538-3636|pmid=19124690}}</ref><ref name=":0">{{Cite journal|last=Morris|first=Gerwyn|last2=Anderson|first2=George|last3=Maes|first3=Michael|date=2016-10-20|title=Hypothalamic-Pituitary-Adrenal Hypofunction in Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS) as a Consequence of Activated Immune-Inflammatory and Oxidative and Nitrosative Pathways|url=https://link.springer.com/article/10.1007/s12035-016-0170-2|journal=Molecular Neurobiology|language=en|volume=54|issue=9|pages=6806–6819|doi=10.1007/s12035-016-0170-2|issn=0893-7648}}</ref>. It has been suggested that HPA axis hypofunction in ME is caused by chronic activation of the inflammatory and oxidative and nitrosative stress pathways<ref name=":0" />. However, this area of research continues to lack studies with direct measures of pituitary function.

Some patients report that there seems to be a period of pituitary/HPA axis hyperfunction in the earlier stage of ME, whereas later in disease progression there's a switch to hypofunction. This could perhaps explain some of the wide variation across studies (e.g.,<ref>{{Cite journal|last=DEMITRACK|first=MARK A.|last2=DALE|first2=JANET K.|last3=STRAUS|first3=STEPHEN E.|last4=LAUE|first4=LOUISA|last5=LISTWAK|first5=SAM J.|last6=KRUESI|first6=MARKUS J. P.|last7=CHROUSOS|first7=GEORGE P.|last8=GOLD|first8=PHILIP W.|date=1991-12|title=Evidence for Impaired Activation of the Hypothalamic-Pituitary-Adrenal Axis in Patients with Chronic Fatigue Syndrome|url=https://academic.oup.com/jcem/article-abstract/73/6/1224/2653522|journal=The Journal of Clinical Endocrinology & Metabolism|language=en|volume=73|issue=6|pages=1224–1234|doi=10.1210/jcem-73-6-1224|issn=0021-972X}}</ref><ref>{{Cite journal|last=Di Giorgio|first=Annabella|last2=Hudson|first2=Marina|last3=Jerjes|first3=Walid|last4=Cleare|first4=Anthony J.|date=2005-5|title=24-hour pituitary and adrenal hormone profiles in chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/15911907|journal=Psychosomatic Medicine|volume=67|issue=3|pages=433–440|doi=10.1097/01.psy.0000161206.55324.8a|issn=1534-7796|pmid=15911907}}</ref><ref>{{Cite journal|date=2004-07-01|title=Basal circadian and pulsatile ACTH and cortisol secretion in patients with fibromyalgia and/or chronic fatigue syndrome|url=https://www.sciencedirect.com/science/article/pii/S0889159104000212|journal=Brain, Behavior, and Immunity|language=en|volume=18|issue=4|pages=314–325|doi=10.1016/j.bbi.2003.12.011|issn=0889-1591}}</ref>).

Patients with ME have also reported other problems with the pituitary, such as [[Empty Sella Syndrome]] and [[pituitary adenoma]]. These may be of note to guide future research.

== Learn more ==
Khan Academy | [https://www.sciencedirect.com/science/article/pii/S0889159104000212 The hypothalamus and pituitary gland]

== References ==
<references />

Pituitary gland

2018-10-25T16:09:55Z

Paulitasofia1:minor changes

The '''pituitary gland''', or hypophysis, is a pea-sized gland of the [[endocrine system]], situated at the base of the brain. As part of the [[Hypothalamic-pituitary-adrenal axis|HPA axis]], it is regulated by the [[hypothalamus]] to produce, store, and secrete various [[hormones]], which target other endocrine glands. The pituitary gland is sometimes referred to as the “master gland” as it regulates the function of the other endocrine glands.<ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>

== Structure and Function ==
[[File:Pituitary lobes.jpg|thumb|Anatomical diagram of the pituitary gland, depicting the posterior, anterior, and intermediate lobes.<ref>{{Cite web|url=http://www.daviddarling.info/encyclopedia/P/pituitary_gland.html|title=pituitary gland|last=Darling|first=David|website=www.daviddarling.info|access-date=2018-10-25}}</ref>]]
The pituitary gland sits at the base of the brain, underneath the hypothalamus. It is surrounded by a protective bony cavity called the [[sella turcica]]. The pituitary is divided into three distinct lobes: posterior, anterior, and intermediate.<ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>
=== Posterior ===
The posterior pituitary develops as an extension of the [[hypothalamus]] (distinct from the anterior pituitary). The posterior pituitary is largely made up of the terminals of nerve cells of the hypothalamus, as neurons in the hypothalamus project directly to the posterior pituitary. Hormones produced by the hypothalamus are stored in the terminals of hypothalamic neurons in the posterior pituitary, and are released by nerve excitation. The two major hormones stored and secreted by the posterior pituitary include:
* [[Antidiuretic hormone]] (ADH, also known as vasopressin)
* [[Oxytocin]] <ref>{{Cite book|url=https://www.ncbi.nlm.nih.gov/books/NBK27/|title=The pituitary gland|last=Nussey|first=Stephen|last2=Whitehead|first2=Saffron|date=2001|publisher=BIOS Scientific Publishers|language=en}}</ref>

=== Anterior ===
The anterior pituitary is structurally distinct from the posterior pituitary. It makes up 80% of the pituitary gland, and is made up of different types of endocrine cells. These cells are classified by the hormones they synthesize and release, and are regulated by the hypothalamus via releasing and inhibiting hormones. The six major hormones of the anterior pituitary are:
* [[Growth hormone]] (GH)
* [[Adrenocorticotropic hormone]] (ACTH)
* [[Thyroid-stimulating hormone]] (TSH)
* [[Follicular-stimulating hormone]] (FSH)
* [[Luteinizing hormone]] (LH)
* [[Prolactin]] <ref>{{Cite book|url=https://www.ncbi.nlm.nih.gov/books/NBK27/|title=The pituitary gland|last=Nussey|first=Stephen|last2=Whitehead|first2=Saffron|date=2001|publisher=BIOS Scientific Publishers|language=en}}</ref><ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>

=== Intermediate ===
The intermediate lobe is present in many lower vertebrates, but is almost absent in humans. The intermediate pituitary synthesizes and secretes:
* [[Melanocyte-stimulating hormone]] (MSH)

=== Function of Hormones ===
{| class="wikitable"
|'''Hormone'''
|'''Target Organ'''
|'''Role'''
|-
|Growth hormone (GH)
|Muscular, skeletal, and fat tissue
|Regulates growth and physical development by stimulating muscle growth and reducing fat tissue
|-
|Adrenocorticotropic hormone (ACTH)
|Adrenal glands
|Stimulates the adrenal glands to produce cortisol and other hormones
|-
|Thyroid-stimulating hormone (TSH)
|Thyroid gland
|Stimulates the thyroid to produce thyroid hormone
|-
|Follicular-stimulating hormone (FSH)
|Ovaries or testes
|Stimulates the ovaries to produce eggs/the testes to produce sperm, and the sex organs to produce sex hormones
|-
|Luteinizing hormone (LH)
|Ovaries or testes
|Stimulates the ovaries to produce eggs/the testes to produce sperm, and the sex organs to produce sex hormones
|-
|Prolactin
|Mammary glands
|Stimulates the mammary glands to produce milk
|-
|Antidiuretic hormone (ADH, also known as vasopressin)
|Kidneys
|Regulates amount of water absorbed and excreted by the kidneys
|-
|Oxytocin
|Uterus and mammary glands
|Causes uterus contraction during childbirth, stimulates contractions of the milk ducts in breast for breastfeeding
|-
|Melanocyte-stimulating hormone (MSH)
|Skin and hair
|Stimulates the production of melanin in skin and hair, suppresses appetite, contributes to sexual arousal
|}
<ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>
[[File:Pituitary diagram.jpg|none|thumb|602x602px|Diagram of the pituitary gland, the hormones it releases, and its target organs.<ref>{{Cite web|url=https://www.earthslab.com/physiology/pituitary-gland-control-hormones-anterior-posterior-lobe/|title=Pituitary Gland – Control And Hormones of Anterior And Posterior Lobe|website=www.earthslab.com|language=en-US|access-date=2018-10-25}}</ref>]]

== '''Dysfunction and Disease''' ==
Dysfunction of the pituitary gland can result in overproduction or underproduction of pituitary hormones, thus having major consequences in bodily function. Conditions of pituitary malfunction include:
* [[Acromegaly]] -- overproduction of GH
* [[Cushing’s disease]] -- overproduction of ACTH
* GH deficiency -- underproduction of GH
* Syndrome of inappropriate antidiuretic hormone -- overproduction of antidiuretic hormone
* [[Diabetes insipidus]] -- underproduction of antidiuretic hormone
* [[Sheehan syndrome]] -- underproduction of any pituitary hormone
* Pickardt-Falhbusch Syndrome -- underproduction of any pituitary hormone aside from prolactin
* Hyperpituitarism (usually pituitary adenoma) -- overproduction of any pituitary hormone
* Hypopituitarism -- underproduction of any pituitary hormone
* Hypophysitis -- inflammation of the pituitary gland
* Autoimmune hypophysitis -- inflammation of the pituitary gland due to autoimmunity
* [[Pituitary adenoma]] -- noncancerous tumor of the pituitary gland <ref>{{Cite journal|date=2018-08-11|title=Pituitary disease|url=https://en.wikipedia.org/w/index.php?title=Pituitary_disease&oldid=854490027|journal=Wikipedia|language=en}}</ref>

=== ME ===
Dysfunction of the endocrine system, with a focus on HPA axis hypofunction, has been reported in individuals with ME.<ref>{{Cite journal|last=Nijhof|first=Sanne L.|last2=Rutten|first2=Juliette M. T. M.|last3=Uiterwaal|first3=Cuno S. P. M.|last4=Bleijenberg|first4=Gijs|last5=Kimpen|first5=Jan L. L.|last6=Putte|first6=Elise M. van de|date=2014-4|title=The role of hypocortisolism in chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/24636516|journal=Psychoneuroendocrinology|volume=42|pages=199–206|doi=10.1016/j.psyneuen.2014.01.017|issn=1873-3360|pmid=24636516}}</ref><ref>{{Cite journal|last=Papadopoulos|first=Andrew S.|last2=Cleare|first2=Anthony J.|date=2011-09-27|title=Hypothalamic-pituitary-adrenal axis dysfunction in chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/21946893|journal=Nature Reviews. Endocrinology|volume=8|issue=1|pages=22–32|doi=10.1038/nrendo.2011.153|issn=1759-5037|pmid=21946893}}</ref><ref>{{Cite journal|last=Heim|first=Christine|last2=Nater|first2=Urs M.|last3=Maloney|first3=Elizabeth|last4=Boneva|first4=Roumiana|last5=Jones|first5=James F.|last6=Reeves|first6=William C.|date=2009-1|title=Childhood trauma and risk for chronic fatigue syndrome: association with neuroendocrine dysfunction|url=https://www.ncbi.nlm.nih.gov/pubmed/19124690|journal=Archives of General Psychiatry|volume=66|issue=1|pages=72–80|doi=10.1001/archgenpsychiatry.2008.508|issn=1538-3636|pmid=19124690}}</ref><ref name=":0">{{Cite journal|last=Morris|first=Gerwyn|last2=Anderson|first2=George|last3=Maes|first3=Michael|date=2016-10-20|title=Hypothalamic-Pituitary-Adrenal Hypofunction in Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS) as a Consequence of Activated Immune-Inflammatory and Oxidative and Nitrosative Pathways|url=https://link.springer.com/article/10.1007/s12035-016-0170-2|journal=Molecular Neurobiology|language=en|volume=54|issue=9|pages=6806–6819|doi=10.1007/s12035-016-0170-2|issn=0893-7648}}</ref>. It has been suggested that HPA axis hypofunction in ME is caused by chronic activation of the inflammatory and oxidative and nitrosative stress pathways<ref name=":0" />. However, this area of research continues to lack studies with direct measures of pituitary function.

Some patients report that there seems to be a period of pituitary/HPA axis hyperfunction in the earlier stage of ME, whereas later in disease progression there's a switch to hypofunction. This could perhaps explain some of the wide variation across studies (e.g.,<ref>{{Cite journal|last=DEMITRACK|first=MARK A.|last2=DALE|first2=JANET K.|last3=STRAUS|first3=STEPHEN E.|last4=LAUE|first4=LOUISA|last5=LISTWAK|first5=SAM J.|last6=KRUESI|first6=MARKUS J. P.|last7=CHROUSOS|first7=GEORGE P.|last8=GOLD|first8=PHILIP W.|date=1991-12|title=Evidence for Impaired Activation of the Hypothalamic-Pituitary-Adrenal Axis in Patients with Chronic Fatigue Syndrome|url=https://academic.oup.com/jcem/article-abstract/73/6/1224/2653522|journal=The Journal of Clinical Endocrinology & Metabolism|language=en|volume=73|issue=6|pages=1224–1234|doi=10.1210/jcem-73-6-1224|issn=0021-972X}}</ref><ref>{{Cite journal|last=Di Giorgio|first=Annabella|last2=Hudson|first2=Marina|last3=Jerjes|first3=Walid|last4=Cleare|first4=Anthony J.|date=2005-5|title=24-hour pituitary and adrenal hormone profiles in chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/15911907|journal=Psychosomatic Medicine|volume=67|issue=3|pages=433–440|doi=10.1097/01.psy.0000161206.55324.8a|issn=1534-7796|pmid=15911907}}</ref><ref>{{Cite journal|date=2004-07-01|title=Basal circadian and pulsatile ACTH and cortisol secretion in patients with fibromyalgia and/or chronic fatigue syndrome|url=https://www.sciencedirect.com/science/article/pii/S0889159104000212|journal=Brain, Behavior, and Immunity|language=en|volume=18|issue=4|pages=314–325|doi=10.1016/j.bbi.2003.12.011|issn=0889-1591}}</ref>).

Patients with ME have also reported other problems with the pituitary, such as [[Empty Sella Syndrome]] and [[pituitary adenoma]]. These may be of note to guide future research.

== Learn more ==
Khan Academy | [https://www.sciencedirect.com/science/article/pii/S0889159104000212 The hypothalamus and pituitary gland]

== References ==
<references />

Pituitary gland

2018-10-25T16:05:51Z

Paulitasofia1:ME section

The '''pituitary gland''', or hypophysis, is a pea-sized gland of the [[endocrine system]], situated at the base of the brain. As part of the [[Hypothalamic-pituitary-adrenal axis|HPA axis]], it is regulated by the [[hypothalamus]] to produce, store, and secrete various [[hormones]], which target other endocrine glands. The pituitary gland is sometimes referred to as the “master gland” as it regulates the function of the other endocrine glands.<ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>

=== Structure and Function ===
[[File:Pituitary lobes.jpg|thumb|Anatomical diagram of the pituitary gland, depicting the posterior, anterior, and intermediate lobes.<ref>{{Cite web|url=http://www.daviddarling.info/encyclopedia/P/pituitary_gland.html|title=pituitary gland|last=Darling|first=David|website=www.daviddarling.info|access-date=2018-10-25}}</ref>]]
The pituitary gland sits at the base of the brain, underneath the hypothalamus. It is surrounded by a protective bony cavity called the [[sella turcica]]. The pituitary is divided into three distinct lobes: posterior, anterior, and intermediate.<ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>

==== Posterior ====
The posterior pituitary develops as an extension of the [[hypothalamus]] (distinct from the anterior pituitary). The posterior pituitary is largely made up of the terminals of nerve cells of the hypothalamus, as neurons in the hypothalamus project directly to the posterior pituitary. Hormones produced by the hypothalamus are stored in the terminals of hypothalamic neurons in the posterior pituitary, and are released by nerve excitation. The two major hormones stored and secreted by the posterior pituitary include:
* [[Antidiuretic hormone]] (ADH, also known as vasopressin)
* [[Oxytocin]] <ref>{{Cite book|url=https://www.ncbi.nlm.nih.gov/books/NBK27/|title=The pituitary gland|last=Nussey|first=Stephen|last2=Whitehead|first2=Saffron|date=2001|publisher=BIOS Scientific Publishers|language=en}}</ref>

==== Anterior ====
The anterior pituitary is structurally distinct from the posterior pituitary. It makes up 80% of the pituitary gland, and is made up of different types of endocrine cells. These cells are classified by the hormones they synthesize and release, and are regulated by the hypothalamus via releasing and inhibiting hormones. The six major hormones of the anterior pituitary are:
* [[Growth hormone]] (GH)
* [[Adrenocorticotropic hormone]] (ACTH)
* [[Thyroid-stimulating hormone]] (TSH)
* [[Follicular-stimulating hormone]] (FSH)
* [[Luteinizing hormone]] (LH)
* [[Prolactin]] <ref>{{Cite book|url=https://www.ncbi.nlm.nih.gov/books/NBK27/|title=The pituitary gland|last=Nussey|first=Stephen|last2=Whitehead|first2=Saffron|date=2001|publisher=BIOS Scientific Publishers|language=en}}</ref><ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>

==== Intermediate ====
The intermediate lobe is present in many lower vertebrates, but is almost absent in humans. The intermediate pituitary synthesizes and secretes:
* [[Melanocyte-stimulating hormone]] (MSH)

=== Function of Hormones ===
{| class="wikitable"
|'''Hormone'''
|'''Target Organ'''
|'''Role'''
|-
|Growth hormone (GH)
|Muscular, skeletal, and fat tissue
|Regulates growth and physical development by stimulating muscle growth and reducing fat tissue
|-
|Adrenocorticotropic hormone (ACTH)
|Adrenal glands
|Stimulates the adrenal glands to produce cortisol and other hormones
|-
|Thyroid-stimulating hormone (TSH)
|Thyroid gland
|Stimulates the thyroid to produce thyroid hormone
|-
|Follicular-stimulating hormone (FSH)
|Ovaries or testes
|Stimulates the ovaries to produce eggs/the testes to produce sperm, and the sex organs to produce sex hormones
|-
|Luteinizing hormone (LH)
|Ovaries or testes
|Stimulates the ovaries to produce eggs/the testes to produce sperm, and the sex organs to produce sex hormones
|-
|Prolactin
|Mammary glands
|Stimulates the mammary glands to produce milk
|-
|Antidiuretic hormone (ADH, also known as vasopressin)
|Kidneys
|Regulates amount of water absorbed and excreted by the kidneys
|-
|Oxytocin
|Uterus and mammary glands
|Causes uterus contraction during childbirth, stimulates contractions of the milk ducts in breast for breastfeeding
|-
|Melanocyte-stimulating hormone (MSH)
|Skin and hair
|Stimulates the production of melanin in skin and hair, suppresses appetite, contributes to sexual arousal
|}
<ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>
[[File:Pituitary diagram.jpg|none|thumb|602x602px|Diagram of the pituitary gland, the hormones it releases, and its target organs.<ref>{{Cite web|url=https://www.earthslab.com/physiology/pituitary-gland-control-hormones-anterior-posterior-lobe/|title=Pituitary Gland – Control And Hormones of Anterior And Posterior Lobe|website=www.earthslab.com|language=en-US|access-date=2018-10-25}}</ref>]]

'''Dysfunction and Disease'''

Dysfunction of the pituitary gland can result in overproduction or underproduction of pituitary hormones, thus having major consequences in bodily function. Conditions of pituitary malfunction include:
* Acromegaly -- overproduction of GH
* Cushing’s disease -- overproduction of ACTH
* GH deficiency -- underproduction of GH
* Syndrome of inappropriate antidiuretic hormone -- overproduction of antidiuretic hormone
* Diabetes insipidus -- underproduction of antidiuretic hormone
* Sheehan syndrome -- underproduction of any pituitary hormone
* Pickardt-Falhbusch Syndrome -- underproduction of any pituitary hormone aside from prolactin
* Hyperpituitarism (usually pituitary adenoma) -- overproduction of any pituitary hormone
* Hypopituitarism -- underproduction of any pituitary hormone
* Hypophysitis -- inflammation of the pituitary gland
* Autoimmune hypophysitis -- inflammation of the pituitary gland due to autoimmunity
* Pituitary adenoma -- noncancerous tumor of the pituitary gland <ref>{{Cite journal|date=2018-08-11|title=Pituitary disease|url=https://en.wikipedia.org/w/index.php?title=Pituitary_disease&oldid=854490027|journal=Wikipedia|language=en}}</ref>

=== ME ===
Dysfunction of the endocrine system, with a focus on HPA axis hypofunction, has been reported in individuals with ME.<ref>{{Cite journal|last=Nijhof|first=Sanne L.|last2=Rutten|first2=Juliette M. T. M.|last3=Uiterwaal|first3=Cuno S. P. M.|last4=Bleijenberg|first4=Gijs|last5=Kimpen|first5=Jan L. L.|last6=Putte|first6=Elise M. van de|date=2014-4|title=The role of hypocortisolism in chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/24636516|journal=Psychoneuroendocrinology|volume=42|pages=199–206|doi=10.1016/j.psyneuen.2014.01.017|issn=1873-3360|pmid=24636516}}</ref><ref>{{Cite journal|last=Papadopoulos|first=Andrew S.|last2=Cleare|first2=Anthony J.|date=2011-09-27|title=Hypothalamic-pituitary-adrenal axis dysfunction in chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/21946893|journal=Nature Reviews. Endocrinology|volume=8|issue=1|pages=22–32|doi=10.1038/nrendo.2011.153|issn=1759-5037|pmid=21946893}}</ref><ref>{{Cite journal|last=Heim|first=Christine|last2=Nater|first2=Urs M.|last3=Maloney|first3=Elizabeth|last4=Boneva|first4=Roumiana|last5=Jones|first5=James F.|last6=Reeves|first6=William C.|date=2009-1|title=Childhood trauma and risk for chronic fatigue syndrome: association with neuroendocrine dysfunction|url=https://www.ncbi.nlm.nih.gov/pubmed/19124690|journal=Archives of General Psychiatry|volume=66|issue=1|pages=72–80|doi=10.1001/archgenpsychiatry.2008.508|issn=1538-3636|pmid=19124690}}</ref><ref name=":0">{{Cite journal|last=Morris|first=Gerwyn|last2=Anderson|first2=George|last3=Maes|first3=Michael|date=2016-10-20|title=Hypothalamic-Pituitary-Adrenal Hypofunction in Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS) as a Consequence of Activated Immune-Inflammatory and Oxidative and Nitrosative Pathways|url=https://link.springer.com/article/10.1007/s12035-016-0170-2|journal=Molecular Neurobiology|language=en|volume=54|issue=9|pages=6806–6819|doi=10.1007/s12035-016-0170-2|issn=0893-7648}}</ref>. It has been suggested that HPA axis hypofunction in ME is caused by chronic activation of the inflammatory and oxidative and nitrosative stress pathways<ref name=":0" />. However, this area of research continues to lack studies with direct measures of pituitary function.

Some patients report that there seems to be a period of pituitary/HPA axis hyperfunction in the earlier stage of ME, whereas later in disease progression there's a switch to hypofunction. This could perhaps explain some of the wide variation across studies (e.g.,<ref>{{Cite journal|last=DEMITRACK|first=MARK A.|last2=DALE|first2=JANET K.|last3=STRAUS|first3=STEPHEN E.|last4=LAUE|first4=LOUISA|last5=LISTWAK|first5=SAM J.|last6=KRUESI|first6=MARKUS J. P.|last7=CHROUSOS|first7=GEORGE P.|last8=GOLD|first8=PHILIP W.|date=1991-12|title=Evidence for Impaired Activation of the Hypothalamic-Pituitary-Adrenal Axis in Patients with Chronic Fatigue Syndrome|url=https://academic.oup.com/jcem/article-abstract/73/6/1224/2653522|journal=The Journal of Clinical Endocrinology & Metabolism|language=en|volume=73|issue=6|pages=1224–1234|doi=10.1210/jcem-73-6-1224|issn=0021-972X}}</ref><ref>{{Cite journal|last=Di Giorgio|first=Annabella|last2=Hudson|first2=Marina|last3=Jerjes|first3=Walid|last4=Cleare|first4=Anthony J.|date=2005-5|title=24-hour pituitary and adrenal hormone profiles in chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/15911907|journal=Psychosomatic Medicine|volume=67|issue=3|pages=433–440|doi=10.1097/01.psy.0000161206.55324.8a|issn=1534-7796|pmid=15911907}}</ref><ref>{{Cite journal|date=2004-07-01|title=Basal circadian and pulsatile ACTH and cortisol secretion in patients with fibromyalgia and/or chronic fatigue syndrome|url=https://www.sciencedirect.com/science/article/pii/S0889159104000212|journal=Brain, Behavior, and Immunity|language=en|volume=18|issue=4|pages=314–325|doi=10.1016/j.bbi.2003.12.011|issn=0889-1591}}</ref>).

Patients with ME have also reported other problems with the pituitary, such as [[Empty Sella Syndrome]] and [[pituitary adenoma]]. These may be of note to guide future research.

=== Learn more ===
Khan Academy | [https://www.sciencedirect.com/science/article/pii/S0889159104000212 The hypothalamus and pituitary gland] <references />

Pituitary gland

2018-10-25T15:49:39Z

Paulitasofia1:small additions, citations

The '''pituitary gland''', or hypophysis, is a pea-sized gland of the [[endocrine system]], situated at the base of the brain. As part of the [[Hypothalamic-pituitary-adrenal axis|HPA axis]], it is regulated by the [[hypothalamus]] to produce, store, and secrete various [[hormones]], which target other endocrine glands. The pituitary gland is sometimes referred to as the “master gland” as it regulates the function of the other endocrine glands.<ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>

=== Structure and Function ===
[[File:Pituitary lobes.jpg|thumb|Anatomical diagram of the pituitary gland, depicting the posterior, anterior, and intermediate lobes.<ref>{{Cite web|url=http://www.daviddarling.info/encyclopedia/P/pituitary_gland.html|title=pituitary gland|last=Darling|first=David|website=www.daviddarling.info|access-date=2018-10-25}}</ref>]]
The pituitary gland sits at the base of the brain, underneath the hypothalamus. It is surrounded by a protective bony cavity called the [[sella turcica]]. The pituitary is divided into three distinct lobes: posterior, anterior, and intermediate.<ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>

==== Posterior ====
The posterior pituitary develops as an extension of the [[hypothalamus]] (distinct from the anterior pituitary). The posterior pituitary is largely made up of the terminals of nerve cells of the hypothalamus, as neurons in the hypothalamus project directly to the posterior pituitary. Hormones produced by the hypothalamus are stored in the terminals of hypothalamic neurons in the posterior pituitary, and are released by nerve excitation. The two major hormones stored and secreted by the posterior pituitary include:
* [[Antidiuretic hormone]] (ADH, also known as vasopressin)
* [[Oxytocin]] <ref>{{Cite book|url=https://www.ncbi.nlm.nih.gov/books/NBK27/|title=The pituitary gland|last=Nussey|first=Stephen|last2=Whitehead|first2=Saffron|date=2001|publisher=BIOS Scientific Publishers|language=en}}</ref>

==== Anterior ====
The anterior pituitary is structurally distinct from the posterior pituitary. It makes up 80% of the pituitary gland, and is made up of different types of endocrine cells. These cells are classified by the hormones they synthesize and release, and are regulated by the hypothalamus via releasing and inhibiting hormones. The six major hormones of the anterior pituitary are:
* [[Growth hormone]] (GH)
* [[Adrenocorticotropic hormone]] (ACTH)
* [[Thyroid-stimulating hormone]] (TSH)
* [[Follicular-stimulating hormone]] (FSH)
* [[Luteinizing hormone]] (LH)
* [[Prolactin]] <ref>{{Cite book|url=https://www.ncbi.nlm.nih.gov/books/NBK27/|title=The pituitary gland|last=Nussey|first=Stephen|last2=Whitehead|first2=Saffron|date=2001|publisher=BIOS Scientific Publishers|language=en}}</ref><ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>

==== Intermediate ====
The intermediate lobe is present in many lower vertebrates, but is almost absent in humans. The intermediate pituitary synthesizes and secretes:
* [[Melanocyte-stimulating hormone]] (MSH)

=== Function of Hormones ===
{| class="wikitable"
|'''Hormone'''
|'''Target Organ'''
|'''Role'''
|-
|Growth hormone (GH)
|Muscular, skeletal, and fat tissue
|Regulates growth and physical development by stimulating muscle growth and reducing fat tissue
|-
|Adrenocorticotropic hormone (ACTH)
|Adrenal glands
|Stimulates the adrenal glands to produce cortisol and other hormones
|-
|Thyroid-stimulating hormone (TSH)
|Thyroid gland
|Stimulates the thyroid to produce thyroid hormone
|-
|Follicular-stimulating hormone (FSH)
|Ovaries or testes
|Stimulates the ovaries to produce eggs/the testes to produce sperm, and the sex organs to produce sex hormones
|-
|Luteinizing hormone (LH)
|Ovaries or testes
|Stimulates the ovaries to produce eggs/the testes to produce sperm, and the sex organs to produce sex hormones
|-
|Prolactin
|Mammary glands
|Stimulates the mammary glands to produce milk
|-
|Antidiuretic hormone (ADH, also known as vasopressin)
|Kidneys
|Regulates amount of water absorbed and excreted by the kidneys
|-
|Oxytocin
|Uterus and mammary glands
|Causes uterus contraction during childbirth, stimulates contractions of the milk ducts in breast for breastfeeding
|-
|Melanocyte-stimulating hormone (MSH)
|Skin and hair
|Stimulates the production of melanin in skin and hair, suppresses appetite, contributes to sexual arousal
|}
<ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>
[[File:Pituitary diagram.jpg|none|thumb|602x602px|Diagram of the pituitary gland, the hormones it releases, and its target organs.<ref>{{Cite web|url=https://www.earthslab.com/physiology/pituitary-gland-control-hormones-anterior-posterior-lobe/|title=Pituitary Gland – Control And Hormones of Anterior And Posterior Lobe|website=www.earthslab.com|language=en-US|access-date=2018-10-25}}</ref>]]

'''Dysfunction and Disease'''

Dysfunction of the pituitary gland can result in overproduction or underproduction of pituitary hormones, thus having major consequences in bodily function. Conditions of pituitary malfunction include:
* Acromegaly -- overproduction of GH
* Cushing’s disease -- overproduction of ACTH
* GH deficiency -- underproduction of GH
* Syndrome of inappropriate antidiuretic hormone -- overproduction of antidiuretic hormone
* Diabetes insipidus -- underproduction of antidiuretic hormone
* Sheehan syndrome -- underproduction of any pituitary hormone
* Pickardt-Falhbusch Syndrome -- underproduction of any pituitary hormone aside from prolactin
* Hyperpituitarism (usually pituitary adenoma) -- overproduction of any pituitary hormone
* Hypopituitarism -- underproduction of any pituitary hormone
* Hypophysitis -- inflammation of the pituitary gland
* Autoimmune hypophysitis -- inflammation of the pituitary gland due to autoimmunity
* Pituitary adenoma -- noncancerous tumor of the pituitary gland <ref>{{Cite journal|date=2018-08-11|title=Pituitary disease|url=https://en.wikipedia.org/w/index.php?title=Pituitary_disease&oldid=854490027|journal=Wikipedia|language=en}}</ref>

=== ME ===
Dysfunction of the endocrine system, with a focus on HPA axis hypofunction, has been reported in individuals with ME.<ref>{{Cite journal|last=Nijhof|first=Sanne L.|last2=Rutten|first2=Juliette M. T. M.|last3=Uiterwaal|first3=Cuno S. P. M.|last4=Bleijenberg|first4=Gijs|last5=Kimpen|first5=Jan L. L.|last6=Putte|first6=Elise M. van de|date=2014-4|title=The role of hypocortisolism in chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/24636516|journal=Psychoneuroendocrinology|volume=42|pages=199–206|doi=10.1016/j.psyneuen.2014.01.017|issn=1873-3360|pmid=24636516}}</ref><ref>{{Cite journal|last=Papadopoulos|first=Andrew S.|last2=Cleare|first2=Anthony J.|date=2011-09-27|title=Hypothalamic-pituitary-adrenal axis dysfunction in chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/21946893|journal=Nature Reviews. Endocrinology|volume=8|issue=1|pages=22–32|doi=10.1038/nrendo.2011.153|issn=1759-5037|pmid=21946893}}</ref><ref>{{Cite journal|last=Heim|first=Christine|last2=Nater|first2=Urs M.|last3=Maloney|first3=Elizabeth|last4=Boneva|first4=Roumiana|last5=Jones|first5=James F.|last6=Reeves|first6=William C.|date=2009-1|title=Childhood trauma and risk for chronic fatigue syndrome: association with neuroendocrine dysfunction|url=https://www.ncbi.nlm.nih.gov/pubmed/19124690|journal=Archives of General Psychiatry|volume=66|issue=1|pages=72–80|doi=10.1001/archgenpsychiatry.2008.508|issn=1538-3636|pmid=19124690}}</ref><ref name=":0">{{Cite journal|last=Morris|first=Gerwyn|last2=Anderson|first2=George|last3=Maes|first3=Michael|date=2016-10-20|title=Hypothalamic-Pituitary-Adrenal Hypofunction in Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS) as a Consequence of Activated Immune-Inflammatory and Oxidative and Nitrosative Pathways|url=https://link.springer.com/article/10.1007/s12035-016-0170-2|journal=Molecular Neurobiology|language=en|volume=54|issue=9|pages=6806–6819|doi=10.1007/s12035-016-0170-2|issn=0893-7648}}</ref>. It has been suggested that HPA axis hypofunction in ME is caused by chronic activation of the inflammatory and oxidative and nitrosative stress pathways<ref name=":0" />. However, this area of research continues to lack studies with direct measures of pituitary function. <references />

Postural orthostatic tachycardia syndrome

2018-10-25T15:15:12Z

Paulitasofia1:additional info

'''Postural orthostatic tachycardia syndrome''' ('''POTS''', or '''postural tachycardia syndrome)''' is a condition in which a change from the supine position (lying horizontally) to an upright position causes an abnormally large increase in [[heart rate]], called [[tachycardia]]. It is a form of [[orthostatic intolerance]] (OI). Other symptoms of an orthostatic nature — occurring in response to upright posture — may accompany the [[tachycardia]].<ref>{{Cite journal|last=Mar|first=Philip L.|last2=Raj|first2=Satish R.|date=2014|title=Neuronal and hormonal perturbations in postural tachycardia syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/24982638|journal=Frontiers in Physiology|volume=5|pages=220|doi=10.3389/fphys.2014.00220|issn=1664-042X|pmc=|pmid=24982638|via=}}</ref> These include headaches, fatigue, sweating, nausea, fainting and dizziness may occur. The [[autonomic nervous system]] is in charge of heart rate and blood pressure but it has become dysregulated. The female to male ratio of patients with POTS is 4:1. <ref>{{Cite news|url=http://www.potsuk.org/|title=PoTS - Postural Tachycardia Syndrome|last=|first=|work=PoTS UK|access-date=2018-08-16|language=en|date=|archive-url=|archive-date=|dead-url=}}</ref><ref>{{Cite news|url=http://www.potsuk.org/what_is_pots2|title=PoTS - Postural Tachycardia Syndrome - What is POTS?|last=|first=|work=PoTS UK|access-date=2018-08-16|language=en|date=|archive-url=|archive-date=|dead-url=}}</ref>

=Signs and symptoms=
[[File:Acrocyanosis in POTS.jpg|thumb|400x400px|Acrocyanosis in POTS. This image shows the legs of a patient with POTS (right) and of a healthy control (left) after standing for 5 minutes. The reddish purple discoloration in the legs is very notable, due to poor circulation in the extremities, which returns to normal upon returning to a reclined position.]]
The main symptom of POTS is an abnormal increase in heart rate upon standing. The specific diagnostic criteria for POTS is an increase in heart rate from the lying to upright position of greater than 30 beats per minute, or a heart rate of greater than 120 beats per minute within 10 minutes of standing. Patients with POTS usually present with other symptoms, commonly occurring in the upright position. These include<ref>{{Cite web|url=http://standinguptopots.org/learning/pots-symptoms|title=Symptoms of Postural Orthostatic Tachycardia Syndrome (POTS)|last=|first=|date=July 9, 2018|website=Standing Up to POTS|archive-url=|archive-date=|dead-url=|access-date=}}</ref><ref>{{Cite journal|last=Raj|first=Satish R|date=2006-04-01|title=The Postural Tachycardia Syndrome (POTS): Pathophysiology, Diagnosis & Management|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1501099/|journal=Indian Pacing and Electrophysiology Journal|volume=6|issue=2|pages=84–99|issn=0972-6292|pmc=PMC1501099|pmid=16943900}}</ref><ref name=":1">{{Cite web|url=http://www.dysautonomiainternational.org/page.php?ID=30|title=Dysautonomia International: Postural Orthostatic Tachycardia Syndrome|website=www.dysautonomiainternational.org|language=en|access-date=2018-10-25}}</ref>:
* Hypovolemia (low blood volume)
* High levels of plasma norepinephrine when standing
* [[Dizziness]]/ [[lightheadedness]] and syncope (fainting)
* [[Headache|Headaches]] and [[migraines]]
* [[Cognitive impairment]] / [[brain fog]]
* Heart palpitations
* Chest pain
* Shortness of breath
* [[Sleep abnormalities]]
* [[Neuropathic pain|Neuropathic pain,]] Coldness or pain in the extremities
* [[Small fiber polyneuropathy]] (in 50% of patients)
* [[Fatigue]]
* Exercise intolerance
* Nausea
* Tremulousness (shaking)
* Acrocyanosis-- reddish purple discoloration in the legs, due to poor circulation in the extremities, which returns to normal upon returning to a reclined position
* [[Sensory sensitivity]]
* [[Abdominal pain]], [[gastroparesis]], or rapid [[gastric emptying]]
* Elevated sympathetic tone

=Testing=
Assessing orthostatic blood pressure can be done in a physician's office by measuring the patient's blood pressure while lying down, sitting, and standing at standardized time increments. Dr. [[Lucinda Bateman]] uses a modified orthostatic blood pressure assessment called the [[NASA 10-minute Lean Test]], a variant of a test used by NASA researchers to test for orthostatic intolerance following space flight. The NASA 10-minute Lean Test is less taxing on the patient and can be done in any physician's office. Instructions are available for printout for both [https://batemanhornecenter.org/wp-content/uploads/2016/09/NASA-Lean-Test-Instructions-1.pdf healthcare providers] and [https://batemanhornecenter.org/wp-content/uploads/2016/09/NASA-Lean-Patient-Preparation-Instructions-1.pdf patients].<ref>{{Cite news|url=https://batemanhornecenter.org/assess-orthostatic-intolerance/|title=Simple Way to Assess Orthostatic Intolerance - Bateman Horne Center|last=Bateman|first=Lucinda|date=2016-09-27|work=Bateman Horne Center Newsletter|access-date=2018-08-16|archive-url=|archive-date=|dead-url=|publisher=|language=en-US|author-link=Lucinda Bateman}}</ref>

If the results of the standard orthostatic blood pressure assessment are inconclusive, a [[tilt table test]] can be used for diagnosis.<ref>{{Cite news|url=http://myheart.net/pots-syndrome/diagnosis-tests/|title=How Doctors Diagnose & Test for POTS • MyHeart|work=MyHeart|access-date=2018-08-16|language=en-US}}</ref>

=Treatment=
A 2012 study [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3390096/ Diagnosis and management of postural orthostatic tachycardia syndrome: A brief review]<ref name=":0" /> concluded:

:"The pathophysiology of POTS is complex and the result of a number of separate mechanisms producing a common pattern of symptoms. The large number of clinical manifestations that characterize this disorder and the wide range of medications available, plus the clear evidence that certain medications and treatment strategies work in some, but not all POTS patients, demonstrates that POTS is a range of disorders requiring comprehensive investigation and characterisation to guide selection of the most appropriate treatment. The recent consensus statement will help to direct further research into the underlying conditions that lead to POTS."
: When the cause of POTS is able to be identified and treated in certain individuals, their POTS symptoms may subside. However, there is currently no cure for POTS on the broader level. The following treatments have been identified to improve symptoms and quality of life:
:* Increasing fluid intake (2-3 liters a day)
:* Increasing salt intake
:* Raising the head of the bed to conserve blood volume (less blood is turned into urine by the kidneys when reclining at an angle)
:* [[Diet]]
:* Reclined [[Exercise|exercise]], such as rowing, biking, swimming (contraindicated in patients with co-morbid [[myalgic encephalomyelitis]])
:* [[Sodium chloride]] 0.9% ([[Normal saline]])
:* Medications:
:** [[Beta-blocker|Beta-blockers]]
:** [[Fludrocortisone]]
:** [[Ivabradine]]
:** [[Erythropoietin]]
:** [[Pyridostigmine]] bromide
:** [[Vasoconstrictor|Vasoconstrictors]]
:** [[NSAID|NSAIDs]]
:** Others such as methyldopa and antidepressants <ref name=":0">{{Cite journal|last=Abed|first=Howraa|last2=Ball|first2=Patrick A|last3=Wang|first3=Le-Xin|date=2012|title=Diagnosis and management of postural orthostatic tachycardia syndrome: A brief review|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3390096/|journal=Journal of Geriatric Cardiology : JGC|volume=9|issue=1|pages=61–67|doi=10.3724/SP.J.1263.2012.00061|issn=1671-5411|pmid=22783324|via=}}</ref><ref name=":1" />
=Conditions associated with POTS =
POTS is not only comorbid with a range of diseases, but its phenotype also resembles that of other disorders (e.g., ME, [[Ehlers-Danlos syndrome|Ehlers-Danlos Syndrome]]).

===ME/CFS ===
POTS can be a co-morbid condition in [[ME/CFS]] patients.<ref>{{Cite web|url=https://www.youtube.com/watch?v=o4OqNPZoqVs|title=POTS in ME/CFS|last=|first=|date=Aug 2, 2014|website=YouTube|publisher=Freedom From ME - The Optimum Health Clinic|archive-url=|archive-date=|dead-url=|access-date=}}</ref><ref>{{Cite web|url=https://ammes.org/overlapping-conditions/|title=Overlapping Conditions – American ME and CFS Society|website=ammes.org|language=en-US|access-date=2018-08-12}}</ref> Estimates on the prevalence of POTS among [[ME/CFS]] patients varies widely, from 11% to 70%. In a 2008 study done in the UK by the Northern CFS/ME Clinical Network, using the [[Fukuda criteria]], 27% of the study population had POTS compared with 9% in the control population.<ref>{{Cite journal|last=Hoad|first=A.|last2=Spickett|first2=G.|last3=Elliott|first3=J.|last4=Newton|first4=J.|date=2008|title=Postural orthostatic tachycardia syndrome is an under-recognized condition in chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/18805903|journal=QJM: monthly journal of the Association of Physicians|volume=101|issue=12|pages=961–965|doi=10.1093/qjmed/hcn123|issn=1460-2393|pmid=18805903|via=|author-link4=Julia Newton}}</ref>

{| class="wikitable"
! colspan="3" |Prevalence of POTS in ME/CFS population samples
|-
!Study:
!number of
ME/CFS patients
!%
POTS
|-
|[[pubmed:10431117|Stewart et al. 1999]]
|25
|70%
|-
|[[pubmed:10189122|Schondorf et al. 1999]]
|75
|40%
|-
|[[pubmed:18805903|Hoad et al. 2008]]
|59
|27%
|-
|[[pubmed:23206180|Lewis et al. 2013]]
|179
|13%
|-
|[[pubmed:24206536|Reynolds et al. 2014]]
|306
|11%
|-
|[[pubmed:27696568|Roerink et al. 2017]]
|419
|5,7%
|}
A 2011 study of 58 POTS patients by the Vanderbilt Autonomic Dysfunction Center (Vanderbilt University School of Medicine, Nashville, TN, U.S.A.), reported that 64% of also met the [[Centers for Disease Control & Prevention]] criteria for [[chronic fatigue syndrome]].<ref>{{Cite journal|last=Okamoto|first=Luis E.|last2=Raj|first2=Satish R.|last3=Peltier|first3=Amanda|last4=Gamboa|first4=Alfredo|last5=Shibao|first5=Cyndya|last6=Diedrich|first6=André|last7=Black|first7=Bonnie K.|last8=Robertson|first8=David|last9=Biaggioni|first9=Italo|date=2012-02-01|title=Neurohumoral and haemodynamic profile in postural tachycardia and chronic fatigue syndromes|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3203411/|journal=Clinical Science (London, England : 1979)|volume=122|issue=Pt 4|pages=183–192|doi=10.1042/CS20110200|issn=0143-5221|pmid=21906029|via=}}</ref>

The proposed [[SEID]] criteria requires either [[orthostatic intolerance]] (of which POTS is one type) or [[cognitive dysfunction]] for a diagnosis.<ref>{{Cite journal|last=|first=|date=2015-03-16|title=Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome|url=https://www.nap.edu/read/19012/chapter/6#114|journal=The National Academies Press|language=en|volume=|pages=114|at=Box 4-3|doi=10.17226/19012|via=NAP.edu}}</ref> POTS is also a symptom of the [[Canadian Consensus Criteria]] (CCC) which diagnoses ME/CFS,<ref>{{Cite web|url=http://me-pedia.org/wiki/Canadian_Consensus_Criteria#Definition|title=Canadian Consensus Criteria - MEpedia|website=me-pedia.org|language=en|access-date=2018-08-16}}</ref> and the [[International Consensus Criteria]] (ICC) for diagnosing myalgic encephalomyelitis.<ref>{{Cite web|url=http://me-pedia.org/wiki/International_Consensus_Criteria#D._Energy_production.2Ftransportation_impairments:_At_least_one_symptom|title=International Consensus Criteria - MEpedia|website=me-pedia.org|language=en|access-date=2018-08-16}}</ref> However, the diagnosis of POTS alone does not automatically support a [[ME/CFS]] diagnosis and cannot be used as a [[diagnostic biomarker]] to determine ME/CFS. POTS can occur independent from ME/CFS, and, likewise, ME/CFS can occur without the symptomatology of POTS.

A September 2016 study in the Netherlands by Roerink et al., found that patients with CFS who fulfilled the [[SEID]] criteria did not have a prevalence of POTS different from that in the overall ME/CFS population. In adults with ME/CFS, the prevalence of POTS was low, between 6% - 18% (depending on age), was not different from the rate in non-ME/CFS fatigued patients, and was not related to disease severity or treatment outcome.<ref name="Roerink, 2016" />

ME patients with POTS can experience impaired neurocognitive abilities (such as working memory, information processing) under increased orthostatic stress (i.e., standing, tilt table test).<ref>{{Cite journal|last=OCON|first=Anthony J.|last2=MESSER|first2=Zachary R.|last3=MEDOW|first3=Marvin S.|last4=STEWART|first4=Julian M.|date=2012-3|title=Increasing orthostatic stress impairs neurocognitive functioning in chronic fatigue syndrome with postural tachycardia syndrome|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3368269/|journal=Clinical Science (London, England : 1979)|volume=122|issue=5|pages=227–238|doi=10.1042/CS20110241|issn=0143-5221|pmc=PMC3368269|pmid=21919887}}</ref>

=== Other conditions associated with POTS ===
[[Ehlers-Danlos syndrome|Ehlers Danlos syndrome]]

[[Fibromyalgia]]

[[Autoimmune disease|Autoimmune diseases]]<ref name=":1" />

[[Chiari malformation]]<ref>{{Cite journal|last=Weig|first=Spencer G.|last2=Buckthal|first2=Paul E.|last3=Choi|first3=Samuel K.|last4=Zellem|first4=Ronald T.|date=1991-10-01|title=Recurrent syncope as the presenting symptom of Arnold‐Chiari malformation|url=http://n.neurology.org/content/41/10/1673|journal=Neurology|language=en|volume=41|issue=10|pages=1673–1673|doi=10.1212/WNL.41.10.1673|issn=0028-3878|pmid=1922816}}</ref><ref>{{Cite journal|last=Prilipko|first=O.|last2=Dehdashti|first2=A. R.|last3=Zaim|first3=S.|last4=Seeck|first4=M.|date=2005-07-01|title=Orthostatic intolerance and syncope associated with Chiari type I malformation|url=https://jnnp.bmj.com/content/76/7/1034|journal=Journal of Neurology, Neurosurgery & Psychiatry|language=en|volume=76|issue=7|pages=1034–1036|doi=10.1136/jnnp.2004.048330|issn=0022-3050|pmid=15965223}}</ref>

Infections such as [[mononucleosis]], [[Epstein Barr|Epstein Barr virus]], [[Lyme disease]], [[Mycoplasma pneumoniae|extra-pulmonary Mycoplasma pneumonia]], and [[Hepatitis C]] <ref>{{Cite journal|last=Kanjwal|first=Khalil|last2=Karabin|first2=Beverly|last3=Kanjwal|first3=Yousuf|last4=Grubb|first4=Blair P.|date=2011|title=Postural orthostatic tachycardia syndrome following Lyme disease|url=https://www.ncbi.nlm.nih.gov/pubmed/21305487|journal=Cardiology Journal|volume=18|issue=1|pages=63–66|issn=1897-5593|pmid=21305487}}</ref><ref>{{Cite journal|last=Kasmani|first=Rahil|last2=Elkambergy|first2=Hossam|last3=Okoli|first3=Kelechi|date=2009-09|title=Postural Orthostatic Tachycardia Syndrome Associated With Mycoplasma pneumoniae|url=http://journals.lww.com/infectdis/Abstract/2009/09000/Postural_Orthostatic_Tachycardia_Syndrome.16.aspx|journal=Infectious Diseases in Clinical Practice|language=en-US|volume=17|issue=5|pages=342–343|doi=10.1097/IPC.0b013e318191781b|issn=1056-9103}}</ref>

[[Mitochondrial disorders|Mitochondrial diseases]]<ref>{{Cite journal|last=Kanjwal|first=Khalil|last2=Karabin|first2=Beverly|last3=Kanjwal|first3=Yousuf|last4=Saeed|first4=Bilal|last5=Grubb|first5=Blair P.|date=2010-10|title=Autonomic dysfunction presenting as orthostatic intolerance in patients suffering from mitochondrial cytopathy|url=https://www.ncbi.nlm.nih.gov/pubmed/20960537|journal=Clinical Cardiology|volume=33|issue=10|pages=626–629|doi=10.1002/clc.20805|issn=1932-8737|pmid=20960537}}</ref>

[[Mast cell activation disorder|Mast cell activation disorders]]<ref>{{Cite journal|last=Raj|first=Satish R|date=2006-04-01|title=The Postural Tachycardia Syndrome (POTS): Pathophysiology, Diagnosis & Management|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1501099/|journal=Indian Pacing and Electrophysiology Journal|volume=6|issue=2|pages=84–99|issn=0972-6292|pmc=PMC1501099|pmid=16943900}}</ref>

[[Vasovagal syncope]]<ref>{{Cite journal|last=Garland|first=Emily M|last2=Celedonio|first2=Jorge E|last3=Raj|first3=Satish R|date=2015-9|title=Postural Tachycardia Syndrome: Beyond Orthostatic Intolerance|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4664448/|journal=Current neurology and neuroscience reports|volume=15|issue=9|pages=60|doi=10.1007/s11910-015-0583-8|issn=1528-4042|pmc=PMC4664448|pmid=26198889}}</ref>

== Studies ==
*2008, [http://www.ncbi.nlm.nih.gov/pubmed/18805903 Postural orthostatic tachycardia syndrome is an under-recognized condition in chronic fatigue syndrome]<ref>{{Cite journal|last=Hoad|first=A.|last2=Spickett|first2=G.|last3=Elliott|first3=J.|last4=Newton|first4=J.|author-link4=Julia Newton|date=Dec 2008|title=Postural orthostatic tachycardia syndrome is an under-recognized condition in chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/18805903|journal=QJM: monthly journal of the Association of Physicians|volume=101|issue=12|pages=961–965|doi=10.1093/qjmed/hcn123|issn=1460-2393|pmid=18805903|via=}}</ref>
*2012, [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3390096/ Diagnosis and management of postural orthostatic tachycardia syndrome: A brief review]<ref>{{Cite journal|last=Abed|first=Howraa|last2=Ball|first2=Patrick A|last3=Wang|first3=Le-Xin|date=2012|title=Diagnosis and management of postural orthostatic tachycardia syndrome: A brief review|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3390096/|journal=Journal of Geriatric Cardiology : JGC|volume=9|issue=1|pages=61–67|doi=10.3724/SP.J.1263.2012.00061|issn=1671-5411|pmid=22783324|via=}}</ref>
*2012, [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3368269/ Increasing orthostatic stress impairs neurocognitive abilities in chronic fatigue syndrome with postural tachycardia syndrome]
*2013, [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3896080/ What is brain fog? An evaluation of the symptom in postural tachycardia syndrome]<ref>{{Cite journal|last=Ross|first=Amanda J.|last2=Medow|first2=Marvin S.|author-link2=Marvin Medow|last3=Rowe|first3=Peter C.|author-link3=Peter Rowe|last4=Stewart|first4=Julian M.|author-link4=Julian Stewart|date=2013-09-03|title=What is brain fog? An evaluation of the symptom in postural tachycardia syndrome|url=https://link.springer.com/article/10.1007%2Fs10286-013-0212-z|journal=Clinical Autonomic Research|language=en|volume=23|issue=6|pages=305–311|doi=10.1007/s10286-013-0212-z|issn=0959-9851|pmc=|pmid=23999934|via=}}</ref>
*2014, [http://hic.sagepub.com/content/2/1/2324709614527812.full Postural Orthostatic Tachycardia With Chronic Fatigue After HPV Vaccination as Part of the “Autoimmune/Auto-inflammatory Syndrome Induced by Adjuvants”]<ref>{{Cite journal|last=Tomljenovic|first=Lucija|last2=Colafrancesco|first2=Serena|last3=Perricone|first3=Carlo|last4=Shoenfeld|first4=Yehuda|date=2014-03-13|title=Postural Orthostatic Tachycardia With Chronic Fatigue After HPV Vaccination as Part of the “Autoimmune/Auto-inflammatory Syndrome Induced by Adjuvants”|url=http://journals.sagepub.com/doi/full/10.1177/2324709614527812|journal=Journal of Investigative Medicine High Impact Case Reports|language=en|volume=2|issue=1|pages=232470961452781|doi=10.1177/2324709614527812|issn=2324-7096|pmid=26425598|via=}}</ref>
*2014, [http://www.ncbi.nlm.nih.gov/pubmed/24206536 Comorbidity of postural orthostatic tachycardia syndrome and chronic fatigue syndrome in an Australian cohort]<ref name="Reynolds2014" />
*2015, An assessment of fatigue in patients with postural orthostatic tachycardia syndrome<ref>{{Cite journal|last=Wise|first=Shelby|last2=Ross|first2=Amanda|last3=Brown|first3=Abigail|author-link3=Abigail Brown|last4=Evans|first4=Meredyth|author-link4=Meredyth Evans|last5=Jason|first5=Leonard|author-link5=Leonard Jason|date=2015-11-04|title=An assessment of fatigue in patients with postural orthostatic tachycardia syndrome|url=https://journals.sagepub.com/action/captchaChallenge?redirectUri=%2Fdoi%2F10.1177%2F1359105315613624|journal=Journal of Health Psychology|language=en|volume=22|issue=6|pages=733–742|doi=10.1177/1359105315613624|issn=1359-1053|via=}}</ref> ''(reprinted in 2017)'' [[pubmed:26537521|(Abstract)]]
*2016, Is Postural Orthostatic Tachycardia a Useful [[Diagnostic biomarker|Diagnostic Marker]] in Chronic Fatigue Syndrome Patients?<ref>{{Cite journal|last=Roerink|first=M.E.|last2=Lenders|first2=J.W.M|last3=Schmits|first3=I.C.|last4=Pistorius|first4=A.|last5=Knoop|first5=H.|last6=van der Meer|first6=J.W.M.|date=2016|title=Is Postural Orthostatic Tachycardia a Useful Diagnostic Marker in Chronic Fatigue Syndrome Patients?|url=http://www.jpsychores.com/article/S0022-3999(16)30280-X/abstract|journal=Journal of Psychosomatic Research|language=English|volume=85|pages=78|doi=10.1016/j.jpsychores.2016.03.193|issn=0022-3999|via=|author-link6=Jos van der Meer}}</ref>[http://www.jpsychores.com/article/S0022-3999%2816%2930280-X/abstract (Abstract)]
*2016, [http://onlinelibrary.wiley.com/doi/10.1111/joim.12564/full Postural orthostatic tachycardia is not a useful diagnostic marker for chronic fatigue syndrome]<ref name="Roerink, 2016" />
*2018, Managing fatigue in postural tachycardia syndrome (PoTS): The Newcastle approach<ref name="Strassheim, 2018" /> [https://www.ncbi.nlm.nih.gov/pubmed/29519643 (Abstract)]

==Learn more==
*[http://www.potsuk.org/ POTS UK website]
*Sep 2010, [https://www.youtube.com/watch?v=5iF30TVLaRE Mangaging Orthostatic Intolerance]<ref>{{Cite web|url=https://www.youtube.com/watch?v=5iF30TVLaRE|title=Managing Orthostatic Intolerance|last=|first=|date=Sep 1, 2010|website=YouTube|publisher=SolveCFS|archive-url=|archive-date=|dead-url=|access-date=}}</ref>
*2016, [https://www.ncbi.nlm.nih.gov/pubmed/26967958 Recognizing postural orthostatic tachycardia syndrome]<ref>{{Cite journal|last=Pavlik|first=Daniel|last2=Agnew|first2=Donna|last3=Stiles|first3=Lauren|last4=Ditoro|first4=Rachel|date=2016|title=Recognizing postural orthostatic tachycardia syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/26967958|journal=JAAPA: official journal of the American Academy of Physician Assistants|volume=29|issue=4|pages=17–23|doi=10.1097/01.JAA.0000481398.76099.09|issn=1547-1896|pmid=26967958|via=}}</ref>
*2016, [http://www.healthrising.org/blog/2016/07/04/exercise-intolerance-fibromyalgia-chronic-fatigue-pots-explained/ The Exercise Intolerance in POTS, ME/CFS and Fibromyalgia Explained?]<ref>{{Cite news|url=http://www.healthrising.org/blog/2016/07/04/exercise-intolerance-fibromyalgia-chronic-fatigue-pots-explained/|title=The Exercise Intolerance in POTS, ME/CFS and Fibromyalgia Explained? - Health Rising|last=Johnson|first=Cort|date=2016-07-04|work=Health Rising|access-date=2018-08-16|archive-url=|archive-date=|dead-url=|language=en-US|author-link=Cort Johnson}}</ref>

==See also==

*[[Tilt table test]]

== References ==
<references>
<ref name="Reynolds2014">{{citation
| last1 = Reynolds | first1 = GK | authorlink1 =
| last2 = Lewis | first2 = Donald P | authorlink2 = Donald Lewis
| last3 = Richardson | first3 = AM | authorlink3 =
| last4 = Lidbury | first4 = Brett A | authorlink4 = Brett Lidbury
| display-authors =
| title = Comorbidity of postural orthostatic tachycardia syndrome and chronic fatigue syndrome in an Australian cohort
| journal = Journal of Internal Medicine | volume = Volume 275, Issue 4 | pages = 409–417
| date = April 2014
| pmid = 24206536 | doi = 10.1111/joim.12161
| url = http://onlinelibrary.wiley.com/doi/10.1111/joim.12161/abstract
}}</ref>
<ref name="Roerink, 2016">{{Cite journal|last=Roerink|first=M. E.|last2=Lenders|first2=J. W. M.|last3=Schmits|first3=I. C.|last4=Pistorius|first4=A. M. A.|last5=Smit|first5=J. W.|last6=Knoop|first6=H.|last7=van der Meer|first7=J. W. M.|date=2016-10-02|title=Postural orthostatic tachycardia is not a useful diagnostic marker for chronic fatigue syndrome|url=https://doi.org/10.1111/joim.12564|journal=Journal of Internal Medicine|language=en|volume=281|issue=2|pages=179–188|doi=10.1111/joim.12564|issn=0954-6820|via=|author-link7=Jos van der Meer}}
</ref>
<ref name="Strassheim, 2018">{{Citation
| last1 = Strassheim | first1 = V | authorlink1 =
| last2 = Welford | first2 = J | authorlink2 =
| last3 = Ballantine | first3 = R | authorlink3 =
| last4 = Newton | first4 = JL | authorlink4 = Julia Newton
| title = Managing fatigue in postural tachycardia syndrome (PoTS): The Newcastle approach.
| journal = Autonomic Neuroscience | volume = | issue = | page =
| date = 2018
| pmid =
| doi = 10.1016/j.autneu.2018.02.003
}}
</ref>
</references>
[[Category:Diagnoses]]
[[Category:Comorbidities]]
[[Category:Signs and symptoms]]
[[Category:Cardiac signs and symptoms]]

Postural orthostatic tachycardia syndrome

2018-10-25T15:07:57Z

Paulitasofia1:adding info

'''Postural orthostatic tachycardia syndrome''' ('''POTS''', or '''postural tachycardia syndrome)''' is a condition in which a change from the supine position (lying horizontally) to an upright position causes an abnormally large increase in [[heart rate]], called [[tachycardia]]. It is a form of [[orthostatic intolerance]] (OI). Other symptoms of an orthostatic nature — occurring in response to upright posture — may accompany the [[tachycardia]].<ref>{{Cite journal|last=Mar|first=Philip L.|last2=Raj|first2=Satish R.|date=2014|title=Neuronal and hormonal perturbations in postural tachycardia syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/24982638|journal=Frontiers in Physiology|volume=5|pages=220|doi=10.3389/fphys.2014.00220|issn=1664-042X|pmc=|pmid=24982638|via=}}</ref> These include headaches, fatigue, sweating, nausea, fainting and dizziness may occur. The [[autonomic nervous system]] is in charge of heart rate and blood pressure but it has become dysregulated. The female to male ratio of patients with POTS is 4:1. <ref>{{Cite news|url=http://www.potsuk.org/|title=PoTS - Postural Tachycardia Syndrome|last=|first=|work=PoTS UK|access-date=2018-08-16|language=en|date=|archive-url=|archive-date=|dead-url=}}</ref><ref>{{Cite news|url=http://www.potsuk.org/what_is_pots2|title=PoTS - Postural Tachycardia Syndrome - What is POTS?|last=|first=|work=PoTS UK|access-date=2018-08-16|language=en|date=|archive-url=|archive-date=|dead-url=}}</ref>

=Signs and symptoms=
[[File:Acrocyanosis in POTS.jpg|thumb|400x400px|Acrocyanosis in POTS. This image shows the legs of a patient with POTS (right) and of a healthy control (left) after standing for 5 minutes. The reddish purple discoloration in the legs is very notable, due to poor circulation in the extremities, which returns to normal upon returning to a reclined position.]]
The main symptom of POTS is an abnormal increase in heart rate upon standing. The specific diagnostic criteria for POTS is an increase in heart rate from the lying to upright position of greater than 30 beats per minute, or a heart rate of greater than 120 beats per minute within 10 minutes of standing. Patients with POTS usually present with other symptoms, commonly occurring in the upright position. These include<ref>{{Cite web|url=http://standinguptopots.org/learning/pots-symptoms|title=Symptoms of Postural Orthostatic Tachycardia Syndrome (POTS)|last=|first=|date=July 9, 2018|website=Standing Up to POTS|archive-url=|archive-date=|dead-url=|access-date=}}</ref><ref>{{Cite journal|last=Raj|first=Satish R|date=2006-04-01|title=The Postural Tachycardia Syndrome (POTS): Pathophysiology, Diagnosis & Management|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1501099/|journal=Indian Pacing and Electrophysiology Journal|volume=6|issue=2|pages=84–99|issn=0972-6292|pmc=PMC1501099|pmid=16943900}}</ref><ref name=":1">{{Cite web|url=http://www.dysautonomiainternational.org/page.php?ID=30|title=Dysautonomia International: Postural Orthostatic Tachycardia Syndrome|website=www.dysautonomiainternational.org|language=en|access-date=2018-10-25}}</ref>:
* Hypovolemia (low blood volume)
* High levels of plasma norepinephrine when standing
* [[Dizziness]]/ [[lightheadedness]] and syncope (fainting)
* [[Headache|Headaches]] and [[migraines]]
* [[Cognitive impairment]] / [[brain fog]]
* Heart palpitations
* Chest pain
* Shortness of breath
* [[Sleep abnormalities]]
* [[Neuropathic pain|Neuropathic pain,]] Coldness or pain in the extremities
* Small fiber polyneuropathy (in 50% of patients)
* [[Fatigue]]
* Exercise intolerance
* Nausea
* Tremulousness (shaking)
* Acrocyanosis-- reddish purple discoloration in the legs, due to poor circulation in the extremities, which returns to normal upon returning to a reclined position
* [[Sensory sensitivity]]
* [[Abdominal pain]], [[gastroparesis]], or rapid [[gastric emptying]]
* Elevated sympathetic tone

=Testing=
Assessing orthostatic blood pressure can be done in a physician's office by measuring the patient's blood pressure while lying down, sitting, and standing at standardized time increments. Dr. [[Lucinda Bateman]] uses a modified orthostatic blood pressure assessment called the [[NASA 10-minute Lean Test]], a variant of a test used by NASA researchers to test for orthostatic intolerance following space flight. The NASA 10-minute Lean Test is less taxing on the patient and can be done in any physician's office. Instructions are available for printout for both [https://batemanhornecenter.org/wp-content/uploads/2016/09/NASA-Lean-Test-Instructions-1.pdf healthcare providers] and [https://batemanhornecenter.org/wp-content/uploads/2016/09/NASA-Lean-Patient-Preparation-Instructions-1.pdf patients].<ref>{{Cite news|url=https://batemanhornecenter.org/assess-orthostatic-intolerance/|title=Simple Way to Assess Orthostatic Intolerance - Bateman Horne Center|last=Bateman|first=Lucinda|date=2016-09-27|work=Bateman Horne Center Newsletter|access-date=2018-08-16|archive-url=|archive-date=|dead-url=|publisher=|language=en-US|author-link=Lucinda Bateman}}</ref>

If the results of the standard orthostatic blood pressure assessment are inconclusive, a [[tilt table test]] can be used for diagnosis.<ref>{{Cite news|url=http://myheart.net/pots-syndrome/diagnosis-tests/|title=How Doctors Diagnose & Test for POTS • MyHeart|work=MyHeart|access-date=2018-08-16|language=en-US}}</ref>

=Treatment=
A 2012 study [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3390096/ Diagnosis and management of postural orthostatic tachycardia syndrome: A brief review]<ref name=":0" /> concluded:

:"The pathophysiology of POTS is complex and the result of a number of separate mechanisms producing a common pattern of symptoms. The large number of clinical manifestations that characterize this disorder and the wide range of medications available, plus the clear evidence that certain medications and treatment strategies work in some, but not all POTS patients, demonstrates that POTS is a range of disorders requiring comprehensive investigation and characterisation to guide selection of the most appropriate treatment. The recent consensus statement will help to direct further research into the underlying conditions that lead to POTS."
: When the cause of POTS is able to be identified and treated in certain individuals, their POTS symptoms may subside. However, there is currently no cure for POTS on the broader level. The following treatments have been identified to improve symptoms and quality of life:
:* Increasing fluid intake (2-3 liters a day)
:* Increasing salt intake
:* Raising the head of the bed to conserve blood volume (less blood is turned into urine by the kidneys when reclining at an angle)
:* [[Diet]]
:* Reclined e[[Exercise|xercise]], such as rowing, biking, swimming (contraindicated in patients with co-morbid [[myalgic encephalomyelitis]])
:* [[Sodium chloride]] 0.9% ([[Normal saline]])
:* Medications:
:** [[Beta-blocker|Beta-blockers]]
:** [[Fludrocortisone]]
:** [[Ivabradine]]
:** [[Erythropoietin]]
:** [[Pyridostigmine]] bromide
:** [[Vasoconstrictor|Vasoconstrictors]]
:** [[NSAID|NSAIDs]]
:** Others such as methyldopa and antidepressants <ref name=":0">{{Cite journal|last=Abed|first=Howraa|last2=Ball|first2=Patrick A|last3=Wang|first3=Le-Xin|date=2012|title=Diagnosis and management of postural orthostatic tachycardia syndrome: A brief review|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3390096/|journal=Journal of Geriatric Cardiology : JGC|volume=9|issue=1|pages=61–67|doi=10.3724/SP.J.1263.2012.00061|issn=1671-5411|pmid=22783324|via=}}</ref><ref name=":1" />
=Conditions associated with POTS =
POTS is not only comorbid with a range of diseases, but its phenotype also resembles that of other disorders (e.g., ME, Ehlers-Danlos Syndrome).

===ME/CFS ===
POTS can be a co-morbid condition in [[ME/CFS]] patients.<ref>{{Cite web|url=https://www.youtube.com/watch?v=o4OqNPZoqVs|title=POTS in ME/CFS|last=|first=|date=Aug 2, 2014|website=YouTube|publisher=Freedom From ME - The Optimum Health Clinic|archive-url=|archive-date=|dead-url=|access-date=}}</ref><ref>{{Cite web|url=https://ammes.org/overlapping-conditions/|title=Overlapping Conditions – American ME and CFS Society|website=ammes.org|language=en-US|access-date=2018-08-12}}</ref> Estimates on the prevalence of POTS among [[ME/CFS]] patients varies widely, from 11% to 70%. In a 2008 study done in the UK by the Northern CFS/ME Clinical Network, using the [[Fukuda criteria]], 27% of the study population had POTS compared with 9% in the control population.<ref>{{Cite journal|last=Hoad|first=A.|last2=Spickett|first2=G.|last3=Elliott|first3=J.|last4=Newton|first4=J.|date=2008|title=Postural orthostatic tachycardia syndrome is an under-recognized condition in chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/18805903|journal=QJM: monthly journal of the Association of Physicians|volume=101|issue=12|pages=961–965|doi=10.1093/qjmed/hcn123|issn=1460-2393|pmid=18805903|via=|author-link4=Julia Newton}}</ref>

{| class="wikitable"
! colspan="3" |Prevalence of POTS in ME/CFS population samples
|-
!Study:
!number of
ME/CFS patients
!%
POTS
|-
|[[pubmed:10431117|Stewart et al. 1999]]
|25
|70%
|-
|[[pubmed:10189122|Schondorf et al. 1999]]
|75
|40%
|-
|[[pubmed:18805903|Hoad et al. 2008]]
|59
|27%
|-
|[[pubmed:23206180|Lewis et al. 2013]]
|179
|13%
|-
|[[pubmed:24206536|Reynolds et al. 2014]]
|306
|11%
|-
|[[pubmed:27696568|Roerink et al. 2017]]
|419
|5,7%
|}
A 2011 study of 58 POTS patients by the Vanderbilt Autonomic Dysfunction Center (Vanderbilt University School of Medicine, Nashville, TN, U.S.A.), reported that 64% of also met the [[Centers for Disease Control & Prevention]] criteria for [[chronic fatigue syndrome]].<ref>{{Cite journal|last=Okamoto|first=Luis E.|last2=Raj|first2=Satish R.|last3=Peltier|first3=Amanda|last4=Gamboa|first4=Alfredo|last5=Shibao|first5=Cyndya|last6=Diedrich|first6=André|last7=Black|first7=Bonnie K.|last8=Robertson|first8=David|last9=Biaggioni|first9=Italo|date=2012-02-01|title=Neurohumoral and haemodynamic profile in postural tachycardia and chronic fatigue syndromes|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3203411/|journal=Clinical Science (London, England : 1979)|volume=122|issue=Pt 4|pages=183–192|doi=10.1042/CS20110200|issn=0143-5221|pmid=21906029|via=}}</ref>

The proposed [[SEID]] criteria requires either [[orthostatic intolerance]] (of which POTS is one type) or [[cognitive dysfunction]] for a diagnosis.<ref>{{Cite journal|last=|first=|date=2015-03-16|title=Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome|url=https://www.nap.edu/read/19012/chapter/6#114|journal=The National Academies Press|language=en|volume=|pages=114|at=Box 4-3|doi=10.17226/19012|via=NAP.edu}}</ref> POTS is also a symptom of the [[Canadian Consensus Criteria]] (CCC) which diagnoses ME/CFS,<ref>{{Cite web|url=http://me-pedia.org/wiki/Canadian_Consensus_Criteria#Definition|title=Canadian Consensus Criteria - MEpedia|website=me-pedia.org|language=en|access-date=2018-08-16}}</ref> and the [[International Consensus Criteria]] (ICC) for diagnosing myalgic encephalomyelitis.<ref>{{Cite web|url=http://me-pedia.org/wiki/International_Consensus_Criteria#D._Energy_production.2Ftransportation_impairments:_At_least_one_symptom|title=International Consensus Criteria - MEpedia|website=me-pedia.org|language=en|access-date=2018-08-16}}</ref> However, the diagnosis of POTS alone does not automatically support a [[ME/CFS]] diagnosis and cannot be used as a [[diagnostic biomarker]] to determine ME/CFS. POTS can occur independent from ME/CFS, and, likewise, ME/CFS can occur without the symptomatology of POTS.

A September 2016 study in the Netherlands by Roerink et al., found that patients with CFS who fulfilled the [[SEID]] criteria did not have a prevalence of POTS different from that in the overall ME/CFS population. In adults with ME/CFS, the prevalence of POTS was low, between 6% - 18% (depending on age), was not different from the rate in non-ME/CFS fatigued patients, and was not related to disease severity or treatment outcome.<ref name="Roerink, 2016" />

ME patients with POTS can experience impaired neurocognitive abilities (such as working memory, information processing) under increased orthostatic stress (i.e., standing, tilt table test).<ref>{{Cite journal|last=OCON|first=Anthony J.|last2=MESSER|first2=Zachary R.|last3=MEDOW|first3=Marvin S.|last4=STEWART|first4=Julian M.|date=2012-3|title=Increasing orthostatic stress impairs neurocognitive functioning in chronic fatigue syndrome with postural tachycardia syndrome|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3368269/|journal=Clinical Science (London, England : 1979)|volume=122|issue=5|pages=227–238|doi=10.1042/CS20110241|issn=0143-5221|pmc=PMC3368269|pmid=21919887}}</ref>

Ehlers Danlos

Fibromyalgia

Autoimmune diseases<ref name=":1" />

Chiari malformation<ref>{{Cite journal|last=Weig|first=Spencer G.|last2=Buckthal|first2=Paul E.|last3=Choi|first3=Samuel K.|last4=Zellem|first4=Ronald T.|date=1991-10-01|title=Recurrent syncope as the presenting symptom of Arnold‐Chiari malformation|url=http://n.neurology.org/content/41/10/1673|journal=Neurology|language=en|volume=41|issue=10|pages=1673–1673|doi=10.1212/WNL.41.10.1673|issn=0028-3878|pmid=1922816}}</ref><ref>{{Cite journal|last=Prilipko|first=O.|last2=Dehdashti|first2=A. R.|last3=Zaim|first3=S.|last4=Seeck|first4=M.|date=2005-07-01|title=Orthostatic intolerance and syncope associated with Chiari type I malformation|url=https://jnnp.bmj.com/content/76/7/1034|journal=Journal of Neurology, Neurosurgery & Psychiatry|language=en|volume=76|issue=7|pages=1034–1036|doi=10.1136/jnnp.2004.048330|issn=0022-3050|pmid=15965223}}</ref>

Infections such as mononucleosis, Epstein Barr virus, Lyme disease, extra-pulmonary Mycoplasma pneumonia, and Hepatitis C <ref>{{Cite journal|last=Kanjwal|first=Khalil|last2=Karabin|first2=Beverly|last3=Kanjwal|first3=Yousuf|last4=Grubb|first4=Blair P.|date=2011|title=Postural orthostatic tachycardia syndrome following Lyme disease|url=https://www.ncbi.nlm.nih.gov/pubmed/21305487|journal=Cardiology Journal|volume=18|issue=1|pages=63–66|issn=1897-5593|pmid=21305487}}</ref><ref>{{Cite journal|last=Kasmani|first=Rahil|last2=Elkambergy|first2=Hossam|last3=Okoli|first3=Kelechi|date=2009-09|title=Postural Orthostatic Tachycardia Syndrome Associated With Mycoplasma pneumoniae|url=http://journals.lww.com/infectdis/Abstract/2009/09000/Postural_Orthostatic_Tachycardia_Syndrome.16.aspx|journal=Infectious Diseases in Clinical Practice|language=en-US|volume=17|issue=5|pages=342–343|doi=10.1097/IPC.0b013e318191781b|issn=1056-9103}}</ref>

Mitochondrial diseases<ref>{{Cite journal|last=Kanjwal|first=Khalil|last2=Karabin|first2=Beverly|last3=Kanjwal|first3=Yousuf|last4=Saeed|first4=Bilal|last5=Grubb|first5=Blair P.|date=2010-10|title=Autonomic dysfunction presenting as orthostatic intolerance in patients suffering from mitochondrial cytopathy|url=https://www.ncbi.nlm.nih.gov/pubmed/20960537|journal=Clinical Cardiology|volume=33|issue=10|pages=626–629|doi=10.1002/clc.20805|issn=1932-8737|pmid=20960537}}</ref>

Mast cell activation disorders

Vasovagal syncope

== Studies ==
*2008, [http://www.ncbi.nlm.nih.gov/pubmed/18805903 Postural orthostatic tachycardia syndrome is an under-recognized condition in chronic fatigue syndrome]<ref>{{Cite journal|last=Hoad|first=A.|last2=Spickett|first2=G.|last3=Elliott|first3=J.|last4=Newton|first4=J.|author-link4=Julia Newton|date=Dec 2008|title=Postural orthostatic tachycardia syndrome is an under-recognized condition in chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/18805903|journal=QJM: monthly journal of the Association of Physicians|volume=101|issue=12|pages=961–965|doi=10.1093/qjmed/hcn123|issn=1460-2393|pmid=18805903|via=}}</ref>
*2012, [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3390096/ Diagnosis and management of postural orthostatic tachycardia syndrome: A brief review]<ref>{{Cite journal|last=Abed|first=Howraa|last2=Ball|first2=Patrick A|last3=Wang|first3=Le-Xin|date=2012|title=Diagnosis and management of postural orthostatic tachycardia syndrome: A brief review|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3390096/|journal=Journal of Geriatric Cardiology : JGC|volume=9|issue=1|pages=61–67|doi=10.3724/SP.J.1263.2012.00061|issn=1671-5411|pmid=22783324|via=}}</ref>
*2012, [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3368269/ Increasing orthostatic stress impairs neurocognitive abilities in chronic fatigue syndrome with postural tachycardia syndrome]
*2013, [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3896080/ What is brain fog? An evaluation of the symptom in postural tachycardia syndrome]<ref>{{Cite journal|last=Ross|first=Amanda J.|last2=Medow|first2=Marvin S.|author-link2=Marvin Medow|last3=Rowe|first3=Peter C.|author-link3=Peter Rowe|last4=Stewart|first4=Julian M.|author-link4=Julian Stewart|date=2013-09-03|title=What is brain fog? An evaluation of the symptom in postural tachycardia syndrome|url=https://link.springer.com/article/10.1007%2Fs10286-013-0212-z|journal=Clinical Autonomic Research|language=en|volume=23|issue=6|pages=305–311|doi=10.1007/s10286-013-0212-z|issn=0959-9851|pmc=|pmid=23999934|via=}}</ref>
*2014, [http://hic.sagepub.com/content/2/1/2324709614527812.full Postural Orthostatic Tachycardia With Chronic Fatigue After HPV Vaccination as Part of the “Autoimmune/Auto-inflammatory Syndrome Induced by Adjuvants”]<ref>{{Cite journal|last=Tomljenovic|first=Lucija|last2=Colafrancesco|first2=Serena|last3=Perricone|first3=Carlo|last4=Shoenfeld|first4=Yehuda|date=2014-03-13|title=Postural Orthostatic Tachycardia With Chronic Fatigue After HPV Vaccination as Part of the “Autoimmune/Auto-inflammatory Syndrome Induced by Adjuvants”|url=http://journals.sagepub.com/doi/full/10.1177/2324709614527812|journal=Journal of Investigative Medicine High Impact Case Reports|language=en|volume=2|issue=1|pages=232470961452781|doi=10.1177/2324709614527812|issn=2324-7096|pmid=26425598|via=}}</ref>
*2014, [http://www.ncbi.nlm.nih.gov/pubmed/24206536 Comorbidity of postural orthostatic tachycardia syndrome and chronic fatigue syndrome in an Australian cohort]<ref name="Reynolds2014" />
*2015, An assessment of fatigue in patients with postural orthostatic tachycardia syndrome<ref>{{Cite journal|last=Wise|first=Shelby|last2=Ross|first2=Amanda|last3=Brown|first3=Abigail|author-link3=Abigail Brown|last4=Evans|first4=Meredyth|author-link4=Meredyth Evans|last5=Jason|first5=Leonard|author-link5=Leonard Jason|date=2015-11-04|title=An assessment of fatigue in patients with postural orthostatic tachycardia syndrome|url=https://journals.sagepub.com/action/captchaChallenge?redirectUri=%2Fdoi%2F10.1177%2F1359105315613624|journal=Journal of Health Psychology|language=en|volume=22|issue=6|pages=733–742|doi=10.1177/1359105315613624|issn=1359-1053|via=}}</ref> ''(reprinted in 2017)'' [[pubmed:26537521|(Abstract)]]
*2016, Is Postural Orthostatic Tachycardia a Useful [[Diagnostic biomarker|Diagnostic Marker]] in Chronic Fatigue Syndrome Patients?<ref>{{Cite journal|last=Roerink|first=M.E.|last2=Lenders|first2=J.W.M|last3=Schmits|first3=I.C.|last4=Pistorius|first4=A.|last5=Knoop|first5=H.|last6=van der Meer|first6=J.W.M.|date=2016|title=Is Postural Orthostatic Tachycardia a Useful Diagnostic Marker in Chronic Fatigue Syndrome Patients?|url=http://www.jpsychores.com/article/S0022-3999(16)30280-X/abstract|journal=Journal of Psychosomatic Research|language=English|volume=85|pages=78|doi=10.1016/j.jpsychores.2016.03.193|issn=0022-3999|via=|author-link6=Jos van der Meer}}</ref>[http://www.jpsychores.com/article/S0022-3999%2816%2930280-X/abstract (Abstract)]
*2016, [http://onlinelibrary.wiley.com/doi/10.1111/joim.12564/full Postural orthostatic tachycardia is not a useful diagnostic marker for chronic fatigue syndrome]<ref name="Roerink, 2016" />
*2018, Managing fatigue in postural tachycardia syndrome (PoTS): The Newcastle approach<ref name="Strassheim, 2018" /> [https://www.ncbi.nlm.nih.gov/pubmed/29519643 (Abstract)]

==Learn more==
*[http://www.potsuk.org/ POTS UK website]
*Sep 2010, [https://www.youtube.com/watch?v=5iF30TVLaRE Mangaging Orthostatic Intolerance]<ref>{{Cite web|url=https://www.youtube.com/watch?v=5iF30TVLaRE|title=Managing Orthostatic Intolerance|last=|first=|date=Sep 1, 2010|website=YouTube|publisher=SolveCFS|archive-url=|archive-date=|dead-url=|access-date=}}</ref>
*2016, [https://www.ncbi.nlm.nih.gov/pubmed/26967958 Recognizing postural orthostatic tachycardia syndrome]<ref>{{Cite journal|last=Pavlik|first=Daniel|last2=Agnew|first2=Donna|last3=Stiles|first3=Lauren|last4=Ditoro|first4=Rachel|date=2016|title=Recognizing postural orthostatic tachycardia syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/26967958|journal=JAAPA: official journal of the American Academy of Physician Assistants|volume=29|issue=4|pages=17–23|doi=10.1097/01.JAA.0000481398.76099.09|issn=1547-1896|pmid=26967958|via=}}</ref>
*2016, [http://www.healthrising.org/blog/2016/07/04/exercise-intolerance-fibromyalgia-chronic-fatigue-pots-explained/ The Exercise Intolerance in POTS, ME/CFS and Fibromyalgia Explained?]<ref>{{Cite news|url=http://www.healthrising.org/blog/2016/07/04/exercise-intolerance-fibromyalgia-chronic-fatigue-pots-explained/|title=The Exercise Intolerance in POTS, ME/CFS and Fibromyalgia Explained? - Health Rising|last=Johnson|first=Cort|date=2016-07-04|work=Health Rising|access-date=2018-08-16|archive-url=|archive-date=|dead-url=|language=en-US|author-link=Cort Johnson}}</ref>

==See also==

*[[Tilt table test]]

== References ==
<references>
<ref name="Reynolds2014">{{citation
| last1 = Reynolds | first1 = GK | authorlink1 =
| last2 = Lewis | first2 = Donald P | authorlink2 = Donald Lewis
| last3 = Richardson | first3 = AM | authorlink3 =
| last4 = Lidbury | first4 = Brett A | authorlink4 = Brett Lidbury
| display-authors =
| title = Comorbidity of postural orthostatic tachycardia syndrome and chronic fatigue syndrome in an Australian cohort
| journal = Journal of Internal Medicine | volume = Volume 275, Issue 4 | pages = 409–417
| date = April 2014
| pmid = 24206536 | doi = 10.1111/joim.12161
| url = http://onlinelibrary.wiley.com/doi/10.1111/joim.12161/abstract
}}</ref>
<ref name="Roerink, 2016">{{Cite journal|last=Roerink|first=M. E.|last2=Lenders|first2=J. W. M.|last3=Schmits|first3=I. C.|last4=Pistorius|first4=A. M. A.|last5=Smit|first5=J. W.|last6=Knoop|first6=H.|last7=van der Meer|first7=J. W. M.|date=2016-10-02|title=Postural orthostatic tachycardia is not a useful diagnostic marker for chronic fatigue syndrome|url=https://doi.org/10.1111/joim.12564|journal=Journal of Internal Medicine|language=en|volume=281|issue=2|pages=179–188|doi=10.1111/joim.12564|issn=0954-6820|via=|author-link7=Jos van der Meer}}
</ref>
<ref name="Strassheim, 2018">{{Citation
| last1 = Strassheim | first1 = V | authorlink1 =
| last2 = Welford | first2 = J | authorlink2 =
| last3 = Ballantine | first3 = R | authorlink3 =
| last4 = Newton | first4 = JL | authorlink4 = Julia Newton
| title = Managing fatigue in postural tachycardia syndrome (PoTS): The Newcastle approach.
| journal = Autonomic Neuroscience | volume = | issue = | page =
| date = 2018
| pmid =
| doi = 10.1016/j.autneu.2018.02.003
}}
</ref>
</references>
[[Category:Diagnoses]]
[[Category:Comorbidities]]
[[Category:Signs and symptoms]]
[[Category:Cardiac signs and symptoms]]

Postural orthostatic tachycardia syndrome

2018-10-25T14:30:24Z

Paulitasofia1:editing page, adding new information

'''Postural orthostatic tachycardia syndrome''' ('''POTS''', or '''postural tachycardia syndrome)''' is a condition in which a change from the supine position (lying horizontally) to an upright position causes an abnormally large increase in [[heart rate]], called [[tachycardia]]. It is a form of [[orthostatic intolerance]] (OI). Other symptoms of an orthostatic nature — occurring in response to upright posture — may accompany the [[tachycardia]].<ref>{{Cite journal|last=Mar|first=Philip L.|last2=Raj|first2=Satish R.|date=2014|title=Neuronal and hormonal perturbations in postural tachycardia syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/24982638|journal=Frontiers in Physiology|volume=5|pages=220|doi=10.3389/fphys.2014.00220|issn=1664-042X|pmc=|pmid=24982638|via=}}</ref> These include headaches, fatigue, sweating, nausea, fainting and dizziness may occur. The [[autonomic nervous system]] is in charge of heart rate and blood pressure but it has become dysregulated. The female to male ratio of patients with POTS is 4:1. <ref>{{Cite news|url=http://www.potsuk.org/|title=PoTS - Postural Tachycardia Syndrome|last=|first=|work=PoTS UK|access-date=2018-08-16|language=en|date=|archive-url=|archive-date=|dead-url=}}</ref><ref>{{Cite news|url=http://www.potsuk.org/what_is_pots2|title=PoTS - Postural Tachycardia Syndrome - What is POTS?|last=|first=|work=PoTS UK|access-date=2018-08-16|language=en|date=|archive-url=|archive-date=|dead-url=}}</ref>

=Signs and symptoms=
The main symptom of POTS is an abnormal increase in heart rate upon standing. The specific diagnostic criteria for POTS is an increase in heart rate from the lying to upright position of greater than 30 beats per minute, or a heart rate of greater than 120 beats per minute within 10 minutes of standing. Patients with POTS usually present with other symptoms, commonly occurring in the upright position. These include<ref>{{Cite web|url=http://standinguptopots.org/learning/pots-symptoms|title=Symptoms of Postural Orthostatic Tachycardia Syndrome (POTS)|last=|first=|date=July 9, 2018|website=Standing Up to POTS|archive-url=|archive-date=|dead-url=|access-date=}}</ref><ref>{{Cite journal|last=Raj|first=Satish R|date=2006-04-01|title=The Postural Tachycardia Syndrome (POTS): Pathophysiology, Diagnosis & Management|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1501099/|journal=Indian Pacing and Electrophysiology Journal|volume=6|issue=2|pages=84–99|issn=0972-6292|pmc=PMC1501099|pmid=16943900}}</ref><ref>{{Cite web|url=http://www.dysautonomiainternational.org/page.php?ID=30|title=Dysautonomia International: Postural Orthostatic Tachycardia Syndrome|website=www.dysautonomiainternational.org|language=en|access-date=2018-10-25}}</ref>:
* Hypovolemia (low blood volume)
* High levels of plasma norepinephrine when standing
* [[Dizziness]]/ [[lightheadedness]] and syncope (fainting)
* [[Headache|Headaches]] and [[migraines]]
* [[Cognitive impairment]] / [[brain fog]]
* Heart palpitations
* Chest pain
* Shortness of breath
* [[Sleep abnormalities]]
* [[Neuropathic pain|Neuropathic pain,]] Coldness or pain in the extremities
* Small fiber polyneuropathy (in 50% of patients)
* [[Fatigue]]
* Exercise intolerance
* Nausea
* Tremulousness (shaking)
* Acrocyanosis-- reddish purple discoloration in the legs, due to poor circulation in the extremities, which returns to normal upon returning to a reclined position
* [[Sensory sensitivity]]
* [[Abdominal pain]], [[gastroparesis]], or rapid [[gastric emptying]]
* Elevated sympathetic tone

=Testing=
Assessing orthostatic blood pressure can be done in a physician's office by measuring the patient's blood pressure while lying down, sitting, and standing at standardized time increments. Dr. [[Lucinda Bateman]] uses a modified orthostatic blood pressure assessment called the [[NASA 10-minute Lean Test]], a variant of a test used by NASA researchers to test for orthostatic intolerance following space flight. The NASA 10-minute Lean Test is less taxing on the patient and can be done in any physician's office. Instructions are available for printout for both [https://batemanhornecenter.org/wp-content/uploads/2016/09/NASA-Lean-Test-Instructions-1.pdf healthcare providers] and [https://batemanhornecenter.org/wp-content/uploads/2016/09/NASA-Lean-Patient-Preparation-Instructions-1.pdf patients].<ref>{{Cite news|url=https://batemanhornecenter.org/assess-orthostatic-intolerance/|title=Simple Way to Assess Orthostatic Intolerance - Bateman Horne Center|last=Bateman|first=Lucinda|date=2016-09-27|work=Bateman Horne Center Newsletter|access-date=2018-08-16|archive-url=|archive-date=|dead-url=|publisher=|language=en-US|author-link=Lucinda Bateman}}</ref>

If the results of the standard orthostatic blood pressure assessment are inconclusive, a [[tilt table test]] can be used for diagnosis.<ref>{{Cite news|url=http://myheart.net/pots-syndrome/diagnosis-tests/|title=How Doctors Diagnose & Test for POTS • MyHeart|work=MyHeart|access-date=2018-08-16|language=en-US}}</ref>

=Treatment=
A 2012 study [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3390096/ Diagnosis and management of postural orthostatic tachycardia syndrome: A brief review]<ref name=":0" /> concluded:

:"The pathophysiology of POTS is complex and the result of a number of separate mechanisms producing a common pattern of symptoms. The large number of clinical manifestations that characterize this disorder and the wide range of medications available, plus the clear evidence that certain medications and treatment strategies work in some, but not all POTS patients, demonstrates that POTS is a range of disorders requiring comprehensive investigation and characterisation to guide selection of the most appropriate treatment. The recent consensus statement will help to direct further research into the underlying conditions that lead to POTS."
The following treatments were identified:
*[[Diet]]
*[[Exercise]] (contraindicated in patients with co-morbid [[myalgic encephalomyelitis]])
*[[Sodium chloride]] 0.9% ([[Normal saline]])
*[[Beta-blocker]]s
*[[Fludrocortisone]]
*[[Ivabradine]]
*[[Erythropoietin]]
*[[Pyridostigmine]] bromide
*[[Vasoconstrictor]]s
*[[NSAID]]s
*Others such as methyldopa and antidepressants<ref name=":0">{{Cite journal|last=Abed|first=Howraa|last2=Ball|first2=Patrick A|last3=Wang|first3=Le-Xin|date=2012|title=Diagnosis and management of postural orthostatic tachycardia syndrome: A brief review|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3390096/|journal=Journal of Geriatric Cardiology : JGC|volume=9|issue=1|pages=61–67|doi=10.3724/SP.J.1263.2012.00061|issn=1671-5411|pmid=22783324|via=}}</ref>

=Related conditions =
===ME/CFS ===
POTS can be a co-morbid condition in [[ME/CFS]] patients.<ref>{{Cite web|url=https://www.youtube.com/watch?v=o4OqNPZoqVs|title=POTS in ME/CFS|last=|first=|date=Aug 2, 2014|website=YouTube|publisher=Freedom From ME - The Optimum Health Clinic|archive-url=|archive-date=|dead-url=|access-date=}}</ref><ref>{{Cite web|url=https://ammes.org/overlapping-conditions/|title=Overlapping Conditions – American ME and CFS Society|website=ammes.org|language=en-US|access-date=2018-08-12}}</ref> Estimates on the prevalence of POTS among [[ME/CFS]] patients varies widely, from 11% to 70%. In a 2008 study done in the UK by the Northern CFS/ME Clinical Network, using the [[Fukuda criteria]], 27% of the study population had POTS compared with 9% in the control population.<ref>{{Cite journal|last=Hoad|first=A.|last2=Spickett|first2=G.|last3=Elliott|first3=J.|last4=Newton|first4=J.|date=2008|title=Postural orthostatic tachycardia syndrome is an under-recognized condition in chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/18805903|journal=QJM: monthly journal of the Association of Physicians|volume=101|issue=12|pages=961–965|doi=10.1093/qjmed/hcn123|issn=1460-2393|pmid=18805903|via=|author-link4=Julia Newton}}</ref>

{| class="wikitable"
! colspan="3" |Prevalence of POTS in ME/CFS population samples
|-
!Study:
!number of
ME/CFS patients
!%
POTS
|-
|[[pubmed:10431117|Stewart et al. 1999]]
|25
|70%
|-
|[[pubmed:10189122|Schondorf et al. 1999]]
|75
|40%
|-
|[[pubmed:18805903|Hoad et al. 2008]]
|59
|27%
|-
|[[pubmed:23206180|Lewis et al. 2013]]
|179
|13%
|-
|[[pubmed:24206536|Reynolds et al. 2014]]
|306
|11%
|-
|[[pubmed:27696568|Roerink et al. 2017]]
|419
|5,7%
|}
A 2011 study of 58 POTS patients by the Vanderbilt Autonomic Dysfunction Center (Vanderbilt University School of Medicine, Nashville, TN, U.S.A.), reported that 64% of also met the [[Centers for Disease Control & Prevention]] criteria for [[chronic fatigue syndrome]].<ref>{{Cite journal|last=Okamoto|first=Luis E.|last2=Raj|first2=Satish R.|last3=Peltier|first3=Amanda|last4=Gamboa|first4=Alfredo|last5=Shibao|first5=Cyndya|last6=Diedrich|first6=André|last7=Black|first7=Bonnie K.|last8=Robertson|first8=David|last9=Biaggioni|first9=Italo|date=2012-02-01|title=Neurohumoral and haemodynamic profile in postural tachycardia and chronic fatigue syndromes|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3203411/|journal=Clinical Science (London, England : 1979)|volume=122|issue=Pt 4|pages=183–192|doi=10.1042/CS20110200|issn=0143-5221|pmid=21906029|via=}}</ref>

The proposed [[SEID]] criteria requires either [[orthostatic intolerance]] (of which POTS is one type) or [[cognitive dysfunction]] for a diagnosis.<ref>{{Cite journal|last=|first=|date=2015-03-16|title=Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome|url=https://www.nap.edu/read/19012/chapter/6#114|journal=The National Academies Press|language=en|volume=|pages=114|at=Box 4-3|doi=10.17226/19012|via=NAP.edu}}</ref> POTS is also a symptom of the [[Canadian Consensus Criteria]] (CCC) which diagnoses ME/CFS,<ref>{{Cite web|url=http://me-pedia.org/wiki/Canadian_Consensus_Criteria#Definition|title=Canadian Consensus Criteria - MEpedia|website=me-pedia.org|language=en|access-date=2018-08-16}}</ref> and the [[International Consensus Criteria]] (ICC) for diagnosing myalgic encephalomyelitis.<ref>{{Cite web|url=http://me-pedia.org/wiki/International_Consensus_Criteria#D._Energy_production.2Ftransportation_impairments:_At_least_one_symptom|title=International Consensus Criteria - MEpedia|website=me-pedia.org|language=en|access-date=2018-08-16}}</ref> However, the diagnosis of POTS alone does not automatically support a [[ME/CFS]] diagnosis and cannot be used as a [[diagnostic biomarker]] to determine ME/CFS. POTS can occur independent from ME/CFS, and, likewise, ME/CFS can occur without the symptomatology of POTS.

A September 2016 study in the Netherlands by Roerink et al., found that patients with CFS who fulfilled the [[SEID]] criteria did not have a prevalence of POTS different from that in the overall CFS population. In adults with CFS, the prevalence of POTS was low, between 6% - 18% (depending on age), was not different from the rate in non-CFS fatigued patients, and was not related to disease severity or treatment outcome.<ref name="Roerink, 2016" />

=== Ehlers Danlos Syndrome ===
{{main article|page_name =Ehlers-Danlos syndrome}}

=== Fibromyalgia ===
{{Main article |page_name = Fibromyalgia}}

== Studies ==
*2008, [http://www.ncbi.nlm.nih.gov/pubmed/18805903 Postural orthostatic tachycardia syndrome is an under-recognized condition in chronic fatigue syndrome]<ref>{{Cite journal|last=Hoad|first=A.|last2=Spickett|first2=G.|last3=Elliott|first3=J.|last4=Newton|first4=J.|author-link4=Julia Newton|date=Dec 2008|title=Postural orthostatic tachycardia syndrome is an under-recognized condition in chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/18805903|journal=QJM: monthly journal of the Association of Physicians|volume=101|issue=12|pages=961–965|doi=10.1093/qjmed/hcn123|issn=1460-2393|pmid=18805903|via=}}</ref>
*2012, [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3390096/ Diagnosis and management of postural orthostatic tachycardia syndrome: A brief review]<ref>{{Cite journal|last=Abed|first=Howraa|last2=Ball|first2=Patrick A|last3=Wang|first3=Le-Xin|date=2012|title=Diagnosis and management of postural orthostatic tachycardia syndrome: A brief review|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3390096/|journal=Journal of Geriatric Cardiology : JGC|volume=9|issue=1|pages=61–67|doi=10.3724/SP.J.1263.2012.00061|issn=1671-5411|pmid=22783324|via=}}</ref>
*2013, [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3896080/ What is brain fog? An evaluation of the symptom in postural tachycardia syndrome]<ref>{{Cite journal|last=Ross|first=Amanda J.|last2=Medow|first2=Marvin S.|author-link2=Marvin Medow|last3=Rowe|first3=Peter C.|author-link3=Peter Rowe|last4=Stewart|first4=Julian M.|author-link4=Julian Stewart|date=2013-09-03|title=What is brain fog? An evaluation of the symptom in postural tachycardia syndrome|url=https://link.springer.com/article/10.1007%2Fs10286-013-0212-z|journal=Clinical Autonomic Research|language=en|volume=23|issue=6|pages=305–311|doi=10.1007/s10286-013-0212-z|issn=0959-9851|pmc=|pmid=23999934|via=}}</ref>
*2014, [http://hic.sagepub.com/content/2/1/2324709614527812.full Postural Orthostatic Tachycardia With Chronic Fatigue After HPV Vaccination as Part of the “Autoimmune/Auto-inflammatory Syndrome Induced by Adjuvants”]<ref>{{Cite journal|last=Tomljenovic|first=Lucija|last2=Colafrancesco|first2=Serena|last3=Perricone|first3=Carlo|last4=Shoenfeld|first4=Yehuda|date=2014-03-13|title=Postural Orthostatic Tachycardia With Chronic Fatigue After HPV Vaccination as Part of the “Autoimmune/Auto-inflammatory Syndrome Induced by Adjuvants”|url=http://journals.sagepub.com/doi/full/10.1177/2324709614527812|journal=Journal of Investigative Medicine High Impact Case Reports|language=en|volume=2|issue=1|pages=232470961452781|doi=10.1177/2324709614527812|issn=2324-7096|pmid=26425598|via=}}</ref>
*2014, [http://www.ncbi.nlm.nih.gov/pubmed/24206536 Comorbidity of postural orthostatic tachycardia syndrome and chronic fatigue syndrome in an Australian cohort]<ref name="Reynolds2014" />
*2015, An assessment of fatigue in patients with postural orthostatic tachycardia syndrome<ref>{{Cite journal|last=Wise|first=Shelby|last2=Ross|first2=Amanda|last3=Brown|first3=Abigail|author-link3=Abigail Brown|last4=Evans|first4=Meredyth|author-link4=Meredyth Evans|last5=Jason|first5=Leonard|author-link5=Leonard Jason|date=2015-11-04|title=An assessment of fatigue in patients with postural orthostatic tachycardia syndrome|url=https://journals.sagepub.com/action/captchaChallenge?redirectUri=%2Fdoi%2F10.1177%2F1359105315613624|journal=Journal of Health Psychology|language=en|volume=22|issue=6|pages=733–742|doi=10.1177/1359105315613624|issn=1359-1053|via=}}</ref> ''(reprinted in 2017)'' [[pubmed:26537521|(Abstract)]]
*2016, Is Postural Orthostatic Tachycardia a Useful [[Diagnostic biomarker|Diagnostic Marker]] in Chronic Fatigue Syndrome Patients?<ref>{{Cite journal|last=Roerink|first=M.E.|last2=Lenders|first2=J.W.M|last3=Schmits|first3=I.C.|last4=Pistorius|first4=A.|last5=Knoop|first5=H.|last6=van der Meer|first6=J.W.M.|date=2016|title=Is Postural Orthostatic Tachycardia a Useful Diagnostic Marker in Chronic Fatigue Syndrome Patients?|url=http://www.jpsychores.com/article/S0022-3999(16)30280-X/abstract|journal=Journal of Psychosomatic Research|language=English|volume=85|pages=78|doi=10.1016/j.jpsychores.2016.03.193|issn=0022-3999|via=|author-link6=Jos van der Meer}}</ref>[http://www.jpsychores.com/article/S0022-3999%2816%2930280-X/abstract (Abstract)]
*2016, [http://onlinelibrary.wiley.com/doi/10.1111/joim.12564/full Postural orthostatic tachycardia is not a useful diagnostic marker for chronic fatigue syndrome]<ref name="Roerink, 2016" />
*2018, Managing fatigue in postural tachycardia syndrome (PoTS): The Newcastle approach<ref name="Strassheim, 2018" /> [https://www.ncbi.nlm.nih.gov/pubmed/29519643 (Abstract)]

==Learn more==
*[http://www.potsuk.org/ POTS UK website]
*Sep 2010, [https://www.youtube.com/watch?v=5iF30TVLaRE Mangaging Orthostatic Intolerance]<ref>{{Cite web|url=https://www.youtube.com/watch?v=5iF30TVLaRE|title=Managing Orthostatic Intolerance|last=|first=|date=Sep 1, 2010|website=YouTube|publisher=SolveCFS|archive-url=|archive-date=|dead-url=|access-date=}}</ref>
*2016, [https://www.ncbi.nlm.nih.gov/pubmed/26967958 Recognizing postural orthostatic tachycardia syndrome]<ref>{{Cite journal|last=Pavlik|first=Daniel|last2=Agnew|first2=Donna|last3=Stiles|first3=Lauren|last4=Ditoro|first4=Rachel|date=2016|title=Recognizing postural orthostatic tachycardia syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/26967958|journal=JAAPA: official journal of the American Academy of Physician Assistants|volume=29|issue=4|pages=17–23|doi=10.1097/01.JAA.0000481398.76099.09|issn=1547-1896|pmid=26967958|via=}}</ref>
*2016, [http://www.healthrising.org/blog/2016/07/04/exercise-intolerance-fibromyalgia-chronic-fatigue-pots-explained/ The Exercise Intolerance in POTS, ME/CFS and Fibromyalgia Explained?]<ref>{{Cite news|url=http://www.healthrising.org/blog/2016/07/04/exercise-intolerance-fibromyalgia-chronic-fatigue-pots-explained/|title=The Exercise Intolerance in POTS, ME/CFS and Fibromyalgia Explained? - Health Rising|last=Johnson|first=Cort|date=2016-07-04|work=Health Rising|access-date=2018-08-16|archive-url=|archive-date=|dead-url=|language=en-US|author-link=Cort Johnson}}</ref>

==See also==

*[[Tilt table test]]

== References ==
<references>
<ref name="Reynolds2014">{{citation
| last1 = Reynolds | first1 = GK | authorlink1 =
| last2 = Lewis | first2 = Donald P | authorlink2 = Donald Lewis
| last3 = Richardson | first3 = AM | authorlink3 =
| last4 = Lidbury | first4 = Brett A | authorlink4 = Brett Lidbury
| display-authors =
| title = Comorbidity of postural orthostatic tachycardia syndrome and chronic fatigue syndrome in an Australian cohort
| journal = Journal of Internal Medicine | volume = Volume 275, Issue 4 | pages = 409–417
| date = April 2014
| pmid = 24206536 | doi = 10.1111/joim.12161
| url = http://onlinelibrary.wiley.com/doi/10.1111/joim.12161/abstract
}}</ref>
<ref name="Roerink, 2016">{{Cite journal|last=Roerink|first=M. E.|last2=Lenders|first2=J. W. M.|last3=Schmits|first3=I. C.|last4=Pistorius|first4=A. M. A.|last5=Smit|first5=J. W.|last6=Knoop|first6=H.|last7=van der Meer|first7=J. W. M.|date=2016-10-02|title=Postural orthostatic tachycardia is not a useful diagnostic marker for chronic fatigue syndrome|url=https://doi.org/10.1111/joim.12564|journal=Journal of Internal Medicine|language=en|volume=281|issue=2|pages=179–188|doi=10.1111/joim.12564|issn=0954-6820|via=|author-link7=Jos van der Meer}}
</ref>
<ref name="Strassheim, 2018">{{Citation
| last1 = Strassheim | first1 = V | authorlink1 =
| last2 = Welford | first2 = J | authorlink2 =
| last3 = Ballantine | first3 = R | authorlink3 =
| last4 = Newton | first4 = JL | authorlink4 = Julia Newton
| title = Managing fatigue in postural tachycardia syndrome (PoTS): The Newcastle approach.
| journal = Autonomic Neuroscience | volume = | issue = | page =
| date = 2018
| pmid =
| doi = 10.1016/j.autneu.2018.02.003
}}
</ref>
</references>
[[Category:Diagnoses]]
[[Category:Comorbidities]]
[[Category:Signs and symptoms]]
[[Category:Cardiac signs and symptoms]]

Pituitary gland

2018-10-25T01:31:12Z

Paulitasofia1:Formatting

The pituitary gland, or hypophysis, is a pea-sized gland of the endocrine system, situated at the base of the brain. As part of the HPA axis, it is regulated by the hypothalamus to produce, store, and secrete various hormones, which target other endocrine glands. The pituitary gland is sometimes referred to as the “master gland” as it regulates the function of the other endocrine glands.<ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>

=== Structure and Function ===
The pituitary gland sits at the base of the brain, underneath the hypothalamus. It is surrounded by a protective bony cavity called the sella turcica. The pituitary is divided into three distinct lobes: posterior, anterior, and intermediate.<ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>

==== Posterior ====
The posterior pituitary develops as an extension of the hypothalamus (distinct from the anterior pituitary). The posterior pituitary is largely made up of the terminals of nerve cells of the hypothalamus, as neurons in the hypothalamus project directly to the posterior pituitary. Hormones produced by the hypothalamus are stored in the terminals of hypothalamic neurons in the posterior pituitary, and are released by nerve excitation. The two major hormones stored and secreted by the posterior pituitary include:
* Antidiuretic hormone (ADH, also known as vasopressin)
* Oxytocin <ref>{{Cite book|url=https://www.ncbi.nlm.nih.gov/books/NBK27/|title=The pituitary gland|last=Nussey|first=Stephen|last2=Whitehead|first2=Saffron|date=2001|publisher=BIOS Scientific Publishers|language=en}}</ref>

==== Anterior ====
The anterior pituitary is structurally distinct from the posterior pituitary. It makes up 80% of the pituitary gland, and is made up of different types of endocrine cells. These cells are classified by the hormones they synthesize and release, and are regulated by the hypothalamus via releasing and inhibiting hormones. The six major hormones of the anterior pituitary are:
* Growth hormone (GH)
* Adrenocorticotropic hormone (ACTH)
* Thyroid-stimulating hormone (TSH)
* Follicular-stimulating hormone (FSH)
* Luteinizing hormone (LH)
* Prolactin <ref>{{Cite book|url=https://www.ncbi.nlm.nih.gov/books/NBK27/|title=The pituitary gland|last=Nussey|first=Stephen|last2=Whitehead|first2=Saffron|date=2001|publisher=BIOS Scientific Publishers|language=en}}</ref><ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>

==== Intermediate ====
The intermediate lobe is present in many lower vertebrates, but is almost absent in humans. The intermediate pituitary synthesizes and secretes:
* Melanocyte-stimulating hormone (MSH)

=== Function of Hormones ===
{| class="wikitable"
|'''Hormone'''
|'''Target Organ'''
|'''Role'''
|-
|Growth hormone (GH)
|Muscular, skeletal, and fat tissue
|Regulates growth and physical development by stimulating muscle growth and reducing fat tissue
|-
|Adrenocorticotropic hormone (ACTH)
|Adrenal glands
|Stimulates the adrenal glands to produce cortisol and other hormones
|-
|Thyroid-stimulating hormone (TSH)
|Thyroid gland
|Stimulates the thyroid to produce thyroid hormone
|-
|Follicular-stimulating hormone (FSH)
|Ovaries or testes
|Stimulates the ovaries to produce eggs/the testes to produce sperm, and the sex organs to produce sex hormones
|-
|Luteinizing hormone (LH)
|Ovaries or testes
|Stimulates the ovaries to produce eggs/the testes to produce sperm, and the sex organs to produce sex hormones
|-
|Prolactin
|Mammary glands
|Stimulates the mammary glands to produce milk
|-
|Antidiuretic hormone (ADH, also known as vasopressin)
|Kidneys
|Regulates amount of water absorbed and excreted by the kidneys
|-
|Oxytocin
|Uterus and mammary glands
|Causes uterus contraction during childbirth, stimulates contractions of the milk ducts in breast for breastfeeding
|-
|Melanocyte-stimulating hormone (MSH)
|Skin and hair
|Stimulates the production of melanin in skin and hair, suppresses appetite, contributes to sexual arousal
|}
<ref>{{Cite news|url=https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland|title=Overview of the Pituitary Gland - Hormonal and Metabolic Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-10-25|language=en-US}}</ref>

'''Dysfunction and Disease'''

Dysfunction of the pituitary gland can result in overproduction or underproduction of pituitary hormones, thus having major consequences in bodily function. Conditions of pituitary malfunction include:
* Acromegaly -- overproduction of GH
* Cushing’s disease -- overproduction of ACTH
* GH deficiency -- underproduction of GH
* Syndrome of inappropriate antidiuretic hormone -- overproduction of antidiuretic hormone
* Diabetes insipidus -- underproduction of antidiuretic hormone
* Sheehan syndrome -- underproduction of any pituitary hormone
* Pickardt-Falhbusch Syndrome -- underproduction of any pituitary hormone aside from prolactin
* Hyperpituitarism (usually pituitary adenoma) -- overproduction of any pituitary hormone
* Hypopituitarism -- underproduction of any pituitary hormone
* Hypophysitis -- inflammation of the pituitary gland
* Autoimmune hypophysitis -- inflammation of the pituitary gland due to autoimmunity
* Pituitary adenoma -- noncancerous tumor of the pituitary gland <ref>{{Cite journal|date=2018-08-11|title=Pituitary disease|url=https://en.wikipedia.org/w/index.php?title=Pituitary_disease&oldid=854490027|journal=Wikipedia|language=en}}</ref>

Pituitary gland

2018-10-25T01:23:38Z

Paulitasofia1:creating pituitary page

The pituitary gland, or hypophysis, is a pea-sized gland of the endocrine system, situated at the base of the brain. As part of the HPA axis, it is regulated by the hypothalamus to produce, store, and secrete various hormones, which target other endocrine glands. The pituitary gland is sometimes referred to as the “master gland” as it regulates the function of the other endocrine glands.
https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland

Structure and Function
The pituitary gland sits at the base of the brain, underneath the hypothalamus. It is surrounded by a protective bony cavity called the sella turcica. The pituitary is divided into three distinct lobes: posterior, anterior, and intermediate. https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland

Posterior
The posterior pituitary develops as an extension of the hypothalamus (distinct from the anterior pituitary). The posterior pituitary is largely made up of the terminals of nerve cells of the hypothalamus, as neurons in the hypothalamus project directly to the posterior pituitary. Hormones produced by the hypothalamus are stored in the terminals of hypothalamic neurons in the posterior pituitary, and are released by nerve excitation. The two major hormones stored and secreted by the posterior pituitary include:
Antidiuretic hormone (ADH, also known as vasopressin)
Oxytocin
https://www.ncbi.nlm.nih.gov/books/NBK27/

*include picture of each anatomical section*

Anterior
The anterior pituitary is structurally distinct from the posterior pituitary. It makes up 80% of the pituitary gland, and is made up of different types of endocrine cells. These cells are classified by the hormones they synthesize and release, and are regulated by the hypothalamus via releasing and inhibiting hormones. The six major hormones of the anterior pituitary are:
Growth hormone (GH)
Adrenocorticotropic hormone (ACTH)
Thyroid-stimulating hormone (TSH)
Follicular-stimulating hormone (FSH)
Luteinizing hormone (LH)
Prolactin
https://www.ncbi.nlm.nih.gov/books/NBK27/
https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland

Intermediate
The intermediate lobe is present in many lower vertebrates, but is almost absent in humans. The intermediate pituitary synthesizes and secretes:
Melanocyte-stimulating hormone (MSH)

Function of Hormones

Hormone
Target Organ
Role
Growth hormone (GH)
Muscular, skeletal, and fat tissue
Regulates growth and physical development by stimulating muscle growth and reducing fat tissue
Adrenocorticotropic hormone (ACTH)
Adrenal glands
Stimulates the adrenal glands to produce cortisol and other hormones
Thyroid-stimulating hormone (TSH)
Thyroid gland
Stimulates the thyroid to produce thyroid hormone
Follicular-stimulating hormone (FSH)
Ovaries or testes
Stimulates the ovaries to produce eggs/the testes to produce sperm, and the sex organs to produce sex hormones
Luteinizing hormone (LH)
Ovaries or testes
Stimulates the ovaries to produce eggs/the testes to produce sperm, and the sex organs to produce sex hormones
Prolactin
Mammary glands
Stimulates the mammary glands to produce milk
Antidiuretic hormone (ADH, also known as vasopressin)
Kidneys
Regulates amount of water absorbed and excreted by the kidneys
Oxytocin
Uterus and mammary glands
Causes uterus contraction during childbirth, stimulates contractions of the milk ducts in breast for breastfeeding
Melanocyte-stimulating hormone (MSH)
Skin and hair
Stimulates the production of melanin in skin and hair, suppresses appetite, contributes to sexual arousal
https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland

Dysfunction and Disease
Dysfunction of the pituitary gland can result in overproduction or underproduction of pituitary hormones, thus having major consequences in bodily function. Conditions of pituitary malfunction include:
Acromegaly -- overproduction of GH
Cushing’s disease -- overproduction of ACTH
GH deficiency -- underproduction of GH
Syndrome of inappropriate antidiuretic hormone -- overproduction of antidiuretic hormone
Diabetes insipidus -- underproduction of antidiuretic hormone
Sheehan syndrome -- underproduction of any pituitary hormone
Pickardt-Falhbusch Syndrome -- underproduction of any pituitary hormone aside from prolactin
Hyperpituitarism (usually pituitary adenoma) -- overproduction of any pituitary hormone
Hypopituitarism -- underproduction of any pituitary hormone
Hypophysitis -- inflammation of the pituitary gland
Autoimmune hypophysitis -- inflammation of the pituitary gland due to autoimmunity
Pituitary adenoma -- noncancerous tumor of the pituitary gland
https://en.wikipedia.org/wiki/Pituitary_disease

Orthostatic intolerance

2018-10-09T17:39:40Z

Paulitasofia1:/* Type of orthostatic intolerance */

'''Orthostatic intolerance''' (OI) is the inability to correctly regulate blood pressure, cerebral blood flow and consciousness when upright, usually when standing, but it can also occur when sitting. If irregular blood pressure and heart rate initiate while in a supine position (lying down, faceup), then officially it is not orthostatic intolerance.<ref name="Stewart2015" />

== Prevalence ==
Orthostatic intolerance is a common dysfunction in [[ME/CFS]].<ref>{{Cite news|url=http://solvecfs.org/guest-blog-dr-peter-rowe-is-the-physical-examination-normal-in-cfs-part-1/|title=Guest Blog: Dr. Peter Rowe – Is The Physical Examination Normal in CFS? Part 1 - Solve ME/CFS Initiative|last=Rowe|first=Peter|date=2014-09-05|work=Solve ME/CFS Initiative|access-date=2018-08-27|archive-url=|archive-date=|dead-url=|language=en-US}}</ref><ref>{{Cite web|url=https://ammes.org/overlapping-conditions/|title=Overlapping Conditions – American ME and CFS Society|website=ammes.org|language=en-US|access-date=2018-08-12}}</ref> Estimates of the rate of orthostatic intolerance in [[Chronic Fatigue Syndrome]] and [[myalgic encephalomyelitis]] patients vary widely, with estimates as low as 50% to as high as 97% of patients.<ref name="Miwa2015" />

Orthostatic intolerance is also commonly associated with [[fibromyalgia]].<ref>{{Cite web|url=https://www.me-pedia.org/wiki/Fibromyalgia#Comorbidities.2C_overlapping_conditions.2C_and_common_symptoms|title=Fibromyalgia - Comorbidities, overlapping conditions, and common symptoms - MEpedia|last=|first=|date=|website=www.me-pedia.org|language=en|archive-url=|archive-date=|dead-url=|access-date=2018-08-27}}</ref><ref>{{Cite web|url=http://drlapp.com/wp-content/uploads/TTT_symptoms.pdf|title=Symptoms Predict the Outcome of Tilt Table Testing in CFS/ME/FM|last=Lapp|first=Charles|last2=Black|first2=Laura|date=|website=drlapp.com|archive-url=|archive-date=|dead-url=|access-date=|last3=Smith|first3=Rebekah S.}}</ref>

==Testing==
Orthostatic intolerance can be diagnosed by a [[tilt table test]], although a tilt table test isn't required. It is part of the [[Institute of Medicine report]]'s proposed diagnostic criteria for [[Systemic Exertion Intolerance Disease]].<ref>{{Cite web|url=http://iom.nationalacademies.org/~/media/Files/Report%20Files/2015/MECFS/MECFS_ProposedDiagnosticCriteria|title=Proposed Diagnostic Criteria for ME/CFS|last=|first=|date=|website=nationalacademies.org|archive-url=|archive-date=|dead-url=|access-date=}}</ref>

The NASA 10-minute Lean Test is a variant of a test used by NASA researchers to test for orthostatic intolerance following space flight. The adaption for [[ME/CFS]] patients was developed by Dr. [[Lucinda Bateman]], which she recommends all [[ME/CFS]] and [[fibromyalgia]] patients undergo to assess for orthostatic intolerance. The NASA 10-minute Lean Test in less taxing on the patient and can be done in any physician's office. Instructions are available for printout for both [https://batemanhornecenter.org/wp-content/uploads/2016/09/NASA-Lean-Test-Instructions-1.pdf healthcare providers] and [https://batemanhornecenter.org/wp-content/uploads/2016/09/NASA-Lean-Patient-Preparation-Instructions-1.pdf patients].<ref>{{Cite news|url=https://batemanhornecenter.org/assess-orthostatic-intolerance/|title=Simple Way to Assess Orthostatic Intolerance - Bateman Horne Center|last=Bateman|first=Lucinda|date=2016-09-27|work=Bateman Horne Center|access-date=2018-08-27|archive-url=|archive-date=|dead-url=|language=en-US}}</ref>

==Symptom recognition==
Orthostatic intolerance (OI) is an optional symptom for diagnosis in [[Systemic Exertion Intolerance Disease]] (SEID), the [[Canadian Consensus Criteria]] (CCC) which diagnoses ME/CFS and the [[International Consensus Criteria]] (ICC) which diagnoses Myalgic encephalomyelitis (ME).<ref>{{Cite web|url=http://me-pedia.org/wiki/Systemic_Exertion_Intolerance_Disease#Diagnostic_Criteria|title=Systemic Exertion Intolerance Disease - MEpedia|website=me-pedia.org|language=en|access-date=2018-08-27}}</ref><ref>{{Cite web|url=http://me-pedia.org/wiki/Canadian_Consensus_Criteria#Definition|title=Canadian Consensus Criteria - MEpedia|website=me-pedia.org|language=en|access-date=2018-08-27}}</ref><ref>{{Cite web|url=http://me-pedia.org/wiki/International_Consensus_Criteria#D._Energy_production.2Ftransportation_impairments:_At_least_one_symptom|title=International Consensus Criteria - MEpedia|website=me-pedia.org|language=en|access-date=2018-08-27}}</ref>In the [[London criteria]] which diagnoses ME, OI is mentioned under the criteria of ''periods of impaired circulation compatible with autonomic dysfunction''.<ref>{{Cite web|url=http://www.axfordsabode.org.uk/me/mecrit2014.htm|title=ME/CFS Medical Update (Layman's version) Winter 2001|last=Howes|first=Sandra|date=2014|website=www.axfordsabode.org.uk|archive-url=|archive-date=|dead-url=|access-date=2018-08-27}}</ref>

== Types of orthostatic intolerance ==

=== Postural orthostatic tachycardia syndrome ===

[[Postural orthostatic tachycardia syndrome]] (POTS) is one of a group of disorders that have orthostatic intolerance (OI) as their primary symptom. The primary symptom of OI is lightheadedness or fainting. In POTS, the lightheadedness or fainting is also accompanied by a rapid increase in heartbeat of more than 30 beats per minute, or a heart rate that exceeds 120 beats per minute, within 10 minutes of rising.<ref>{{Cite web|url=https://www.ninds.nih.gov/Disorders/All-Disorders/Postural-Tachycardia-Syndrome-Information-Page|title=Postural Tachycardia Syndrome Information Page {{!}} National Institute of Neurological Disorders and Stroke|website=www.ninds.nih.gov|access-date=2018-08-27}}</ref>

=== Orthostatic hypotension ===

Also called postural hypotension, it is a form of sudden low blood pressure that occurs upon standing. It can often cause dizziness. it is defined as a fall in systolic blood pressure of at least 20 mm Hg or diastolic blood pressure of at least 10 mm Hg when a person assumes a standing position.<ref>{{Cite news|url=http://www.potsuk.org/living_with_low_blood_pressure|title=PoTS - Postural Tachycardia Syndrome|last=Stream|first=Creative|work=PoTS UK|access-date=2018-08-27|language=en}}</ref>

=== Neurally mediated hypotension ===

Also called neurally mediate syncope, in NMH, peripheral vasodilation causes blood to pool in the extremities. It is associated with a decrease in blood pressure, and a slow or lowered heart rate upon standing.<ref>{{Cite web|url=http://www.dysautonomiainternational.org/page.php?ID=31|title=Dysautonomia International: Summary of Syncope and Neurally Mediated Syncope|website=www.dysautonomiainternational.org|language=en|access-date=2018-08-27}}</ref>

=== Vasovagal syncope ===

== Potential treatments ==
===Drugs===
* [[wikipedia:Beta_blocker|Beta-blockers]] (Metopropol)

*[[Fludrocortisone]] (Florinef)
*[[Mestinon|Pyridostigmine]]<ref>{{Cite news|url=https://www.prohealth.com/library/evergreen_pages/pharmaceutical-medications-for-chronic-fatigue-syndrome-myalgic-encephalomyelitis|title=Pharmaceutical Medications for Chronic Fatigue Syndrome & Myalgic Encephalomyelitis - Prohealth|work=Prohealth|access-date=2018-08-28|language=en-US}}</ref>

===Management===
*increase fluids and salt<ref name=":0">{{Cite web|url=https://www.cdc.gov/me-cfs/treatment/index.html|title=Treatment {{!}} Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) {{!}} CDC|date=2018-05-18|website=www.cdc.gov|language=en-us|access-date=2018-08-28}}</ref>
*monitoring [[heart rate]]<ref>{{Cite news|url=https://www.prohealth.com/library/orthostatic-intolerance-part-2-treating-oi-82949|title=Orthostatic Intolerance, Part 2: Treating OI - Prohealth|date=2018-06-15|work=Prohealth|access-date=2018-08-28|language=en-US}}</ref>
*raising head of bed<ref>{{Cite web|url=http://www.theoicenter.com/Taking-Care/Head-Up.html|title=Head of Bed Up|website=www.theoicenter.com|access-date=2018-08-28}}</ref><ref>{{Cite journal|last=Fan|first=C. W.|last2=Walsh|first2=C.|last3=Cunningham|first3=C. J.|date=2011-01-13|title=The effect of sleeping with the head of the bed elevated six inches on elderly patients with orthostatic hypotension: an open randomised controlled trial|url=https://academic.oup.com/ageing/article/40/2/187/47278|journal=Age and Ageing|language=en|volume=40|issue=2|pages=187–192|doi=10.1093/ageing/afq176|issn=0002-0729}}</ref>
*shower chair, handheld shower head, cooler water<ref>{{Cite web|url=http://www.theoicenter.com/Taking-Care/Showers-and-Stuff.html|title=Cleaning Up - Shower, Hair, Skin|website=www.theoicenter.com|access-date=2018-08-28}}</ref>
*support stockings<ref name=":0" />

==Notable studies==
*1999, [https://www.researchgate.net/publication/13372595_Orthostatic_Intolerance_in_Adolescent_Chronic_Fatigue_Syndrome Orthostatic intolerance in the chronic fatigue syndrome]<ref>{{Cite web|url=https://www.researchgate.net/profile/Julian_Stewart2/publication/13372595_Orthostatic_Intolerance_in_Adolescent_Chronic_Fatigue_Syndrome/links/5747411808aef66a78b079bf.pdf|title=Orthostatic Intolerance in Adolescent Chronic Fatigue Syndrome|last=Stewart|first=Julian Mark|last2=Gewitz|first2=Michael|date=Feb 1999|website=researchgate.net|publisher=PubMed|via=Research Gate|archive-url=|archive-date=|dead-url=|access-date=|last3=Weldon|first3=A|last4=Munoz|first4=J}}</ref>
*2000, [http://www.ncbi.nlm.nih.gov/pubmed/10910366 The Roles of Orthostatic Hypotension, Orthostatic Tachycardia, and Subnormal Erythrocyte Volume in the Pathogenesis of the Chronic Fatigue Syndrome]<ref>{{Cite journal|last=Streeten|first=D. H.|last2=Thomas|first2=D.|last3=Bell|first3=D. S.|date=2000|title=The roles of orthostatic hypotension, orthostatic tachycardia, and subnormal erythrocyte volume in the pathogenesis of the chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/10910366|journal=The American Journal of the Medical Sciences|volume=320|issue=1|pages=1–8|issn=0002-9629|pmid=10910366|via=}}</ref>
*2000, [https://www.tandfonline.com/doi/abs/10.1300/J092v08n02_05 Orthostatic Intolerance: A Review with Application to the Chronic Fatigue Syndrome]<ref>{{Cite journal|last=Stewart|first=Julian M.|date=2000|title=Orthostatic Intolerance|url=http://dx.doi.org/10.1300/J092v08n02_05|journal=Journal of Chronic Fatigue Syndrome|language=en|volume=8|issue=2|pages=45–64|doi=10.1300/j092v08n02_05|issn=1057-3321|via=}}</ref>
*2015, [http://link.springer.com/article/10.1007/s00246-015-1274-6 Intravenous Hydration for Management of Medication-Resistant Orthostatic Intolerance in Adolescents and Young Adults]<ref name="Moak2015" />
*2016, [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4460014/ Orthostatic Changes in Hemodynamics and Cardiovascular Biomarkers in Dysautonomic Patients]<ref name="Nilsson2015" />

==Talks & interviews==
*2010, [https://www.youtube.com/watch?v=5iF30TVLaRE Mangaging Orthostatic Intolerance]<ref>{{Cite web|url=https://link.springer.com/article/10.1007%2Fs00246-015-1274-6|title=Managing Orthostatic Intolerance|last=Rowe|first=Peter|date=Sep 1, 2010|website=YouTube|publisher=SolveCFS|archive-url=|archive-date=|dead-url=|access-date=}}</ref>
*2016, [https://www.youtube.com/watch?v=_eydfpVtb0c Remaining Upright: Approach to Orthostatic Intolerance]<ref>{{Cite web|url=https://www.youtube.com/watch?v=_eydfpVtb0c|title=Remaining Upright: Approach to Orthostatic Intolerance - Melissa Cortes|last=Cortes|first=Melissa|date=Apr 7, 2016|website=YouTube|publisher=Bateman Horne Center|archive-url=|archive-date=|dead-url=|access-date=}}</ref>

==Learn more==
*2015, [http://emedicine.medscape.com/article/902155-overview#showall Orthostatic Intolerance]<ref>{{Cite journal|last=Stewart|first=Julian|date=2018-01-04|title=Orthostatic Intolerance: Background, Pathophysiology, Etiology|url=https://emedicine.medscape.com/article/902155-overview|journal=MedScape|volume=|pages=|via=}}</ref>
*2016, [https://batemanhornecenter.org/remaining-upright-approach-to-orthostatic-intolerance/ Remaining Upright: Approach to Orthostatic Intolerance]<ref>{{Cite news|url=https://batemanhornecenter.org/remaining-upright-approach-to-orthostatic-intolerance/|title=Remaining Upright: Approach to Orthostatic Intolerance - Bateman Horne Center|last=Reynolds|first=Leigh|date=2016-04-08|work=Bateman Horne Center|access-date=2018-08-28|archive-url=|archive-date=|dead-url=|language=en-US}}</ref>
*2016, [http://www.meaction.net/2016/02/21/nih-gives-246000-for-study-of-oral-rehydration-in-mecfs-patients-with-orthostatic-intolerance/ NIH gives $246,000 for study of oral rehydration in ME/CFS patients with orthostatic intolerance]<ref>{{Cite news|url=https://www.meaction.net/2016/02/21/nih-gives-246000-for-study-of-oral-rehydration-in-mecfs-patients-with-orthostatic-intolerance/|title=NIH gives $246,000 for study of oral rehydration in ME/CFS patients with orthostatic intolerance - #MEAction|last=Anderssen|first=Alex|date=2016-02-21|work=#MEAction|access-date=2018-08-28|archive-url=|archive-date=|dead-url=|language=en-US}}</ref>
*[http://www.theoicenter.com/Index.html The Orthostatic Intolerance (OI) Center]<ref>{{Cite web|url=http://www.theoicenter.com/Index.html|title=Orthostatic Intolerance (OI) Center|website=www.theoicenter.com|access-date=2018-08-28}}</ref>

==See Also==
*[[Tilt table test]]
*[[Dizziness]]
*[[Neurally mediated hypotension]]
*[[Postural orthostatic tachycardia]]

==References==
<references>
<ref name="Miwa2015">{{Citation
| last = Miwa | first = Kunihisa
| title = Cardiac dysfunction and orthostatic intolerance in patients with myalgic encephalomyelitis and a small left ventricle
| journal = Heart and Vessels | volume = 30| issue = 4| pages = 484–489
| date = Jul 2015
| pmid = 24736946
| doi = 10.1007/s00380-014-0510-y
| url = http://www.ncbi.nlm.nih.gov/pubmed/24736946
}}</ref>
<ref name="Stewart2015">{{Citation
| last = Stewart | first = Julian M | authorlink1 = Julian Stewart
| last2 = Medow | first2 = Marvin S | authorlink2 = Marvin Medow
| title = Orthostatic Intolerance
| journal = Medscape
| date = 2 Feb 2015
| url = http://emedicine.medscape.com/article/902155-overview#showall
}}</ref>
<ref name="Moak2015">{{Cite journal|last=Moak|first=Jeffrey P.|last2=Leong|first2=Derek|last3=Fabian|first3=Robin|last4=Freedenberg|first4=Vicki|last5=Jarosz|first5=Elizabeth|last6=Toney|first6=Carol|last7=Hanumanthaiah|first7=Sridhar|last8=Darbari|first8=Anil|date=2015-10-07|title=Intravenous Hydration for Management of Medication-Resistant Orthostatic Intolerance in the Adolescent and Young Adult|url=https://link.springer.com/article/10.1007/s00246-015-1274-6|journal=Pediatric Cardiology|language=en|volume=37|issue=2|pages=278–282|doi=10.1007/s00246-015-1274-6|issn=0172-0643}}</ref>
<ref name="Nilsson2015">{{citation
| last1 = Nilsson | first1 = David
| last2 = Sutton | first2 = Richard
| last3 = Tas | first3 = Widet
| last4 = Burri | first4 = Philippe
| last5 = Melander | first5 = Olle
| last6 = Fedorowski | first6 = Artur
| display-authors = 3
| title = Orthostatic Changes in Hemodynamics and Cardiovascular Biomarkers in Dysautonomic Patients
| journal = PLoS ONE | volume = 10| issue = 6
| date = 6 Aug 2015
| pmid = 26053073
| doi = 10.1371/journal.pone.0128962
| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4460014/
}}</ref>
</references>

[[Category:Signs and symptoms]]
[[Category:Cardiac signs and symptoms]]
[[Category:Comorbidities]]

Autonomic nervous system

2018-08-31T03:55:35Z

Paulitasofia1:edits

[[File:Autonomic Nervous System.jpg|400px|thumb|right|Autonomic Nervous System]]
The '''autonomic nervous system''' (ANS) is the branch of the peripheral nervous system that allows for communication between the internal organs and the [[brain]], and is responsible for regulating many involuntary processes in the body. The ANS is constantly active, responding to information from an individual’s environment and his or her body to regulate functions such as heart rate, breathing, and digestion.<ref name=":0">{{Cite journal|last=McCorry|first=Laurie Kelly|date=2007-08-15|title=Physiology of the Autonomic Nervous System|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1959222/|journal=American Journal of Pharmaceutical Education|volume=71|issue=4|issn=0002-9459|pmc=PMC1959222|pmid=17786266}}</ref><ref name=":1">{{Cite news|url=https://www.merckmanuals.com/home/brain,-spinal-cord,-and-nerve-disorders/autonomic-nervous-system-disorders/overview-of-the-autonomic-nervous-system|title=Overview of the Autonomic Nervous System - Brain, Spinal Cord, and Nerve Disorders - Merck Manuals Consumer Version|work=Merck Manuals Consumer Version|access-date=2018-08-31|language=en-US}}</ref><ref name=":2">{{Cite news|url=https://www.verywellmind.com/what-is-the-autonomic-nervous-system-2794823|title=How the Autonomic Nervous System Regulates Body Functions|work=Verywell Mind|access-date=2018-08-31}}</ref><ref>{{Cite web|url=https://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0025455/|title=Autonomic Nervous System - National Library of Medicine|last=pmhdev|website=PubMed Health|language=en|access-date=2018-08-31}}</ref>

== Function ==
The ANS is split into two main divisions: the sympathetic nervous system (SNS) and parasympathetic nervous system (PNS). The PNS and SNS serve the same organs, but one system will activate a bodily function while the other will inhibit it.<ref name=":2" /> This opposition is operated by two main chemical messengers: [[norepinephrine]], which activates (excitatory) and [[acetylcholine]], which inhibits (inhibitory).<ref name=":0" /> The two divisions complement each other to regulate the body’s responses.<ref name=":2" /> Functions regulated by the ANS include:
* Blood pressure
* Heart rate
* Urination
* Digestion and hunger
* Respiratory rate
* Sexual response
* Body temperature
* Metabolism
* Production of sweat, saliva
* Emotional responses <ref name=":0" /><ref name=":1" />

=== Sympathetic nervous system ===
The [[sympathetic nervous system]] (SNS) regulates what is referred to as the “fight-or-flight” response, which prepares the body against a perceived stress or threat. Stimulation of the SNS activates an internal alarm response. This causes an increase in:
* Heart rate (more blood pumped throughout the body)
* Width of airways (maximizing the intake of oxygen/elimination of carbon dioxide)
* Muscle strength
* The release of stored energy
During perceived stress, the SNS is activated while the PNS is less predominant. This redirects the body’s resources toward processes that are important in an emergency situation, resulting in a decrease in bodily functions controlled by the PNS, which are less important in an emergency situation.<ref name=":0" />

=== Parasympathetic nervous system ===
The [[parasympathetic nervous system]] (PNS) is dominant in conditions referred to as “rest and digest”. It controls body processes during ordinary situations. This division of the ANS helps return the body to resting state after confronting a stressor, helping to conserve energy.<ref name=":0" />

Functions of the PNS include:
* Stimulating the digestive tract, including gland secretion
* Contraction of the bladder
* Slowing heart rate
* Reducing blood pressure<ref name=":0" /><ref name=":1" />

== Autonomic disorder and dysfunction ==
Symptoms of autonomic dysfunction include:
* [[Orthostatic intolerance]]: dizziness or light-headedness when a person stands up due to a significant decrease in blood pressure, attributed to cardiovascular deconditioning and/or postural idiopathic autonomic neuropathy
* Alterations in sweating, resulting in heat intolerance
* Exercise intolerance: inability to regulate heart rate during exercise
* [[Gastroparesis]]: feeling prematurely full due to slow emptying of stomach
* Constipation or loss of bowel control
* Hyper or hypoactive bladder
* [[Visual dysfunction|Vision problems]]: inability of pupils to react to light quickly, blurry vision
* Sexual response problems (men and women)<ref name=":1" /><ref name=":3" />

== Myalgic encephalomyelitis and the ANS ==
Altered ANS functioning has been seen in many [[myalgic encephalomyelitis]] (ME) patients, as they experience various altered autonomic responses. Symptoms of autonomic dysfunction in ME include:
* Blood pressure
** Impaired blood pressure variability<ref>{{Cite journal|last=Frith|first=J.|last2=Zalewski|first2=P.|last3=Klawe|first3=J. J.|last4=Pairman|first4=J.|last5=Bitner|first5=A.|last6=Tafil-Klawe|first6=M.|last7=Newton|first7=J. L.|date=2012-9|title=Impaired blood pressure variability in chronic fatigue syndrome--a potential biomarker|url=https://www.ncbi.nlm.nih.gov/pubmed/22670061|journal=QJM: monthly journal of the Association of Physicians|volume=105|issue=9|pages=831–838|doi=10.1093/qjmed/hcs085|issn=1460-2393|pmid=22670061}}</ref>
** [[Orthostatic intolerance]]<ref name=":4">{{Cite journal|last=Van Cauwenbergh|first=Deborah|last2=Nijs|first2=Jo|last3=Kos|first3=Daphne|last4=Van Weijnen|first4=Laura|last5=Struyf|first5=Filip|last6=Meeus|first6=Mira|date=2014-04-17|title=Malfunctioning of the autonomic nervous system in patients with chronic fatigue syndrome: a systematic literature review|url=https://onlinelibrary.wiley.com/doi/epdf/10.1111/eci.12256|journal=European Journal of Clinical Investigation|language=en|volume=44|issue=5|pages=516–526|doi=10.1111/eci.12256|issn=0014-2972}}</ref><ref>{{Cite journal|last=Rowe|first=Peter C.|last2=Lucas|first2=Katherine E.|date=2007-03|title=Orthostatic Intolerance in Chronic Fatigue Syndrome|url=https://www.amjmed.com/article/S0002-9343(06)00316-0/fulltext|journal=The American Journal of Medicine|language=English|volume=120|issue=3|pages=e13|doi=10.1016/j.amjmed.2006.02.033|issn=0002-9343}}</ref>
** Higher prevalence and severity of [[Postural orthostatic tachycardia syndrome|POTS]]<ref name=":4" />
* Heart rate
** Elevated baseline heart rate in some studies<ref name=":4" />
** Reduced [[heart rate variability]] at night<ref>{{Cite journal|date=2013-10-01|title=Heart rate variability in patients with fibromyalgia and patients with chronic fatigue syndrome: A systematic review|url=https://www.sciencedirect.com/science/article/pii/S0049017213000516|journal=Seminars in Arthritis and Rheumatism|language=en|volume=43|issue=2|pages=279–287|doi=10.1016/j.semarthrit.2013.03.004|issn=0049-0172}}</ref>
** Reduced [[Small heart syndrome|left ventricular mass]], end-diastolic volume and cardiac output, and increased residual torsion in diastole<ref name=":5">{{Cite journal|last=Jones|first=David E. J.|last2=Hollingsworth|first2=Kieren G.|last3=Jakovljevic|first3=Djordje G.|last4=Fattakhova|first4=Gulnar|last5=Pairman|first5=Jessie|last6=Blamire|first6=Andrew M.|last7=Trenell|first7=Michael I.|last8=Newton|first8=Julia L.|date=2011-07-12|title=Loss of capacity to recover from acidosis on repeat exercise in chronic fatigue syndrome: a case-control study|url=https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2362.2011.02567.x|journal=European Journal of Clinical Investigation|language=en|volume=42|issue=2|pages=186–194|doi=10.1111/j.1365-2362.2011.02567.x|issn=0014-2972}}</ref>
* Digestion
** Delayed gastric emptying<ref>{{Cite journal|last=Burnet|first=Richard B|last2=Chatterton|first2=Barry E|date=2004-12|title=Gastric emptying is slow in chronic fatigue syndrome|url=https://bmcgastroenterol.biomedcentral.com/articles/10.1186/1471-230X-4-32|journal=BMC Gastroenterology|language=En|volume=4|issue=1|doi=10.1186/1471-230x-4-32|issn=1471-230X}}</ref>
** Increased gut-intestinal permeability (dysfunction of the PNS via abnormal glandular secretion in digestion)<ref>{{Cite journal|last=Maes|first=Michael|last2=Mihaylova|first2=Ivana|last3=Leunis|first3=Jean-Claude|date=2007-4|title=Increased serum IgA and IgM against LPS of enterobacteria in chronic fatigue syndrome (CFS): indication for the involvement of gram-negative enterobacteria in the etiology of CFS and for the presence of an increased gut-intestinal permeability|url=https://www.ncbi.nlm.nih.gov/pubmed/17007934|journal=Journal of Affective Disorders|volume=99|issue=1-3|pages=237–240|doi=10.1016/j.jad.2006.08.021|issn=0165-0327|pmid=17007934}}</ref>
* Body temperature
** Impaired thermoregulation, including significantly increased shivering and sweating compared to controls<ref>{{Cite web|url=http://pediatrics.aappublications.org.ezproxy.library.tufts.edu/content/120/1/e129.short|title=Tufts Libraries EZproxy Login|website=pediatrics.aappublications.org.ezproxy.library.tufts.edu|language=en|access-date=2018-08-31}}</ref>
* Exercise intolerance
** Reduced capacity to recover from exercise-induced muscle acidosis (can be attributed to dysfunction of vascular runoff, in part controlled by the ANS)<ref name=":5" />
* Neurological correlates with ANS dysfunction
** Altered communication between some parts of the [[brain]] that regulate the ANS<ref>{{Cite journal|date=2016-01-01|title=Autonomic correlations with MRI are abnormal in the brainstem vasomotor centre in Chronic Fatigue Syndrome|url=https://www.sciencedirect.com/science/article/pii/S2213158216300584|journal=NeuroImage: Clinical|language=en|volume=11|pages=530–537|doi=10.1016/j.nicl.2016.03.017|issn=2213-1582}}</ref>

=== The vagus nerve hypothesis ===
{{Main article | page_name = Vagus nerve infection hypothesis}}
The [[Vagus nerve infection hypothesis|vagus nerve hypothesis]] suggests that infection and inflammation of the vagus nerve, a prominent nerve within the ANS, would disrupt normal autonomic function. The vagus nerve communicates information between numerous internal organs and the brain. Infection of the vagus nerve could signal an exaggerated sickness response and perpetuate further dysfunction.<ref>{{Cite journal|last=VanElzakker|first=Michael B.|date=2013-9|title=Chronic fatigue syndrome from vagus nerve infection: a psychoneuroimmunological hypothesis|url=https://www.ncbi.nlm.nih.gov/pubmed/23790471|journal=Medical Hypotheses|volume=81|issue=3|pages=414–423|doi=10.1016/j.mehy.2013.05.034|issn=1532-2777|pmid=23790471}}</ref>

== See also ==
*[[Central nervous system]]
*[[Nervous system]]
*[[Parasympathetic nervous system]]
== Learn more ==
*[https://www.youtube.com/watch?v=7dZHmKMLdC0 Neurology | Autonomic Nervous System]<ref name=":3">{{Cite web|url=https://www.youtube.com/watch?v=7dZHmKMLdC0|title=Neurology {{!}} Autonomic Nervous System|last=|first=|date=Nov 11, 2017|website=YouTube|via=Ninja Nerd Science|archive-url=|archive-date=|dead-url=|access-date=}}</ref>
*[https://www.youtube.com/watch?v=71pCilo8k4M Crash Course | Autonomic Nervous System]
*[https://www.youtube.com/watch?v=0IDgBlCHVsA Crash Course | Sympathetic Nervous System]
*[https://www.youtube.com/watch?v=qqU-VjqjczE Crash Course | Parasympathetic Nervous System]

== References ==

[[Category:Neurology]]
<references />

Autonomic nervous system

2018-08-30T16:31:46Z

Paulitasofia1:minor edits

{{stub}}
[[File:Autonomic Nervous System.jpg|400px|thumb|right|Autonomic Nervous System]]
The autonomic nervous system (ANS) is the branch of the peripheral nervous system that allows for communication between the internal organs and the brain, and is responsible for regulating many involuntary processes in the body. The ANS is constantly active, responding to information from an individual’s environment and his or her body to regulate functions such as heart rate, breathing, and digestion (1,2,3,4).

== Function ==
The ANS is split into two main divisions: the sympathetic nervous system (SNS) and parasympathetic nervous system (PNS). The PNS and SNS serve the same organs, but one system will activate a bodily function while the other will inhibit it (3). This opposition is operated by two main chemical messengers: norepinephrine, which activates (excitatory) and acetylcholine, which inhibits (inhibitory) (1). The two divisions complement each other to regulate the body’s responses (3). Functions regulated by the ANS include:
* Blood pressure
* Heart rate
* Urination
* Digestion and hunger
* Respiratory rate
* Sexual response
* Body temperature
* Metabolism
* Production of sweat, saliva
* Emotional responses (1,2)

=== Sympathetic Nervous System ===
The sympathetic nervous system (SNS) regulates what is referred to as the “fight-or-flight” response, which prepares the body against a perceived stress or threat. Stimulation of the SNS activates an internal alarm response. This causes an increase in:
* Heart rate (more blood pumped throughout the body)
* Width of airways (maximizing the intake of oxygen/elimination of carbon dioxide)
* Muscle strength
* The release of stored energy
During perceived stress, the SNS is activated while the PNS is less predominant. This redirects the body’s resources toward processes that are important in an emergency situation, resulting in a decrease in bodily functions controlled by the PNS, which are less important in an emergency situation (1).

=== Parasympathetic Nervous System ===
The parasympathetic nervous system (PNS) is dominant in conditions referred to as “rest and digest”. It controls body processes during ordinary situations. This division of the ANS helps return the body to resting state after confronting a stressor, helping to conserve energy (1).

Functions of the PNS include:
* Stimulating the digestive tract, including gland secretion
* Contraction of the bladder
* Slowing heart rate
* Reducing blood pressure (1,2)

== Autonomic Disorder and Dysfunction ==
Symptoms of autonomic dysfunction include:
* Orthostatic intolerance: dizziness or light-headedness when a person stands up due to a significant decrease in blood pressure, attributed to cardiovascular deconditioning and/or postural idiopathic autonomic neuropathy
* Alterations in sweating, resulting in heat intolerance
* Exercise intolerance: inability to regulate heart rate during exercise
* Gastroparesis: feeling prematurely full due to slow emptying of stomach
* Constipation or loss of bowel control
* Hyper or hypoactive bladder
* Vision problems: inability of pupils to react to light quickly, blurry vision
* Sexual response problems (men and women) (2,5)

== Myalgic Encephalomyelitis and the ANS ==
Altered ANS functioning has been seen in many myalgic encephalomyelitis (ME) patients, as they experience various altered autonomic responses. Symptoms of autonomic dysfunction in ME include:
* Blood pressure
** Impaired blood pressure variability (9)
** Orthostatic intolerance (7,10)
** Higher prevalence and severity of POTS (7)
* Heart rate
** Elevated baseline heart rate in some studies (7)
** Reduced heart rate variability at night (8)
** Reduced left ventricular mass, end-diastolic volume and cardiac output, and increased residual torsion in diastole (11)
* Digestion
** Delayed gastric emptying (12)
** Increased gut-intestinal permeability (dysfunction of the PNS via abnormal glandular secretion in digestion) (13)
* Body temperature
** Impaired thermoregulation, including significantly increased shivering and sweating compared to controls (6)
* Exercise intolerance
** Reduced capacity to recover from exercise-induced muscle acidosis (can be attributed to dysfunction of vascular runoff, in part controlled by the ANS) (11)
* Neurological correlates with ANS dysfunction
** Altered communication between some parts of the brain that regulate the ANS (16)

=== The Vagus Nerve Hypothesis ===
The vagus nerve hypothesis suggests that infection and inflammation of the vagus nerve, a prominent nerve within the ANS, would disrupt normal autonomic function. The vagus nerve communicates information between numerous internal organs and the brain. Infection of the vagus nerve could signal an exaggerated sickness response and perpetuate further dysfunction (17).

== Learn more ==
*[https://www.youtube.com/watch?v=7dZHmKMLdC0 Neurology | Autonomic Nervous System]<ref>{{Cite web|url=https://www.youtube.com/watch?v=7dZHmKMLdC0|title=Neurology {{!}} Autonomic Nervous System|last=|first=|date=Nov 11, 2017|website=YouTube|via=Ninja Nerd Science|archive-url=|archive-date=|dead-url=|access-date=}}</ref>
*<nowiki>https://www.youtube.com/watch?v=71pCilo8k4M</nowiki> Autonomic Nervous System <nowiki>https://www.youtube.com/watch?v=0IDgBlCHVsA</nowiki> (Sympathetic Nervous System) <nowiki>https://www.youtube.com/watch?v=qqU-VjqjczE</nowiki> (Parasympathetic Nervous System)

== See also ==
*[[Nervous system]]
*[[Parasympathetic nervous system]]

== References ==

[[Category:Neurology]]
<references />

Autonomic nervous system

2018-08-30T16:27:41Z

Paulitasofia1:adding to page

{{stub}}
[[File:Autonomic Nervous System.jpg|400px|thumb|right|Autonomic Nervous System]]
The autonomic nervous system (ANS) is the branch of the peripheral nervous system that allows for communication between the internal organs and the brain, and is responsible for regulating many involuntary processes in the body. The ANS is constantly active, responding to information from an individual’s environment and his or her body to regulate functions such as heart rate, breathing, and digestion (1,2,3,4).

== Function ==
The ANS is split into two main divisions: the sympathetic nervous system (SNS) and parasympathetic nervous system (PNS). The PNS and SNS serve the same organs, but one system will activate a bodily function while the other will inhibit it (3). This opposition is operated by two main chemical messengers: norepinephrine, which activates (excitatory) and acetylcholine, which inhibits (inhibitory) (1). The two divisions complement each other to regulate the body’s responses (3). Functions regulated by the ANS include:
* Blood pressure
* Heart rate
* Urination
* Digestion and hunger
* Respiratory rate
* Sexual response
* Body temperature
* Metabolism
* Production of sweat, saliva
* Emotional responses (1,2)

=== Sympathetic Nervous System ===
The sympathetic nervous system (SNS) regulates what is referred to as the “fight-or-flight” response, which prepares the body against a perceived stress or threat. Stimulation of the SNS activates an internal alarm response. This causes an increase in:
* Heart rate (more blood pumped throughout the body)
* Width of airways (maximizing the intake of oxygen/elimination of carbon dioxide)
* Muscle strength
* The release of stored energy
During perceived stress, the SNS is activated while the PNS is less predominant. This redirects the body’s resources toward processes that are important in an emergency situation, resulting in a decrease in bodily functions controlled by the PNS, which are less important in an emergency situation (1).

=== Parasympathetic Nervous System ===
The parasympathetic nervous system (PNS) is dominant in conditions referred to as “rest and digest”. It controls body processes during ordinary situations. This division of the ANS helps return the body to resting state after confronting a stressor, helping to conserve energy (1).

Functions of the PNS include:
* Stimulating the digestive tract, including gland secretion
* Contraction of the bladder
* Slowing heart rate
* Reducing blood pressure (1,2)

== Autonomic Disorder and Dysfunction ==
Symptoms of autonomic dysfunction include:
* Orthostatic intolerance: dizziness or light-headedness when a person stands up due to a significant decrease in blood pressure, attributed to cardiovascular deconditioning and/or postural idiopathic autonomic neuropathy
* Alterations in sweating, resulting in heat intolerance
* Exercise intolerance: inability to regulate heart rate during exercise
* Gastroparesis: feeling prematurely full due to slow emptying of stomach
* Constipation or loss of bowel control
* Hyper or hypoactive bladder
* Vision problems: inability of pupils to react to light quickly, blurry vision
* Sexual response problems (men and women) (2,5)

== Myalgic Encephalomyelitis and the ANS ==
Altered ANS functioning has been seen in many myalgic encephalomyelitis (ME) patients, as they experience various altered autonomic responses. Symptoms of autonomic dysfunction in ME include:
* Blood pressure
** Impaired blood pressure variability (9)
** Orthostatic intolerance (7,10)
** Higher prevalence and severity of POTS (7)
* Heart rate
** Elevated baseline heart rate in some studies (7)
** Reduced heart rate variability at night (8)
** Reduced left ventricular mass, end-diastolic volume and cardiac output, and increased residual torsion in diastole (11)
* Digestion
** Delayed gastric emptying (12)
** Increased gut-intestinal permeability (dysfunction of the PNS via abnormal glandular secretion in digestion) (13)???
* Body temperature
** Impaired thermoregulation, including significantly increased shivering and sweating compared to controls (6)
* Exercise intolerance
** Reduced capacity to recover from exercise-induced muscle acidosis (can be attributed to dysfunction of vascular runoff, in part controlled by the ANS) (11)
* Neurological correlates with ANS dysfunction
** Altered communication between some parts of the brain that regulate the ANS (16)

=== The Vagus Nerve Hypothesis ===
The vagus nerve hypothesis suggests that infection and inflammation of the vagus nerve, a prominent nerve within the ANS, would disrupt normal autonomic function. The vagus nerve communicates information between numerous internal organs and the brain. Infection of the vagus nerve could signal an exaggerated sickness response and perpetuate further dysfunction (17).

== Learn more ==
*[https://www.youtube.com/watch?v=7dZHmKMLdC0 Neurology | Autonomic Nervous System]<ref>{{Cite web|url=https://www.youtube.com/watch?v=7dZHmKMLdC0|title=Neurology {{!}} Autonomic Nervous System|last=|first=|date=Nov 11, 2017|website=YouTube|via=Ninja Nerd Science|archive-url=|archive-date=|dead-url=|access-date=}}</ref>
*<nowiki>https://www.youtube.com/watch?v=71pCilo8k4M</nowiki> Autonomic Nervous System <nowiki>https://www.youtube.com/watch?v=0IDgBlCHVsA</nowiki> (Sympathetic Nervous System) <nowiki>https://www.youtube.com/watch?v=qqU-VjqjczE</nowiki> (Parasympathetic Nervous System)

== See also ==
*[[Nervous system]]
*[[Parasympathetic nervous system]]

== References ==

[[Category:Neurology]]
<references />