Wirth-Scheibenbogen hypothesis

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Prof Dr Klaus Wirth and Prof Dr Carmen Scheibenbogen

Theory[edit | edit source]

Hypothesis[edit | edit source]

Endothelial dysfunction is proposed to be key to ME/CFS, which is regarded as a neurovascular disease.[1][2][3]

Evidence[edit | edit source]

Treatment[edit | edit source]

Self-administered Immunoglobulin G (IgG) is a proposed treatment, with a proof of concept trial completed in 2021.[4]

Notable studies[edit | edit source]

  • 2021, An attempt to explain the neurological symptoms of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome[3] - (Full text)
  • 2021, Pathophysiology of skeletal muscle disturbances in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)[2] - (Full text)
  • 2021, Tolerability and Efficacy of s.c. IgG Self-Treatment in ME/CFS Patients with IgG/IgG Subclass Deficiency: A Proof-of-Concept Study[4] - (Full text)
  • 2020, A Unifying Hypothesis of the Pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): Recognitions from the finding of autoantibodies against ß2-adrenergic receptors[1] - (Full text)

Evidence and related studies[edit | edit source]

  • 2012, Differences in metabolite-detecting, adrenergic, and immune gene expression after moderate exercise in patients with chronic fatigue syndrome, patients with multiple sclerosis, and healthy controls[5] - (Full text)
  • 2011, Gene expression alterations at baseline and following moderate exercise in patients with Chronic Fatigue Syndrome and Fibromyalgia Syndrome[6] - (Abstract)
  • 2009, Moderate exercise increases expression for sensory, adrenergic, and immune genes in chronic fatigue syndrome patients but not in normal subjects[7] - (Abstract)

See also[edit | edit source]

Learn more[edit | edit source]

References[edit | edit source]

  1. ↑ 1.0 1.1 Wirth, Klaus; Scheibenbogen, Carmen (June 1, 2020). "A Unifying Hypothesis of the Pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): Recognitions from the finding of autoantibodies against ß2-adrenergic receptors". Autoimmunity Reviews. 19 (6): 102527. doi:10.1016/j.autrev.2020.102527. ISSN 1568-9972.
  2. ↑ 2.0 2.1 Wirth, Klaus J.; Scheibenbogen, Carmen (April 21, 2021). "Pathophysiology of skeletal muscle disturbances in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)". Journal of Translational Medicine. 19 (1): 162. doi:10.1186/s12967-021-02833-2. ISSN 1479-5876. PMC 8058748. PMID 33882940.
  3. ↑ 3.0 3.1 Wirth, Klaus J.; Scheibenbogen, Carmen; Paul, Friedemann (November 22, 2021). "An attempt to explain the neurological symptoms of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome". Journal of Translational Medicine. 19 (1): 471. doi:10.1186/s12967-021-03143-3. ISSN 1479-5876. PMC 8607226. PMID 34809664.
  4. ↑ 4.0 4.1 Scheibenbogen, Carmen; Sotzny, Franziska; Hartwig, Jelka; Bauer, Sandra; Freitag, Helma; Wittke, Kirsten; Doehner, Wolfram; Scherbakov, Nadja; Loebel, Madlen; Grabowski, Patricia Grabowski (January 2021). "Tolerability and Efficacy of s.c. IgG Self-Treatment in ME/CFS Patients with IgG/IgG Subclass Deficiency: A Proof-of-Concept Study". Journal of Clinical Medicine. 10 (11): 2420. doi:10.3390/jcm10112420. PMC 8198960. PMID 34072494.
  5. ↑ White, Andrea T; Light, Alan R; Hughen, Ronald W; VanHaitsma, Timothy A; Light, Kathleen C (December 30, 2011). "Differences in metabolite-detecting, adrenergic, and immune gene expression after moderate exercise in patients with chronic fatigue syndrome, patients with multiple sclerosis, and healthy controls". Psychosom Med. 74 (1): 46-54. doi:10.1097/PSY.0b013e31824152ed. PMID 22210239.
  6. ↑ Light, Alan R; Bateman, Lucinda; Jo, Daehyun; Hughen, Ronald W; Vanhaitsma, TA; White, Andrea T; Light, Kathleen C (July 13, 2011). "Gene expression alterations at baseline and following moderate exercise in patients with Chronic Fatigue Syndrome and Fibromyalgia Syndrome". J Intern Med. 271 (1): 64-81. doi:10.1111/j.1365-2796.2011.02405.x. PMID 21615807.
  7. ↑ Light, Alan R; White, Andrea T; Hughen, Ronald W; Light, Kathleen C (July 31, 2009). "Moderate exercise increases expression for sensory, adrenergic, and immune genes in chronic fatigue syndrome patients but not in normal subjects". J Pain. 10 (10): 1099-112. doi:10.1016/j.jpain.2009.06.003. PMID 19647494.

myalgic encephalomyelitis (M.E.) - A disease often marked by neurological symptoms, but fatigue is sometimes a symptom as well. Some diagnostic criteria distinguish it from chronic fatigue syndrome, while other diagnostic criteria consider it to be a synonym for chronic fatigue syndrome. A defining characteristic of ME is post-exertional malaise (PEM), or post-exertional neuroimmune exhaustion (PENE), which is a notable exacerbation of symptoms brought on by small exertions. PEM can last for days or weeks. Symptoms can include cognitive impairments, muscle pain (myalgia), trouble remaining upright (orthostatic intolerance), sleep abnormalities, and gastro-intestinal impairments, among others. An estimated 25% of those suffering from ME are housebound or bedbound. The World Health Organization (WHO) classifies ME as a neurological disease.

autoantibody An antibody that works against the body's own antigens, a hallmark of autoimmune diseases. Autoantibodies are the opposite of an antibodies.

metabolite A chemical compound produced by, or involved in, metabolism. The term is often used to refer to the degradation products of drugs in the body.

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