Kenny De Meirleir

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Professor Dr. Kenny L. De Meirleir is a Belgian Internal Medicine doctor who specializes in ME/CFS. He frequently partners with numerous myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) researchers in the EU, UK, US, and Australia to further the understanding of the pathophysiology of ME/CFS. He was an editor of the former Journal of Chronic Fatigue Syndrome. He participated in an earlier clinical trial of Ampligen, an immunomodulator for ME/CFS.

Clinic location[edit]

Professor De Meirleir runs a clinic in Brussels, Hummunitas, and also at the Nevada Center for Biomedical Research in Reno, Nevada, in the United States.

Education[edit]

(As per bio page at Nevada Center for Biomedical Research)[1]

  • 1970 – 1977 Medical Education, Vrije Universiteit Brussel, Doctor in Medicine (Belgium), Magna cum Laude
  • 1977 – 1982 Internal medicine Residency, Department of Internal Medicine, university Hospital Vrije Universiteit Brussel, under supervision of Prof. Dr. R. Six. Certification in Internal Medicine
  • 1982 – 1984 Resident in Cardiology, Algemeen Ziekenhuis, Vrije Universiteit Brussel, under supervision of Prof. Dr. P. Block, interrupted by military service
  • 1985 Ph.D. in Physiology

Awards[edit]

  • Solvay Prize
  • NATO Research Award

International Consensus Criteria[edit]

He is one of the authors of the 2011 case definition, International Consensus Criteria.[2]

Canadian Consensus Criteria[edit]

  • 2003, Canadian Consensus Criteria for Myalgic Encephalomyelitis, PDF File
  • 2003, Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Clinical Working Case Definition, Diagnostic and Treatment Protocols
    Abstract - Recent years have brought growing recognition of the need for clinical criteria for myalgic encephalomyelitis (ME), which is also called chronic fatigue syndrome (CFS). An Expert Subcommittee of Health Canada established the Terms of Reference, and selected an Expert Medical Consensus Panel representing treating physicians, teaching faculty and researchers. A Consensus Workshop was held on March 30 to April 1, 2001 to culminate the review process and establish consensus for a clinical working case definition, diagnostic protocols and treatment protocols. We present a systematic clinical working case definition that encourages a diagnosis based on characteristic patterns of symptom clusters, which reflect specific areas of pathogenesis. Diagnostic and treatment protocols, and a short overview of research are given to facilitate a comprehensive and integrated approach to this illness. Throughout this paper, “myalgic encephalomyelitis” and “chronic fatigue syndrome” are used interchangeably and this illness is referred to as “ME/CFS.”[3]

Pediatric Case Definition[edit]

  • 2006, "A Pediatric Case Definition for Myalgic Encephalomyelitis and Chronic Fatigue Syndrome"
    "Summary: For a diagnosis of chronic fatigue syndrome (CFS), most researchers use criteria that were developed by Fukuda et al. (1994), with modifications suggested by Reeves et al. (2003). However, this case definition was established for adults rather than children. A Canadian Case Definition (ME/CFS; Myalgic Encephalomyelitis/CFS) has recently been developed, with more specific inclusion criteria (Carruthers et al., 2003). Again, the primary aim of this case definition is to diagnose adult CFS. A significant problem in the literature is the lack of both a pediatric definition of ME/CFS and a reliable instrument to assess it. These deficiencies can lead to criterion variance problems resulting in studies labeling children with a wide variety of symptoms as having ME/CFS. Subsequently, comparisons between articles become more difficult, decreasing the possibility of conducting a meta-analysis. This article presents recommendations developed by the International Association of Chronic Fatigue Syndrome Pediatric Case Definition Working group for a ME/CFS pediatric case definition. It is hoped that this pediatric case definition will lead to more appropriate identification of children and adolescents with ME/CFS."[4]

Books[edit]

Notable studies[edit]

  • 2016, Humoral Immunity Profiling of Subjects with Myalgic Encephalomyelitis Using a Random Peptide Microarray Differentiates Cases from Controls with High Specificity and Sensitivity (FULL TEXT)
    Abstract - "Myalgic encephalomyelitis (ME) is a complex, heterogeneous illness of unknown etiology. The search for biomarkers that can delineate cases from controls is one of the most active areas of ME research; however, little progress has been made in achieving this goal. In contrast to identifying biomarkers that are directly involved in the pathological process, an immunosignature identifies antibodies raised to proteins expressed during, and potentially involved in, the pathological process. Although these proteins might be unknown, it is possible to detect antibodies that react to these proteins using random peptide arrays. In the present study, we probe a custom 125,000 random 12-mer peptide microarray with sera from 21 ME cases and 21 controls from the USA and Europe and used these data to develop a diagnostic signature. We further used these peptide sequences to potentially uncover the naturally occurring candidate antigens to which these antibodies may specifically react with in vivo. Our analysis revealed a subset of 25 peptides that distinguished cases and controls with high specificity and sensitivity. Additionally, Basic Local Alignment Search Tool (BLAST) searches suggest that these peptides primarily represent human self-antigens and endogenous retroviral sequences and, to a minor extent, viral and bacterial pathogens."[5]
  • 2016, Genome-wide association analysis identifies genetic variations in subjects with myalgic encephalomyelitis/chronic fatigue syndrome (FULL TEXT)
    Abstract - "Myalgic encephalomyelitis, also known as chronic fatigue syndrome or ME/CFS, is a multifactorial and debilitating disease that has an impact on over 4 million people in the United States alone. The pathogenesis of ME/CFS remains largely unknown; however, a genetic predisposition has been suggested. In the present study, we used a DNA single-nucleotide polymorphism (SNP) chip representing over 906,600 known SNPs to analyze DNA from ME/CFS subjects and healthy controls. To the best of our knowledge, this study represents the most comprehensive genome-wide association study (GWAS) of an ME/CFS cohort conducted to date. Here 442 SNPs were identified as candidates for association with ME/CFS (adjusted P-value<0.05). Whereas the majority of these SNPs are represented in non-coding regions of the genome, 12 SNPs were identified in the coding region of their respective gene. Among these, two candidate SNPs resulted in missense substitutions, one in a pattern recognition receptor and the other in an uncharacterized coiled-coil domain-containing protein. We also identified five SNPs that cluster in the non-coding regions of T-cell receptor loci. Further examination of these polymorphisms may help identify contributing factors to the pathophysiology of ME/CFS, as well as categorize potential targets for medical intervention strategies.[6]
  • 2013, Plasmacytoid Dendritic Cells in the Duodenum of Individuals Diagnosed with Myalgic Encephalomyelitis Are Uniquely Immunoreactive to Antibodies to Human Endogenous Retroviral Proteins[7]
  • 2009, Detection of Herpesviruses and Parvovirus B19 in Gastric and Intestinal Mucosa of Chronic Fatigue Syndrome Patients
    Abstract: "Background: Human herpesvirus-6 (HHV-6), Epstein-Barr virus and parvovirus B19 have been suggested as etiological agents of chronic fatigue syndrome but none of these viruses is consistently detected in all patients. However, active viral infections may be localized in specific tissues, and, therefore, are not easily detectable. The aim of this study was to investigate the presence of HHV-6, HHV-7, EBV and parvovirus B19 in the gastro-intestinal tract of CFS patients. Patients and Methods: Using real-time PCR, viral DNA loads were quantified in gastro-intestinal biopsies of 48 CFS patients and 35 controls. Results: High loads of HHV-7 DNA were detected in most CFS and control biopsies. EBV and HHV-6 were detected in 15-30% of all biopsies. Parvovirus B19 DNA was detected in 40% of the patients versus less than 15% of the controls. Conclusion: Parvovirus B19 may be involved in the pathogenesis of CFS, at least for a subset of patients. The gastro-intestinal tract appears as an important reservoir of infection for several potentially pathogenic viruses."[8]
  • 2009, Increased D-Lactic Acid Intestinal Bacteria in Patients with Chronic Fatigue Syndrome[9]
  • 2007, Physiological Responses to Arm and Leg Exercise in Women Patients with Chronic Fatigue Syndrome
    "Abstract - Patients affected by chronic fatigue syndrome (CFS) characteristically show easy and unexplained fatigue after minimal exertion that does not resolve with rest and is associated with specific symptoms lasting for more than six months. Cardiopulmonary exercise testing is a valid procedure for determining functional capacity in patients with CFS. We compare cardioventilatory adaptation to exercise between a group of eighty-five consecutive women patients affected by CFS and a group of fifteen healthy women extremely sedentary individuals, with the use of maximum incremental exercise testing on a cycle ergometer and arm ergometer, assessing possible differences. The majority of values achieved at peak exhaustive exercise were significantly lower in CFS patients than controls, including the percentage of maximum oxygen uptake in arm physical test (37.4±10.0% in CFS vs. 58.9± 15.8% in controls) and leg physical test (53.4±15.0% in CFS patients vs. 76.2 ± 18.0%in controls). In conclusion, the CFS group shows a lower work capacity in arm or leg exercise that would not be justified exclusively by their personal characteristics or deconditioning."[10]
  • 2007, Defining the Occurrence and Influence of Alpha-Delta Sleep in Chronic Fatigue Syndrome
    "Abstract: BACKGROUND: Patients with chronic fatigue syndrome (CFS) present a disordered sleep pattern and frequently undergo polysomnography to exclude a primary sleep disorder. Such studies have shown reduced sleep efficiency, a reduction of deep sleep, prolonged sleep initiation, and alpha-wave intrusion during deep sleep. Deregulation of the 2-5A synthetase/RNase L antiviral pathway and a potential acquired channelopathy are also found in a subset of CFS patients and could lead to sleep disturbances. This article compiles a large sleep study database on CFS patients and correlates these data with a limited number of immune parameters as it has been thought that RNase L could be associated with these sleep disturbances. METHODS: Forty-eight patients who fulfilled 1994 Centers for Disease Control and Prevention criteria for CFS underwent extensive medical evaluation, routine laboratory testing, and a structured psychiatric interview. Subjects then completed a complaint checklist and a two-night polysomnographic investigation. RNase L analysis was performed by gel electrophoresis using a radiolabeled 2',5'-oligoadenylate trimer. Basic descriptive statistical parameters were calculated. RESULTS: Patients experienced a prolonged sleep latency, showed a low sleep efficiency index, and had a low percentage of slow wave sleep. The present alpha-delta intrusion correlated with anxiety; no correlations appeared, however, between alpha-delta sleep and immunologic parameters, including RNase L. CONCLUSIONS: The main findings are 1) validation of sleep latency problems and other sleep disturbances as already suggested by several authors; 2) alpha-delta intrusion seems associated with anxiety; and 3) elevated RNase L did not correlate with alpha-delta sleep.[11]
  • 2006, Pediatric Chronic Fatigue Syndrome and Munchausen-By-Proxy: A Case Study
    "Abstract - Pediatric chronic fatigue syndrome (CFS) posits even more challenges for professional caregivers in comparison with adult CFS samples. Most children with CFS display a decrease in school attendance and a decrease in social activities. As several conditions such as school phobia, primary psychiatric disorders or family disturbance present the same characteristics, the diagnostic process appears more complex. Family disturbance, moreover, is often specified as child abuse, neglect or even Munchausen-by-proxy. As skepticism is frequently associated with a diagnosis of CFS, patients and parents must fend for themselves, fighting allegations of child abuse and neglect. This case study illustrates what happens when such allegations are put forward."[12]
  • 2006, Antiviral Pathway Deregulation of Chronic Fatigue Syndrome Induces Nitric Oxide Production in Immune Cells That Precludes a Resolution of the Inflammatory Response
    "Abstract - Chronic fatigue syndrome (CFS) is a poorly defined medical condition diagnosed by exclusion, which, besides severe chronic fatigue as the hallmark symptom, involves inflammatory and immune activation stigma. Although viral infections are not systematically found in CFS patients, the type I interferon antiviral pathway has been repeatedly shown to be activated in peripheral blood mononuclear cells (PBMC) of the most afflicted patients. An abnormal truncated form of ribonuclease L (37-kDa RNase L) is also found in the PBMC of CFS patients and this protein has been proposed as a biological marker for CFS. Recently, the levels of this abnormal protein have been significantly correlated to the extent of inflammatory symptoms displayed by CFS patients. We report here that active double-stranded RNA-dependent kinase (PKR) is expressed and activated in parallel to the presence of the 37-kDa RNase L and to an increase in nitric oxide production by immune cells. However, PKR upregulation results also in a significant increase followed by a decrease in caspase 3 activity for the samples containing the highest levels of 37-kDa RNase L. This caspase 3 downregulation does not result from increased expression of the anti-apoptotic proteins Bcl-2 and Bcl-XL. These results therefore suggest that chronic inflammation due to excess nitric oxide production plays a role in CFS and that the normal resolution of the inflammatory process by NF-kB activation and apoptotic induction is impaired. These observations draw new directions for the therapeutic approach of CFS."[13]
  • 2004, The Influence of Chronic Fatigue Syndrome on the Personality Profile: A Case Report
    "Abstract - Objective: Chronic fatigue syndrome (CFS) functionally impairs many patients. Despite numerous studies and reviews in CFS, little is known about the behavioral consequences. Several researchers have already suggested the influential role of personality as a possible predisposing or perpetuating factor. Method: A case study is presented of a 34-year-old man with a history of CFS. Psychological profiling using the MMPI-2 was performed during the course of his condition. Results: His passive-aggressive manner during the medical encounter was underscored by his personality profile (code type 3-2). After his recovery, however, a spike 3 profile emerged indicating a fulfilled individual. Somatic items included in the inventory, created a secondary increase of the clinical scales. Physical complaints diminished as his condition improved and subsequently, decreased the clinical scales. Conclusion: The relevance of classifying personality characteristics in CFS patients as traits could not be supported by this case report."[14]
  • 2004, Association Between Fennell Phase Inventory Scores and Immune and RNase-L Parameters in Chronic Fatigue Syndrome
    "Abstract - All patients suffering from a chronic condition, are challenged to manage the reality of their disease, the accompanying anxiety, the problems of daily living, and the effect on relationships. Therefore, when confronted with debilitating complaints, patients suffering from chronic fatigue syndrome (CFS) need to adapt to a new way of living during the course of their illness. Fennell developed an integrated model to manage CFS. This article is a follow-up of a study by Jason et al. (9, 10) to verify the existence of the different phases. Although not all differences are statistically significant, a clear distinction is made according to the conclusions drawn by Jason et al. (9, 10). Relationships between these distinctions and measures of symptoms, disability, psychological distress, coping, and immune parameters were revealed using non-parametric statistical tests."[15]
  • 2004, The Fennell Phase Inventory in a Belgian Sample
    "Abstract: The present study is a follow-up of the research conducted by Jason, Fennell et al. (1995, 1999, 2000) on a multistage theory for chronic fatigue syndrome (CFS). This multistage model is a very promising method for the evaluation of patients suffering from CFS and could facilitate the appropriate selection of various psychosocial therapies that improve the patient’s ability to cope with their illness. Four predictive factors emerged with moderate to excellent reliability. A Spearman’s rank correlation revealed positive correlations between our four-factor model and the three-factor model identified by Jason et al.(1999). A correlation matrix between the dimensional psychological investigation and the Fennell Phases revealed characteristics as suggested by previous research. Biological parameters varied over the different phases suggesting an important interaction between body and psyche."[16]
  • 2003, Evidence for Bacterial (Mycoplasma, Chlamydia) and Viral (HHV-6) Co-Infections in Chronic Fatigue Syndrome Patients
    "Abstract - Using the blood of 100 CFS patients and forensic polymerase chain reaction we have found that a majority of Chronic Fatigue Syndrome (CFS) patients show evidence of multiple, systemic bacterial and viral infections (OR = 18.0, 95%CL 8.5–37.9, P >0.001) that could play an important role in CFS morbidity. CFS patients had a high prevalence (51%) of one of four Mycoplasma species (OR = 13.8, 95%CL 5.8–32.9, P >0.001) and often showed evidence of co-infections with different Mycoplasma species, Chlamydia pneumoniae (OR = 8.6,95%CL 1.0–71.1, P >0.01) and/or active Human Herpes Virus-6 (HHV-6) (OR = 4.5,95%CL 2.0–10.2, P >0.001). We found that 8% of the CFS patients showed evidence of C. pneumoniae and 31% of active HHV-6 infections. Since the presence of one or more chronic systemic infections may predispose patients to other infections, we examined the prevalence of C. pneumoniae and active HHV-6 infections in mycoplasma-positive and -negative patients. The incidence of C. pneumoniae or HHV-6 was similar in mycoplasma-positive and -negative patients, suggesting that such infections occur independently in CFS patients. Also, the incidence of C. pneumoniae in active HHV-6-positive and -negative patients was similar. Control subjects (N = 100) had low rates of mycoplasma (6%), active HHV-6 (9%) or chlamydia (1%) infections, and there were no coinfections in control subjects. Differences in bacterial and/or viral infections in CFS patients compared to control subjects were significant. The results indicate that a relatively large subset of CFS patients show evidence of bacterial and viral co-infections."[17]
  • 2004, Comparison of Activity Limitations/Participation Restrictions Among Fibromyalgia and Chronic Fatigue Syndrome Patients
    "Abstract - Fibromyalgia (FM) and Chronic Fatigue Syndrome (CFS) are related yet overlapping disorders; the current case definitions prohibit a clear-cut differential diagnosis. These diagnostic criteria mainly address the impairment level of the World Health Organization's International Classification of Functioning, Disability and Health. This study aimed at comparing activity limitations and participation restrictions in patients with FM (n = 90) and CFS (n = 47). The Chronic Fatigue Syndrome Activities and Participation Questionnaire (CFS-APQ) was used for assessing functionality in both groups. The convergent validity of the scores obtained with the questionnaire with visual analogue scales for pain, fatigue and concentration was investigated in FM patients, as well as the content validity. No differences in total scores and 25 out of 26 individual items on the CFS-APQ were observed between the 2 groups (independent samples Mann-Whitney U test). This sample of FM patients reported to be more disabled in ‘sitting for two hours’ as compared to the CFS group (mean scores 3.0 ± 1.0 and 2.3 ± 1.0; P = .004). Four hundred and thirty-seven of the 497 (87.9%) responses to the request to list difficult activities matched the content of the CFS-APQ. The overall scores of the CFS-APQ correlated statistically significant in respect to visual analogue scales for pain and concentration (Spearman rho for the total scores ranged between .44 and .49). These data question the disease specificity of the CFS-APQ for CFS, but suggests its applicability in ‘the Chronic Pain-Fatigue Syndromes.’ The present report provides evidence for both the content and convergent validity of the CFS-APQ in FM patients.[18]
  • 2003, Hyperbaric Therapy in Chronic Fatigue Syndrome
    "Abstract - The aim of this study was to determine if hyperbaric oxygen treatment (HBOT) could be used as adjunctive therapy and if HBOT could increase the quality of life in such a way that the functional status would improve in patients with an infection. A randomized, controlled trial was conducted on 15 Mycoplasma sp. infected CFS (CDC 1994) patients and 14 CFS (CDC 1994) patients with no evidence of a Mycoplasma infection were enrolled in a convenience randomization sample from our referral clinic. No statistical differences were found by use of univariate repeated measures although Bodily Pain as measured by the SF-36 seems to decrease after hyperbaric therapy (Greenhouse-Geisser: p = .010). Trends were found using paired t-testing for Mycoplasma infected CFS patients. The general perceived fatigue seemed to decrease after hyperbaric therapy (General Fatigue: p = .06). Directly after one week of hyperbaric therapy general fatigue improved (p = .03) but there was a reduction of activity (reduced activity: p = .05) and general perceived health (general health: p = .04). One month later the physical role increased (Role-Physical: p = .07). Although more data is required to make firm conclusions, trends were found. Reduced fatigue, increased levels of activity and an improved reaction time improved significantly their quality of life and therefore, enhanced also their functional status and thus could be used as an adjunctive therapy."[19]
  • 2003, Deregulation of the 2,5A Synthetase RNase L Antiviral Pathway by Mycoplasma spp. in Subsets of Chronic Fatigue Syndrome
    "Abstract - The deregulation of the 2,5A synthetase RNase L antiviral pathway and the prevalence of Mycoplasma spp. in subsets of Chronic Fatigue Syndrome (CFS) have been separately reported in the scientific literature. We hypothesised that a comorbid pathophysiological mechanism involving infection by Mycoplasma spp. and the deregulation of the 2,5A synthetase/RNase L antiviral pathway may exist in CFS. Therefore, 186 consecutive CFS patients were enrolled. Mycoplasma detection was performed using forensic polymerase chain reaction. For RNase L determination, a radioactive probe was used to label 2,5A binding proteins in unfractionated peripheral blood mononuclear cell extracts. Mycoplasma-infected CFS patients presented with significantly elevated RNase L-ratio, compared to non-infected age- and sex-matched patients (p = 0.016). These results suggest that mycoplasma infections may cause deregulation of the 2,5A synthetase RNase L antiviral pathway in patients with CFS."[20]
  • 2003, Immunophenotyping Predictive of Mycoplasma Infection in Patients with Chronic Fatigue Syndrome?
    "Abstract - An impaired immune system and opportunistic infections are considered important characteristics in the pathophysiology of Chronic Fatigue Syndrome (CFS). Using immunofluorescence we examined healthy subjects (N = 35) and two subsets of CFS patients: those without evidence of Mycoplasma (N = 55) and those with evidence of a Mycoplasma infection in their blood (N = 131). Using monoclonal antibodies and forensic polymerase chain reaction for detection of M. hominis, M. fermentans, M. pneumoniae and M. penetrans, we examined leukocytes in peripheral blood samples. Both patient groups presented with significantly elevated CD25+ (activated) cells as compared to healthy volunteers. CFS patients without evidence of mycoplasma infection(s) had increased amounts of CD5+ B-cells. Stepwise discriminant analysis indicated the number of activated cells, number of memory CD4+ cells and percentage of suppressor T-cells (lower in Mycoplasma+ patients as compared to Mycoplasma- patients) as the discriminant variables. A classification tree, for predicting the presence of Mycoplasma species in CFS patients, was constructed. Taken together, these data confirm earlier reports on immune activation among CFS patients, but this does not appear to be specific for Mycoplasma-infected CFS patients."[21]
  • 2003, The Symptoms and Psychiatric Status of the Bijlmermeer Plane Crash Disaster: Similarities with Chronic Fatigue Syndrome and Gulf War Syndrome
    "Abstract - On October 4, 1992, the El Al Boeing crashed in the residential quarter ‘Bijlmermeer’ in Amsterdam (The Netherlands). In the years after the plane crash, local residents and assistance personnel began reporting a variety of unusual symptoms not unlike those reported by patients with chronic fatigue syndrome (CFS) and Gulf War Syndrome (GWS). The aim of this study was to define the symptom constellations reported by the patients and assess the possible causes of the illness. Standardized psychological questionnaires (MMPI-II, SCL-90, KPS and a complaints checklist) were used to screen for psychological changes and to describe the symptoms reported by the patients. Differences between local residents and assistance personnel, gender differences, Mycoplasma-infected and Mycoplasma non-infected patients were monitored. The major symptoms reported were extreme fatigue, non-restorative sleep, concentration-problems, memory problems and muscle and joint pains. There were no changes in the SCL-90 responses that indicated any alteration of psychological distress. Assessment using the MMPI-II revealed a profile typically seen in chronic physical illness and assessment of the Harris-Lingoes scales revealed no elevations in pathogenic scales. Twelve subjects (67%) had a positive Mycoplasma PCR response. Victims of the Bijlmermeer plane crash disaster had increases in symptoms similar to patients with Gulf War Syndrome and CFS and no evidence of somatoform disorder, anxiety or depression. Similar to patients with Gulf War Syndrome and CFS, a deregulation of the immune-competence through a combination of toxic material exposure and psychological stressors associated with increased opportunistic infections may be the most likely etiological hypothesis."[22]
  • 2002, Activity Limitations and Participation Restrictions in Patients with Chronic Fatigue Syndrome—Construction of a Disease Specific Questionnaire
    "Abstract - Review of the literature indicated the lack of disease specific measures for assessing activity limitations and participation restriction in patients with Chronic Fatigue Syndrome. Retrospective analysis of Karnofsky Performance Status questionnaires and Activities of Daily Living questionnaires (a Dutch version of the Barthel index, modified for CFS) of 141 subjects was performed to create a new questionnaire. Data analysis resulted in the following item selection, based on most frequently reported activity limitations and participation restriction; cleaning, washing dishes and returning them to cupboard, iron, do the wash, gardening, replace light bulb, walking, climb one flight of stairs, stand one hour, sit two hours, doing groceries, thirty minutes of computer work, carrying heavy objects, write a full page letter, use a screwdriver, hammer a nail, make one bed, reading, social activities, doing sports, studying, driving a car, going to school/working, preparing meals and caring for a child. These data were used to create the CFS-Activities and Participation Questionnaire (CFS-APQ). The reliability and different aspects of validity of this new measure still need to be established."[23]
  • 2002, Possible Triggers and Mode of Onset of Chronic Fatigue Syndrome
    "Abstract - To identify the possible triggering events of CFS, we collected data on 1546 CFS patients and 309 excluded fatigued patients. Using extensive present and past medical history and lab reports as close as possible to the date of onset, an attempt was made to identify the agents that could play a role in the disease process. Significant differences were found between the events at onset, between the Fukuda or Holmes definitions and a sudden as distinct from a gradual onset. We further found a series of subgroups of events that occurred at onset of CFS. Each of these onset event clusters was associated with an infectious event, blood transfusion or hepatitis B vaccination. In a large percentage of our study group an infectious event was combined with a non-infectious event. In summary, we can conclude that a number of different stressors and consequent immunological and neuroendocrinological changes can contribute to the onset of CFS."[24]
  • 2001, A definition-based analysis of symptoms in a large cohort of patients with chronic fatigue syndrome.[25]
  • 2001, G-Actin Cleavage Parallels 2-5A-Dependent RNase L Cleavage in Peripheral Blood Mononuclear Cells—Relevance to a Possible Serum-Based Screening Test for Dysregulations in the 2-5A Pathway
    "Summary - A dysregulation in the 2N,5N-oligoadenylate (2-5A)-dependent RNase L antiviral pathway has been detected in peripheral blood mononuclear cells (PBMC) of chronic fatigue syndrome (CFS) patients, which is characterized by an unregulated RNase L activity and the presence of a low molecular weight (LMW) 2-5A-binding protein (37-kDa 2-5A-BP). This study was undertaken to test the possibility that the 37-kDa 2-5A-BP of CFS is produced by proteolytic cleavage of the 80-kDa monomeric enzyme. Incubation of the 80-kDa human recombinant RNase L (r-hRNase L) with PBMC extracts either positive or negative for the presence of 37-kDa 2-5A-BP, respectively, demonstrates that the LMW protein is produced by the former, not the latter, and that the size of the fragment generated from the recombinant protein matches the 37-kDa size of the fragment observed in the original PBMC. Digestion of r-hRNase L with calpain generated the same 37-kDa 2-5A-BP observed in PBMC extracts, and calpain immunoprecipitation from PBMC extracts reduced their proteolytic activity, an observation that suggests that calpain may be involved in the cleavage. We further examined G-actin, a known calpain substrate, for possible cleavage in PBMC. Actin fragments were observed of which the presence correlated with the presence of 37-kDa 2-5-BP. Since G-actin is cleared by serum transport, we further screened serum samples for the presence of LMW forms. A single LMW actin fragment could be detected in serum, the presence of which correlated significantly with the presence of both G-actin and RNase L fragments in PBMC. This latter observation offers the opportunity to screen large populations of patients for dysregulations in the RNase L pathway by a serum-based assay."[26]
  • 2001, Interactions Between Rnase L Ankyrin-Like Domain and ABC Transporters as a Possible Origin for Pain, Ion Transport, CNS and Immune Disorders of Chronic Fatigue Immune Dysfunction Syndrome
    "Summary - Low molecular weight (LMW) ribonuclease L (RNase L) forms have been identified in peripheral blood mononuclear cells (PBMC) of patients with chronic fatigue immune dysfunction syndrome (CFIDS). Data from our laboratory indicate that these LMW RNase L proteins are produced by proteolytic cleavage of the native monomeric enzyme and we have identified calpain as one of the possible proteases involved. Using human recombinant RNase L (r-hRNase L) His-tagged at the N-terminus, we show here at the one hand that both calpain and PBMC extracts from CFIDS patients cleave the protein in fragments of identical sizes containing ankyrin-like repeat sequences. At the other hand, the activity of RNase L is modulated by its interaction with a specific inhibitor (RLI), a member of the ATP binding cassette (ABC) superfamily. RLI interacts with the ankyrin domain of RNase L, which results in a blockade of the 2N,5N-oligoadenylate (2-5A)-binding site of the enzyme. We show that RLI contains a small ankyrin-interacting peptide cluster through which it interacts with the first two β-hairpin coils of the RNase L ankyrin domain. A similarity search performed at the NCBI using RLI aminoacid sequence as the entry allowed to identify several other ABC transporter proteins sharing significant identities with RLI, including the ankyrin-interacting peptide. Taken together, these results show that upon pathological cleavage of RNase L, fragments containing the ankyrin domain are released, which could be capable of interacting with selected members of the human ABC superfamily, preventing their interaction with the normal cognate ankyrin protein and hence impairing their proper cellular function. This interaction constitutes a common physiological mechanism explaining numerous and currently unexplained symptoms experienced by patients with CFIDS, which are otherwise totally unrelated."[27]

Talks & interviews[edit]

Wetenschap voor Patiënten - ME/cvs Vereniging[edit]

Invest in ME Conference Speeches[edit]

ME/CFS Alert[edit]

IAMECFS Conference[edit]

Other[edit]

Online presence[edit]

Learn more[edit]

See also[edit]

Nevada Center for Biomedical Research

References[edit]

  1. http://nvcbr.org/meet-the-team/?team_member=kennydemeirleir#tab-2fc81613def7f57b934
  2. Carruthers, BM; van de Sande, MI; De Meirleir, KL; Klimas, NG; Broderick, G; Mitchell, T; Staines, D; Powles, A C P; Speight, N; Vallings, R; Bateman, L; Baumgarten-Austrheim, B; Bell, DS; Carlo-Stella, N; Chia, J; Darragh, A; Jo, D; Lewis, D; Light, A; Marshall-Gradisnik, S; Mena, I; Mikovits, JA; Miwa, K; Murovska, M; Pall, ML; Stevens, S (2011), "Myalgic encephalomyelitis: International Consensus Criteria.", Journal of Internal Medicine, 270 (4): 327-38, PMID 21777306, doi:10.1111/j.1365-2796.2011.02428.x 
  3. Carruthers, Bruce M.; Jain, Anil Kumar; De Meirleir, Kenny L.; Peterson, Daniel L.; Klimas, Nancy G.; Lerner, A. Martin; Bested, Alison C.; Flor-Henry, Pierre; Joshi, Pradip; Powles, A C Peter; Sherkey, Jeffrey A.; van de Sande, Marjorie I. (2003), "Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Clinical Working Case Definition, Diagnostic and Treatment Protocols", Journal of Chronic Fatigue Syndrome, 11 (2): 7-115, doi:10.1300/J092v11n01_02 
  4. Jason, Leonard A; Jordan, Karen; Miike, Teruhisa; Bell, David S; Lapp, Charles; Torres-Harding, Susan; Rowe, Kathy; Gurwitt, Alan; De Meirleir, Kenny; Van Hoof, Elke LS (2006), "A Pediatric Case Definition for Myalgic Encephalomyelitis and Chronic Fatigue Syndrome", Journal of Chronic Fatigue Syndrome, 13 (2-3): 1-44, doi:10.1300/J092v13n02_01 
  5. Singh, Sahajpreet; Stafford, Phillip; Schlauch, Karen A.; Tillett, Richard R.; Gollery, Martin; Johnston, Stephen Albert; Khaiboullina, Svetlana F.; De Meirleir, Kenny L.; Rawat, Shanti; Mijatovic, Tatjana; Subramanian, Krishnamurthy; Palotás, András; Lombardi, Vincent C. (2016), "Humoral Immunity Profiling of Subjects with Myalgic Encephalomyelitis Using a Random Peptide Microarray Differentiates Cases from Controls with High Specificity and Sensitivity", Molecular Neurobiology, doi:10.1007/s12035-016-0334-0 
  6. Schlauch, Karen A.; Khaiboullina, Svetlana F.; De Meirleir, Kenny L.; Rawat, Shanti; Petereit, J; Rizvanov, Albert A; Blatt, Nataliya; Mijatovic, Tatjana; Kulick, D; Palotás, András; Lombardi, Vincent C. (2016), "Genome-wide association analysis identifies genetic variations in subjects with myalgic encephalomyelitis/chronic fatigue syndrome", Translational Psychiatry, 6 (2): e730, doi:10.1038/tp.2015.208 
  7. De Meirleir, KL; Khaiboullina, SF; Frémont, M; Hulstaert, J; Rizvanov, AA; Palotás, A; Lombardi, VC (2013), "Plasmacytoid Dendritic Cells in the Duodenum of Individuals Diagnosed with Myalgic Encephalomyelitis Are Uniquely Immunoreactive to Antibodies to Human Endogenous Retroviral Proteins", In Vivo, 27 (2): 177–187, PMID 23422476 
  8. Frémont, Marc; Metzger, Kristine; Rady, Hamada; Hulstaert, Jan; De Meirleir, Kenny (2009), "Detection of Herpesviruses and Parvovirus B19 in Gastric and Intestinal Mucosa of Chronic Fatigue Syndrome Patients" (PDF), In Vivo, 23 (2): 209-213 
  9. Sheedy, John R.; Wettenhall, Richard E.H.; Scanlon, Denis; Gooley, Paul R.; Lewis, Donald P.; McGregor, Neil; Stapleton, David; Butt, Henry L.; De Meirleir, Kenny L. (2009), "Increased D-Lactic Acid Intestinal Bacteria in Patients with Chronic Fatigue Syndrome", In Vivo, 23 (4): 621-628, PMID 19567398 
  10. Casimiro Javierre, José Alegre, José Luis Ventura, Ana García-Quintana, Ramon Segura, Andrea Suarez, Alberto Morales, Agusti Comella & Kenny De Meirleir. (2007). Physiological Responses to Arm and Leg Exercise in Women Patients with Chronic Fatigue Syndrome. Journal of Chronic Fatigue Syndrome, Vol. 14, Iss. 1, pp. 43-53. http://dx.doi.org/10.1300/J092v14n01_05
  11. Van Hoof E, De Becker P, Lapp C, Cluydts R, De Meirleir K. (2009). Defining the Occurrence and Influence of Alpha-Delta Sleep in Chronic Fatigue Syndrome. The American Journal of the Medical Sciences. Vol 333, Iss 2, pp. 78-84. PMID: 17301585.
  12. E. Van Hoof, P. De Becker & K. De Meirleir. (2006). Pediatric Chronic Fatigue Syndrome and Munchausen-By-Proxy: A Case Study. Journal of Chronic Fatigue Syndrome, Vol. 13, Iss. 2-3, pp. 45-53. http://dx.doi.org/10.1300/J092v13n02_02
  13. Marc Frémont, Freya Vaeyens, C. Vincent Herst, Kenny De Meirleir & Patrick Englebienne. (2006). Antiviral Pathway Deregulation of Chronic Fatigue Syndrome Induces Nitric Oxide Production in Immune Cells That Precludes a Resolution of the Inflammatory Response. Journal of Chronic Fatigue Syndrome, Vol. 13, Iss. 4, pp. 17-28. http://dx.doi.org/10.1300/J092v13n04_03
  14. Elke Van Hoof & Kenny De Meirleir. (2004). The Influence of Chronic Fatigue Syndrome on the Personality Profile: A Case Report. Journal of Chronic Fatigue Syndrome, Vol. 12, Iss. 3, pp. 63-71. http://dx.doi.org/10.1300/J092v12n03_05
  15. Elke Van Hoof, Danny Coomans, Raymond Cluydts & Kenny De Meirleir. Association Between Fennell Phase Inventory Scores and Immune and RNase-L Parameters in Chronic Fatigue Syndrome. Journal of Chronic Fatigue Syndrome, Vol. 12, Iss. 2, pp. 19-34. http://dx.doi.org/10.1300/J092v12n02_03
  16. Van Hoof, Elke; Coomans, Danny; Cluydts, Raymond; De Meirleir, Kenny (2004), "The Fennell Phase Inventory in a Belgian Sample", Journal of Chronic Fatigue Syndrome, 12 (1): 53-69, doi:10.1300/J092v12n01_04 
  17. Garth L. Nicolson, Marwan Y. Nasralla, Kenny De Meirleir, Robert Gan & Joerg Haier. (2003). Evidence for Bacterial (Mycoplasma, Chlamydia) and Viral (HHV-6) Co-Infections in Chronic Fatigue Syndrome Patients. Journal of Chronic Fatigue Syndrome, Vol. 11, Iss. 2, pp. 7-19. http://dx.doi.org/10.1300/J092v11n02_02
  18. Jo Nijs, Peter Vaes, Neil McGregor, Luc Lambrecht, Elke Van Hoof & Kenny De Meirleir. (2003). Comparison of Activity Limitations/Participation Restrictions Among Fibromyalgia and Chronic Fatigue Syndrome Patients. Journal of Chronic Fatigue Syndrome, Vol. 11, Iss. 4, pp. 3-18. http://dx.doi.org/10.1300/J092v11n04_02
  19. Elke Van Hoof, Danny Coomans, Pascale De Becker, Romain Meeusen, Raymond Cluydts & Kenny De Meirleir. (2003). Hyperbaric Therapy in Chronic Fatigue Syndrome Journal of Chronic Fatigue Syndrome, Vol. 11, Iss. 3, pp. 37-49. http://dx.doi.org/10.1300/J092v11n03_04
  20. Jo Nijs, Kenny De Meirleir, Danny Coomans, Pascale De Becker & Garth L. Nicolson. (2003). Deregulation of the 2,5A Synthetase RNase L Antiviral Pathway by Mycoplasma spp. in Subsets of Chronic Fatigue Syndrome. Journal of Chronic Fatigue Syndrome, Vol. 11, Iss. 2, pp. 37-50. http://dx.doi.org/10.1300/J092v11n02_04
  21. Jo Nijs, Danny Coomans, Garth L. Nicolson, Pascale De Becker, Demanet Christian & Kenny De Meirleir. (2003). Immunophenotyping Predictive of Mycoplasma Infection in Patients with Chronic Fatigue Syndrome? Journal of Chronic Fatigue Syndrome, Vol. 11, Iss. 2, pp. 51-69. http://dx.doi.org/10.1300/J092v11n02_05
  22. Van Hoof, Elke; De Meirleir, Kenny; Cluydts, Raymond; Coomans, Danny (2003), "The Symptoms and Psychiatric Status of the Bijlmermeer Plane Crash Disaster: Similarities with Chronic Fatigue Syndrome and Gulf War Syndrome", Journal of Chronic Fatigue Syndrome, 11 (3): 3-21, doi:10.1300/J092v11n03_02 
  23. Jo Nijs, Peter Vaes, Elke Van Hoof, Pascale De Becker, Neil McGregor & Kenny De Meirleir. (2002). Activity Limitations and Participation Restrictions in Patients with Chronic Fatigue Syndrome—Construction of a Disease Specific Questionnaire. Journal of Chronic Fatigue Syndrome, Vol. 10, Iss. 2, pp. 3-23. http://dx.doi.org/10.1300/J092v10n03_02
  24. P. De Becker, N. McGregor & K. De Meirleir. (2002). Possible Triggers and Mode of Onset of Chronic Fatigue Syndrome. Journal of Chronic Fatigue Syndrome, Vol. 10, Iss. 2, pp. 3-18. http://dx.doi.org/10.1300/J092v10n02_02
  25. De Becker, P; McGregor, N; De Meirleir, K (Sep 2001), "A definition-based analysis of symptoms in a large cohort of patients with chronic fatigue syndrome.", Journal of Internal Medicine, 250 (3): 234-240, PMID 11555128 
  26. Simon Roelens, C. Vincent Herst, Anne D'Haese, Karen De Smet, Marc Frémont, Kenny De Meirleir & Patrick Englebienne. (2001). G-Actin Cleavage Parallels 2-5A-Dependent RNase L Cleavage in Peripheral Blood Mononuclear Cells—Relevance to a Possible Serum-Based Screening Test for Dysregulations in the 2-5A Pathway. Journal of Chronic Fatigue Syndrome, Vol. 8, Iss. 3-4, pp. 63-82. http://dx.doi.org/10.1300/J092v08n03_07
  27. Patrick Englebienne, C. Vincent Herst, Karen De Smet, Anne D'Haese & Kenny De Meirleir. (2001). Interactions Between Rnase L Ankyrin-Like Domain and ABC Transporters as a Possible Origin for Pain, Ion Transport, CNS and Immune Disorders of Chronic Fatigue Immune Dysfunction Syndrome. Journal of Chronic Fatigue Syndrome, Vol. 8, Iss. 3-4, pp. 83-102. http://dx.doi.org/10.1300/J092v08n03_08
  28. http://www.investinme.eu/IIMEC6.shtml#agenda
  29. http://www.investinme.eu/IIMEC4.shtml#agenda
  30. http://www.investinme.eu/IIMEC2.shtml#agenda


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