Kenny De Meirleir

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
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
(As per bio page at Nevada Center for Biomedical Research)
 * 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

 * Solvay Prize
 * NATO Research Award

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

Canadian Consensus Criteria

 * 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.”"

Pediatric Case Definition

 * 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.'"

Books

 * 2011, Gezond of gezondigd? by Kenny de Meirleir and Christine Tobback
 * 2006, Pediatric Chronic Fatigue Syndrome by Kenny de Meirleir, [[Neil McGregor], and Elke L.S. Van Hoof]
 * 2002, Chronic Fatigue Syndrome: A Biological Approach Edited by Patrick Englebienne and Kenny De Meirleir
 * 2000, Chronic Fatigue Syndrome: Critical Reviews and Clinical Advances; What Does the Research Say? by Roberto Patarca-Montero and Kenny De Meirleir

Notable studies

 * 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.'"
 * 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."
 * 2013, Plasmacytoid Dendritic Cells in the Duodenum of Individuals Diagnosed with Myalgic Encephalomyelitis Are Uniquely Immunoreactive to Antibodies to Human Endogenous Retroviral Proteins
 * 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."
 * 2009, Increased D-Lactic Acid Intestinal Bacteria in Patients with Chronic Fatigue Syndrome
 * 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.'"
 * 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.'"
 * 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.'"
 * 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.'"
 * 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.'"
 * 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.'"
 * 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.'"
 * 2001, A definition-based analysis of symptoms in a large cohort of patients with chronic fatigue syndrome.
 * 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.'"
 * 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.'"

Wetenschap voor Patiënten - ME/cvs Vereniging

 * 2012, 01. Is ME and/or CFS a disease?/ Is ME en/of CVS een ziekte? - Prof. Dr. K. de Meirleir
 * 2012, 02. Is it possible to diagnose ME/CFS? / Valt ME/CVS re diagnosticeren? - Prof. Dr. K. de Meirleir
 * 2012, 03. Is ME a hereditary condition?/ Is ME een erfelijke aandoening? - Prof. Dr. K. de Meirleir
 * 2012, 04. ME and sleep disorders / ME en slaapproblemen - prof. Dr. K. de Meirleir
 * 2012, 05. ME and Pain / ME en Pijn - prof. Dr. K. de Meirleir
 * 2012, 06. ME and Hormones / ME en Hormonen - prof. Dr. K. de Meirleir
 * 2012, 07. ME, the immune system and several viruses / ME, het immuunsysteem en diverse virussen - prof. Dr. K. de Meirleir
 * 2012, 08. ME, Blood Circulation and the Brain / ME, de bloedsomloop en de hersenen - prof. Dr. K. de Meirleir
 * 2012, 09. ME and gastrointestinal Problems / ME en maag-darmproblemen - prof. Dr. K. de Meirleir
 * 2013, 10. ME, comorbidity and exclusion criteria / ME, comorbiditeit en uitsluitingscriteria - prof. Dr. K. de Meirleir
 * 2013, 11. Twelve Answers to Questions - ME Irigins and Causes / Bestaan en oorzaken ME - prof. Dr. K. de Meirleir
 * 2013, 12. Misdiagnosis, related Diagnosis and Tests / Verkeerde diagnoses, verwante diagnoses en testen - prof. Dr. K. de Meirleir
 * 2013, 13. Sleep, Pain and Nightmares / Slaap, pijn en nachtzweten - prof. Dr. K. de Meirleir
 * 2013, 14. ME and Treatment / Behandeling - prof. Dr. K. de Meirleir
 * 2013, 15. ME, Remedy and Hope / Remedies en hoop - prof. Dr. K. de Meirleir
 * 2013, 16. ME and Low-Dose Naltrexone (LDN) / Low Dose Naltrexone (LDN) - prof. Dr. K. de Meirleir
 * 2013, 17. ME and the Brain / ME en de hersenen -prof. Dr. K. de Meirleir
 * 2013, 18. ME, Th1, Th2 and Th17 / ME, Th1, Th2 en Th17 - prof. Dr. K. de Meirleir
 * 2013, 19. Subgroups of Patients / Subgroepen patienten - prof. Dr. K. de Meirleir
 * 2013, 20. Sense and Nonsense of Tests / Zin en onzin van testen - prof. Dr. K. de Meirleir

Invest in ME Conference Speeches

 * 2011, Speaker at the 6th Invest in ME International ME Conference on Clinical Diagnosis, Treatments and Trials of ME/CFS DVD available
 * 2009, Speaker at the 4th Invest in ME International ME Conference on Research on Extremely Debilitated M.E. Patients Reveals the True Nature of the Disorder DVD available
 * 2007, Speaker at the 2nd Invest in ME International ME Conference on Treatments for ME/CFS Integrative & Complimentary Medicine DVD available

ME/CFS Alert

 * Episode 45 - Interview with Dr. Kenny de Meirleir, Part 4
 * Episode 44 - Interview with Dr. Kenny de Meirleir, Part 3
 * Episode 43 - Interview with Dr. Kenny de Meirleir, Part 2
 * Episode 42 - Interview with Dr. Kenny de Meirleir

IAMECFS Conference

 * 2016, 12th International IACFS/ME Biennial Clinical and Research Conference, Emerging Science and Clinical Care, Paper presentation:A panel of biomarkers accurately identifies CFS/ME patients and contributes to the understanding of the pathophysiology of the disorder

Other

 * 17 April 2010, Professor Kenny De Meirleir on Chronic Fatigue in Perth, Western Australia at Sir Charles Gairdner Hospital

Online presence

 * PubMed
 * Twitter
 * Facebook
 * Website
 * Wikipedia

Learn more

 * 2013, The De Meirleir Experience
 * 2009, Dr. Kenny de Meirleir
 * 2008, Dr. Kenny De Meirleir – Man on the Move for ME/CFS
 * 2007, ME/CFS & Chronic Infection of the Gut – Notes on Dr. Kenny De Meirleir’s Presentation in Perth