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Monitoring a Hypothetical Channelopathy in Chronic Fatigue Syndrome

  [ 24 votes ]   [ Discuss This Article ] • June 20, 2002

J Nijs,[1,6] PT; C Demanet, [5] MD, PhD; N McGregor, [3] MDSc, PhD; P De Becker, [1] PhD; M Verhas, [4] MD, PhD; P Englebienne, [4] PhD; and K De Meirleir, [1,2] MD, PhD

1: Department of Human Physiology, Faculty of Physical Education and Physical Therapy, Vrije Universiteit Brussel,Belgium

2: Fatigue Clinic, Vrije Universiteit Brussel, Belgium

3: Collaborative Pain Research Unit, Department of Biological Sciences, Faculty of Science, University of Newcastle,, Callaghan, New South Wales, Australia

4: Department of Nuclear Medicine, Brugmann Hospital / Academic Hospital, Vrije Universiteit Brussel and UniversitŽ Libre Bruxelles (V.U.B Ð U.L.B.), Brussels, Belgium

5: Division of Hematology and Immunology, Academic Hospital Vrije Universiteit, Brussel, Belgium

6: To whom correspondence should be addressed: Vakgroep MFYS, AZ-VUB KRO gebouw, 1, Laarbeeklaan 101, 1090, Brussel, Belgium
Tel: +32 2 477 4604. Fax: +32 2 477 4607. E-mail:

This study aimed at monitoring of a previously suggested channelopathy in Chronic Fatigue Syndrome, and at searching for possible explanations by means of immune system characteristics.

Twenty-seven CFS patients and 20 age and sex matched healthy volunteers were recruited. RNase L-ratio, % of the norm of whole body potassium content, serum electrolytes (sodium, calcium and potassium), immune cells, blood cell count and erythrocyte sedimentation rate were determined.

More than fifty percent of our patients presented with abnormal whole body potassium content. Eight patients had increased, while six had depleted potassium content. Discriminant function analysis revealed that the CFS patients and control subjects could be differentiated on immunophenotyping with the predominant cell differences being the increase in CD19+CD5+ (mature B-) cells and the decrease in CD3-CD16+CD56+ (NK) cells in both the percentage and count distributions. The fall in NK-cells was very strongly associated with increases in the RNase L-ratio and falls in serum calcium levels. In addition, four patients with low serum calcium levels showed lower whole body potassium levels.

In conclusion, these observations provide evidence for a channelopathy in an important subset of CFS-patients, probably induced by the deregulated 2,5A RNase L antiviral pathway. Proteolytic cleavage of 80 kDa RNase L generates ankyrin repeat motif-containing fragments. RLI (RNase L inhibitor) takes part of the ATP binding cassette (ABC) superfamily, and is capable of binding ankyrin-like fragments in CFS-patients. Consequently, ankyrin fragments, released by RNase L cleavage, interacts with the ABC-ankyrin domain interaction and deregulation of proper ABC transporters function is inevitable.

Source: Presented at the 2001 Clinical and Scientific Meeting: Myalgic Encephalopathy/Chronic Fatigue Syndrome: "The Medical Practitioners' Challenge in 2001."

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