Immunological Similarities between Cancer and Chronic Fatigue Syndrome

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  Immunological Similarities between Cancer and Chronic Fatigue Syndrome: The Common Link to Fatigue?

  MIRA MEEUS 1 ,2 , WILHELM MISTIAEN 1, LUC LAMBRECHT 3 ,4 and JO NIJS 1 ,2

  Author Affiliations  * 1Division of Musculoskeletal Physiotherapy, Department of Health Sciences, Artesis University College Antwerp (AHA), Antwerp  * 2Department of Human Physiology, Faculty of Physical Education and Physiotherapy, Vrije Universiteit Brussel (VUB), Brussel  * 3Private Practice for Internal Medicine, Ghent & Aalst;  * 4CVS Contactgroep, Belgium  * Correspondence to: Jo Nijs, Artesis Hogeschool Antwerpen (AHA), Department of Health Sciences, Division of Musculoskeletal Physiotherapy, Van Aertselaerstraat 31, 2170 Merksem, Belgium. Tel: +32 36418205, e-mail: jo.nijs@vub.ac.be  or jo.nijs@artesis.be

  Abstract Cancer and chronic fatigue syndrome (CFS) are both characterised by fatigue and severe disability. Besides fatigue, certain aspects of immune dysfunctions appear to be present in both illnesses. In this regard, a literature review of overlapping immune dysfunctions in CFS and cancer is provided. Special emphasis is given to the relationship between immune dysfunctions and fatigue.

  Abnormalities in ribonuclease (RNase) L and hyperactivation of nuclear factor kappa beta (NF-κB) are present in CFS and in prostate cancer. Malfunctioning of natural killer (NK) cells has long been recognised as an important factor in the development and reoccurrence of cancer, and has been documented repeatedly in CFS patients.

  The dysregulation of the RNase L pathway, hyperactive NF-κB leading to disturbed apoptotic mechanisms and oxidative stress or excessive nitric oxide, and low NK activity may play a role in the two diseases and in the physiopathology of the common symptom fatigue. However, in cancer the relation between the immune dysfunctions and fatigue has been poorly studied.

  Immunological abnormalities to such as a dysregulated RNase L pathway, hyperactive NF-κB, increased oxidative stress and reduced NK cytotoxicity, among others, are present in both diseases. These anomalies may be part of the physiopathology of some of the common complaints, such as fatigue. Further studies to confirm the hypotheses given here are warranted.