Immunological aspects of chronic fatigue syndrome.
Journal: Autoimmun Rev. 2008 Sep 15. [Epub ahead of print]
Authors: Lorusso L, Mikhaylova SV, Capelli E, Ferrari D, Ngonga GK, Ricevuti G.
Affiliation: Department of Neurology, Mellino Mellini Hospital, Chiari, Brescia, Italy.
NLM Citation: PMID: 18801465
Chronic fatigue syndrome (CFS) is a specific clinical condition that characterises unexplained disabling fatigue and a combination of non-specific accompanying symptoms for at least 6 months, in the absence of a medical diagnosis that would otherwise explain the clinical presentation. Other common symptoms include headaches, myalgia, arthralgia, and post-exertional malaise; cognitive difficulties, with impaired memory and concentration; unrefreshing sleep; and mood changes.
Similar disorders have been described for at least two centuries and have been differently named neurasthenia, post-viral fatigue, myalgic encephalomyelitis and chronic mononucleosis. Recent longitudinal studies suggest that some people affected by chronic fatigue syndrome improve with time but that most remain functionally impaired for several years. The estimated worldwide prevalence of CFS is 0.4-1% and it affects over 800,000 people in the United States and approximately 240,000 patients in the UK. No physical examination signs are specific to CFS and no diagnostic tests identify this syndrome. The pathophysiological mechanism of CFS is unclear.
The main hypotheses include altered central nervous system functioning resulting from an abnormal immune response against a common antigen; a neuroendocrine disturbance; cognitive impairment caused by response to infection or other stimuli in sentient people. The current concept is that CFS pathogenesis is a multifactorial condition. Various studies have sought evidence for a disturbance in immunity in people with CFS. An alteration in cytokine profile, a decreased function of natural killer (NK) cells, a presence of autoantibodies and a reduced responses of T cells to mitogens and other specific antigens have been reported.
The observed high level of pro-inflammatory cytokines may explain some of the manifestations such as fatigue and flu-like symptoms and influence NK activity. Abnormal activation of the T lymphocyte subsets and a decrease in antibody-dependent cell-mediated cytotoxicity have been described. An increased number of CD8+ cytotoxic T lymphocytes and CD38 and HLA-DR activation markers have been reported, and a decrease in CD11b expression associated with an increased expression of CD28+ T subsets has been observed. This review discusses the immunological aspects of CFS and offers an immunological hypothesis for the disease processes.
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Yet, despite all this evidence of a biological, rather than psychiatric, basis for CFS, there are still people who insist that there's nothing physically wrong with us.
And despite the fact that something very similar has been around for hundreds of years, there are still those who insist that it's caused by electromagnetic forces, the stress of modern living, watching too much TV, eating too much processed food, cell phones, or any number of other reasons that could not have been the cause of the identical symptoms 200 years ago.
The only thing that makes sense is the observation that this is caused by an enterovirus, and causes symptoms similar to another known enterovirus (read more at http://journals.aol.com/kmc528/Lifeasweknowit/entries/2008/02/13/dr.-bruno-parallels-in-cfsfmspolio/1905 )
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