by Nicola Bassi, MD, et al.
February 28, 2008
[Note: A free full text pdf of this article is available at http://www.ima.org.il/imaj/ar08jan-21.pdf]
Chronic fatigue syndrome (CFS) is a heterogeneous disorder with unknown pathogenesis and etiology, characterized by disabling fatigue, difficulty in concentration and memory, and concomitant skeletal and muscular pain.
Several mechanisms have been suggested to play a role in CFS, such as:
Excessive oxidative stress following exertion [oxidative stress exists when levels of "reactive oxygen species" (ROS) molecules exceed the cells' ability to consistently defend, via antioxidants, against the damage they can do],
Immune imbalance characterized by decreased Natural Killer cell and macrophage activity, immunoglobulin G subclass deficiencies (IgG1, IgG3) and decreased serum concentrations of complement component.
Autoantibodies were also suggested as a possible factor in the pathogenesis of CFS. Recent studies indicate that anti-serotonin, anti-microtubule-associated protein 2, and anti-muscarinic cholinergic receptor 1 may play a role in the pathogenesis of CFS.
It has been demonstrated that impairment in vasoactive neuropeptide metabolism may explain the symptoms of CFS. [Neuropetides are chemical signals released by nerve cells; “vasoactive” is defined as having a relaxing or contricting effect on blood vessels.]
Source: The Israel Medical Association Journal: 2008 Jan;10(1):79-82. PMID: 18300582, by Bassi N, Amital D, Amital H, Doria A, Shoenfeld Y. Department of Rheumatology, University of Padova, Padova, Italy; Departments of Psychiatry & Medicine and Center for Autoimmune Diseases, Tel Aviv University, Israel.
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