New research has found high levels of several autoimmune disease indicators in chronic fatigue syndrome (CFS).
Researchers examined the sera of 40 CFS patients for anticardiolipin antibodies (ACAs) and demonstrated that 95% of CFS samples tested showed elevated ACA of the immunoglobulin M isotype in patient sera.1
The presence of immunoglobulin G and immunoglobulin A isotypes were also detected in a subset of the samples.
Testing for antibodies to cardiolipin (CL) is routinely performed as one of a panel of tests for autoimmune disorders.2
The presence of ACA at relatively high titers in patients with CFS suggests the possibility of alterations to the inner membranes of liver mitochondria, thereby exposing CL in a manner so as to elicit an antibody response to CL.
For comparison, in clinically ‘‘normal’’ individuals, which can be generally classified as those who meet the following criteria: (a) no severe diseases, (b) no drug or alcohol dependence, (c) no clinical or laboratory evidence of systemic lupus erythematosus or other autoimmune disorder, and (d) no antibodies that might cross react with ACAs, one study showed that 77.3% of assayed individuals had negative ACA titers, 15.0% were considered low positives, and 7.7% had moderately high titers.3
As a possible autoimmune disease, CFS patients may be treated by suppression of the ACA or by diminishing the antigen CL in serum.
Previous studies have shown that treatment with monoclonal antibodies to B cells reduces ACA levels to normal in patients with autoimmune disease, leading to clinical improvements.
Specifically, Rituximab, a chimeric monoclonal CD20 antibody, has been shown to normalize high ACA serum titers of patients with autoimmune systemic lupus erythematosus, rheumatoid arthritis, autoimmune thrombocytopenia, and autoimmune hemolytic anemia.
Rituximab may serve as an effective therapeutic agent for ameliorating the symptoms of CFS. Therefore, classification of CFS as an autoimmune disorder may serve to increase the availability of treatment options for patients suffering from the disease.
Anticardiolipin antibodies in autoimmune disorders
Anti-cardiolipin antibodies are “anti-mitochondrial” antibodies that attack certain molecules that are common constituents of cell membranes and tend to increase clot formation – e.g., in veins and arteries. They are associated with many disorders, including immune disturbances such as lupus and Behcet’s disease, syphilis and recurrent miscarriage.
“Anticardiolipin antibodies are found in most autoimmune disorders and especially in those that involve decreased mitochondrial function (essentially all fatiguing illnesses and many other chronic illnesses, such as neurodegenerative diseases, neurobehavioral diseases, among other diseases),” he said.
Cardiolipin is a specialized lipid that is mostly found in the inner mitochondrial membrane where it is essential for oxidative phosphorylation or the production of high-energy molecules in the cell that are necessary for metabolism and cell function.
Reduction of the cardiolipin molecules results in leaky mitochondrial membranes, and these membranes must not be leaky or high-energy molecules can’t be produced, resulting in fatigue.
Infections damage cardiolipin and other membrane phospholipids by oxidation—the infections produce peroxides that oxidize the membrane lipids, and cardiolipin molecules are particularly sensitive. Once damaged, they must be removed and antibodies can be made against them during this process.
These same oxidative events can damage the endothelial cells lining the blood vessels, resulting in increased platelet aggregation and increased production of platelets to compensate for this.
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- Hokama Y1, Campora CE, Hara C, Kuribayashi T, Le Huynh D, Yabusaki K. Anticardiolipin antibodies in the sera of patients with diagnosed chronic fatigue syndrome. J Clin Lab Anal. 2009;23(4):210-2. doi: 10.1002/jcla.20325. [PubMed], [Full Text] ↩
- Ioannou Y, Lambrianides A, Cambridge G, Leandro MJ, Edwards JCW, Isenberg DA. B cell depletion therapy for patients with systemic lupus erythematosus results in a significant drop in anticardiolipin antibody titers. Ann Rheum Dis 2008;67:425–426. [Abstract] ↩
- Schmidt R, Auer-Grumbach P, Fazekas F, Offenbacher H, Kapeller P. Anticardiolipin antibodies in normal subjects. Stroke 1995;26:749–754. [Full Text] ↩