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Anticardiolipin antibodies found in CFS

Evidence of autoimmunity: 95% of CFS samples showed ACA in patient sera

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.



of CFS patients showed high ACA titers


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


Read the full text of this paper, co-sponsored by the National CFIDS Foundation, here.


Treatment options

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.

In a MedHep discussion, Professor Garth Nicolson elaborated on the role of anticardiolipin antibodies in autoimmune disorders.

“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.


To see the full abstract of this study, tap on the toggle below.

Anticardiolipin antibodies in the sera of patients with diagnosed chronic fatigue syndrome.


Examination of anticardiolipin antibodies (ACAs) in the sera of patients clinically diagnosed with chronic fatigue syndrome (CFS) using an enzyme-linked immunoassay procedure demonstrated the presence of immunoglobulin M isotypes in 95% of CFS serum samples tested. The presence of immunoglobulin G and immunoglobulin A isotypes were also detected in a subset of the samples. Future studies will focus on elucidating whether alterations to mitochondrial inner membranes and/or metabolic functions play a possible role in the expression of ACAs.


FEATURE PHOTO: Antibody lights by Isabelle


  1. 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] []
  2. 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] []
  3. Schmidt R, Auer-Grumbach P, Fazekas F, Offenbacher H, Kapeller P. Anticardiolipin antibodies in normal subjects. Stroke 1995;26:749–754. [Full Text] []

Written by Russell Logan


Russell Logan worked as a magazine publisher and editor until forced into early retirement through ill health with ME. He has battled with moderate to severe ME for 25 years. He now lives in Noosaville, Australia.

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  1. Having had ME for at least 15 years and having experienced a recent onset severe headache (before christmas) I have just been diagnosed with a right transverse cerebral venous sinus thrombosis (CVST).

    Your article is very interesting with regards to the development of blod clots in the brain, because having ACA is apparently a risk factor for developing CVST.

    It would also be interesting to see how Fluge and Mella’s Rituximab studies might potentially develop this theme further.

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