Yoshitsugi Hokama, Cara Empey Campora, Cynthia Hara, Tina Kuribayashi, Diana Le Huynh, and Kenichi Yabusaki
Department of Pathology, John A. Burns School of Medicine, University of Hawaii at Maˆnoa,
Journal of Clinical Laboratory Analysis 23 : 210–212 (2009)
A survey of the literature reports ACAs as common
serological markers in many different types of diseases,
including viral diseases such as illnesses resulting from
chemical (1) and marine toxin exposure (4,5,6), HIV
(7,8) and Epstein-Barr virus (9), hematological cancers
including CLL and acute myelocytic leukemias, exposure
to fungal organisms, malaria, and staphylococcus
infections (10,11), and autoimmune diseases such as
multiple sclerosis, systemic lupus erythematosus, autoimmune
hepatitis, and more (2).
This study demonstrates that a large percentage of patients clinically diagnosed with CFS have elevated levels of the IgM isotype to CL (95%), suggesting that CFS may be an autoimmune condition.
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 (11,13).
classification of CFS as an autoimmune disorder
may serve to increase the availability of treatment
options for patients suffering from the disease.
Experiments are underway to further elucidate why
ACAs are produced in individuals afflicted with CFS.
Such studies include investigating the effects of specific
chemical agents, marine toxins, and ACAs on mitochondrial
metabolic pathways that are indicative of
reduced or blocked energy production that may lead to
the fatigued state in CFS.
Such studies may lead to the
development of potential therapeutic agents to block or
reduce such interactions.