Rituximab works by destroying white blood cells that make antibodies. White blood cells are part of the immune system response and ME/CFS studies point to chronic activation of the immune system following an acute infection.
A clear or possible clinical infection preceding CFS onset could be identified in 73% and 67% of the patients in the Rituximab and placebo groups, respectively according to the authors, however, patients with ongoing infections were excluded from the trial.
Like all immune cells, white blood cells are created in the bone marrow. The NIAID reports, that at the heart of the immune system is the ability to distinguish between self and non-self. Immune cells and other cells in the body usually coexist peaceably in a state known as self-tolerance. In abnormal situations (such as an autoimmune disease), the immune system can wrongly identify self as non-self and execute a misdirected immune attack.
A limitation of this study is the lack of predetermined exact definitions of clinical response with respect to duration and extent of improvement. According to the authors, an alternative explanation for the observed clinical improvement from B-cell depletion could be elimination or reduction of B-lymphotrophic viruses such as cytomegalovirus (CMV) or Epstein-Barr virus (EBV).
Two new open-label phase-II studies in Norway (Study 1, Study 2) investigating Rituximab treatment with two infusions two weeks apart (as in the present study) followed by maintenance Rituximab infusions at 3, 6, 10 and 15 months, are being conducted to further explore this treatment principle in CFS (
The anti-cancer drug is also being investigated for treatment of rheumatoid arthritis, lupus/systemic lupus erythematosus, Sjogren’s syndrome multiple sclerosis, and Behcet’s disease.
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See also: Cancer drug Rituximab/Rituxan-study in ME/CFS in PLoS ONE: major improvements in all symptoms in 67 % of patients
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