A new clinical trial published in the online journal PloS ONE studied the effects of the anti-cancer drug Rituxan (rituximab) on chronic fatigue syndrome (ME/CFS). In addition to symptom reduction, the results of this study gave credence to the theory that ME/CFS may be an autoimmune disease.
Study Design and Results
You may be wondering why anyone would even think of treating ME/CFS with an anti-cancer drug. The idea for this study came about when an ME/CFS patient, who also had non-Hodgkins lymphoma, experienced significant ME/CFS symptom improvement while undergoing chemotherapy for the cancer.
In this double-blind, placebo-controlled study, 30 ME/CFS patients were given an infusion of either Rituxan or saline followed by a second infusion two weeks later. The participants were then followed for 12 months.
Major or moderate improvement was seen in 10 of the 15 patients in the Rituxan group while only two of the placebo group reported improvement. The average duration of the improvement was 25 weeks, however, four from the Rituxan group continued to experience the improvement even after the end of the year-long study.
It's important to note that the Rituxan group did not begin to experience improvements for two to seven months after they were treated. This delayed response supports the theory that ME/CFS may indeed be an autoimmune disease.
The Autoimmune Connection
B cells are lymphocytes that make and secrete antibodies which attach themselves to foreign invaders, marking them for destruction by the immune system. Autoimmune diseases occur when, instead of just attacking foreign invaders, the immune system mistakenly attacks and destroys healthy body tissues as well.
The drug Rituxan works by destroying B cells that have a protein called CD20 on their surface. (CD20 has been linked to certain types of cancer, such as lymphoma.) This is referred to as B-cell depletion. Rituxan is increasingly being tested and used in the treatment of a number of different autoimmune diseases including rheumatoid arthritis and lupus.
Although the scientists don't know exactly why B-cell depletion improves ME/CFS symptoms, they think that the delayed responses experienced by the ME/CFS patients who were treated with Rituxan “suggests that CFS is an autoimmune disease and may be consistent with the gradual elimination of autoantibodies...”
The researchers went on to say, “...we believe that B-cell depletion targets a central player in the pathogenesis of the CFS disease, directly or indirectly. Whether this mechanism applies to specific subsets of CFS patients or the group as a whole is a subject for further research.”
These same researchers have already begun two new open-label phase-II studies investigating Rituxan treatment with two infusions two weeks apart (as in this study) followed by maintenance infusions at 3, 6, 10 and 15 months.
Whether or not ME/CFS is an autoimmune disease has been debated for many years. Even though previous research showed that more than half of ME/CFS patients develop autoantibodies indicative of autoimmune reactions, it has not “officially” been considered to be an autoimmune disease. Based on this study, however, that designation may soon have to change.
Although there are still many questions left to be answered and much more research to be done, I think this study provides pretty strong evidence that autoimmunity plays a role in at least a subset of ME/CFS patients.
I found it particularly encouraging that, as of the time the authors were writing this research paper, two people in the Rituxan group were still experiencing major improvements and had returned to full-time work. I'll be looking forward to hearing the results of the new studies to see if maintenance infusions of Rituxan will allow even more patients to regain the lives they had before ME/CFS entered the picture.
Fluge Ø, Bruland O, Risa K, Storstein A, Kristoffersen EK, et al. 2011 Benefit from B-Lymphocyte Depletion Using the Anti-CD20 Antibody Rituxan in Chronic Fatigue Syndrome. A Double-Blind and Placebo-Controlled Study. PLoS ONE 6(10): e26358. doi:10.1371/journal.pone.0026358
Published On: October 31, 2011