This short video demonstrates the action of rituximab, a drug which shows promise for those with severe CFS/ME. Rituximab (trade names: Rituxan, MabThera) was first approved by the FDA in 1997 for the treatment of non-Hodgkin's lymphoma. It is believed that rituximab destroys tumors by attaching to the CD20 receptor on B cells, causing the tumor cells to disintegrate. In some non-Hodgkin's B-cell lymphomas, rituximab prevents the production of more tumor cells.
Rituximab is also used in the treatment of autoimmune disorders, such as rheumatoid arthritis and Wegener's granulomatosis. In these cases, rituximab works by temporarily depleting the total number of B cells, which are important in promoting inflammation. Rich Van Konynenburg proposed that this is why rituximab works for CFS/ME patients – by reducing B cells, rituximab reduces inflammation.
The effect of rituximab on CFS/ME patients was discovered by accident. Two Norwegian doctors, Øystein Fluge and Olav Mella of Haukeland University Hospital, noticed that after treating a CFS/ME patient for Hodgkin's lymphoma with rituximab, she recovered from CFS/ME. This led the doctors to initiate a small study of rituximab on CFS/ME patients.
Three CFS/ME patients were given rituximab in an open-label trial (that is, the patients knew they were receiving the drug). All three patients experienced significant improvement; two of them responded within six weeks and the third had a delayed response, occurring six months after treatment. The positive effects lasted for between 16 and 44 weeks. After relapse, the patients were administered another dose of rituximab, with the same positive results. The investigators hypothesized that B cells of the immune system might play a significant role in CFS, at least for a subset of patients, and that “CFS may be amenable to therapeutic interventions aimed at modifying B-cell number and function.”
The positive results of this, as well as a second open-label trial, led Drs. Fluge and Mella to conduct a larger study with a more rigorous design to test the effects of the drug. In 2009 they initiated a double-blind, placebo-controlled phase trial with 30 CFS/ME patients. As in the earlier open-label studies, the responses to rituximab were significant. Sustained overall improvements were noted in 67% of the patients (as opposed to 13% of the control group). Four of the rituximab patients showed improvement past the study period. The authors concluded that the delayed responses starting from 2–7 months after rituximab treatment, in spite of rapid B-cell depletion, “suggests that CFS is an autoimmune disease and may be consistent with the gradual elimination of autoantibodies preceding clinical responses.”
Dr. David Bell, a now retired CFS/ME specialist, says “I've not seen results like this in any medical study in the 25 years that I have been in this field."