In people with rheumatoid arthritis, the behavior of certain memory B cell subsets may play a role in the efficacy of rituximab, response to the drug and disease relapse after taking it, according to research published in the June issue of Arthritis & Rheumatism.

Petra Roll, M.D., of the University of Wurzburg in Germany, and colleagues analyzed data from 17 patients with rheumatoid arthritis refractory to standard disease-modifying anti-rheumatic drugs and/or TNFα, who were treated with rituximab. Twelve showed a good response after one cycle, and 11 of the responders were retreated.

After each cycle, B cell reconstitution showed a similar pattern, with an early phase marked by immature CD38++,IgD+,CD10+ B cells, followed by an increase in naive B cells. At the second depletion, memory B cells were still reduced, but they recovered to levels similar to those seen after the first cycle.

"In summary, the current study demonstrated that repeated cycles of rituximab led to a comparable repopulation pattern in B cell subpopulations, with no further reduction in the number of memory B cells. A high number of memory B cells before therapy may be a less favorable biomarker for early relapse. Moreover, the data provide evidence that effective repletion or suspended production of IgD+ memory B cells was strongly correlated to the response to treatment. Overall, the data are consistent with the conclusion that depletion of memory B cells seems to be a key target for the clinical effects of rituximab in rheumatoid arthritis," the authors write.

A co-author disclosed financial relationships with Roche and Genentech, and another disclosed a financial relationship with Roche.

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Prepared jointly by the editors of RN and HealthDay's Physicians' Briefing (www.physiciansbriefing.com).