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NEW YORK (Reuters Health) Jan 29 - Rituximab inhibits joint damage progression in rheumatoid arthritis (RA) patients who have an inadequate response to tumor necrosis factor (TNF) inhibitor therapies, according to a report in the January issue of the Annals of the Rheumatic Diseases.
As many as 40% of RA patients fail to achieve an adequate response with TNF inhibitors, the authors explain, and no biological agent has been shown to slow joint damage in such patients.
Dr. E. Keystone from the University of Toronto and colleagues investigated whether treatment with rituximab, a monoclonal antibody that selectively targets CD20-positive B cells, would inhibit the progression of structural joint damage in 517 RA patients who exhibit an inadequate response to TNF inhibitors.
In this phase 3 study, patients received either rituximab plus methotrexate or placebo plus methotrexate.
The mean progression of joint damage after 56 weeks of treatment (as measured by the total Genant-modified Sharp score) was significantly lower in the rituximab group than in the placebo group, the authors report.
Patients in the rituximab group had fewer erosions and less joint space narrowing than did patients in the placebo group, the report indicates.
Significantly more patients in the rituximab group (61%) than in the placebo group (52%) showed no erosive progression between baseline and week 56, the investigators say.
"This study provides the first evidence that a B cell-targeted therapy, rituximab, inhibits the progression of structural damage in RA," the authors conclude. "These data also show for the first time that, in patients with RA with long-standing, active disease inadequately controlled by prior biologic therapy, inhibition of progressive joint damage is an achievable therapeutic goal."
Ann Rheum Dis 2009;68:216-221.
[QUOTE=Lynn49]