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Effect of tumor necrosis factor a inhibitors on heart failure risk in RA Patients
Date:2/27/2008

A chronic autoimmune disease, rheumatoid arthritis (RA) is characterized by persistent inflammation of the synovial membrane and progressive joint destruction. Beyond loss of mobility, sufferers face a high risk of heart failure. An inflammatory cytokine known for contributing to the development of RA, tumor necrosis factor a (TNFa) has also been implicated in cardiovascular disorders. Inhibition of TNFa has opened promising new treatment options for RA patients. Anti-TNF drugs such as infliximab, etanercept, and adalimumab have been shown to not only diminish signs and symptoms of the disease, but also prevent joint damage. However, in cardiac trials, TNFa inhibitors have shown no more positive effects on heart failure risk -- and sometimes less -- than placebo.

Does TNFa inhibition prevent heart failure in RA patients -- or promote it? That's the critical question Dr. Joachim Listing and a team of specialists with the German Rheumatism Research Centre in Berlin set out to answer. Featured in the March 2008 issue of Arthritis & Rheumatism (http://www.interscience.wiley.com/journal/arthritis), their study indicates that anti-TNF therapy does a patients heart more good than harm, when it successfully reduces the inflammatory toll of RA.

To clearly assess the role of TNFa inhibitors in heart failure risk, the researchers analyzed a 3-year span of disease activity and cardiovascular incidents in 4,248 RA patients enrolled in an ongoing Germany-wide study of biologic therapy. At the time of enrollment, 2,757 of the subjects had started treatment with an anti-TNF drug -- infliximab, etanercept, or adalimumab -- and 1,491 had started a new disease-modifying antirheumatic drug (DMARD). Within the study period, several hundred of the patients were also treated with glucocorticoids, nonsteroidal anti-inflammatory drugs (NSAIDs), or COX-2 inhibitors. Over 78 percent of the p
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Contact: Amy Molnar
amolnar@wiley.com
Wiley-Blackwell
Source:Eurekalert

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