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ANTI TNF ANTIBODY IN RHEUMATOID ARTHRITIS

$0M01FY2000RRNIH

Duke University, Durham NC

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Abstract

RA is a chronic autoimmune disorder of unknown etiology that occurs in approximately 1% of the population. Methotrexate (MTX) has become the drug of choice for many rheumatologists because of its superior efficacy and faster mode of action. However, despite treatment with MTX, many patients only experience partial relief of symptoms and continue to exhibit active disease. Cytokines are protein or glycoprotein molecules that deliver important intercellular messages that regulate chronic inflammation and tissue damage in RA. Cytokines such as tumor necrosis factor alpha (TNF-a), interleukin-1 (IL-1), interleukin-6 (IL-6), and granulocyte macrophage colony stimulating factor (GM-CSF) are abundant in inflamed joints and promote the influx of neutrophils into synovial fluid and entry of lymphocytes and monocytes into the synovial tissue. TNF-a appears to be a key mediator since it regulates other proinflammatory cytokines. This study evaluates the efficacy and safety of chronic Anti-TNF Chimeric Monoclonal Antibody (Remicade) treatment in patients with active RA despite treatment with MTX. Additional objectives of the study are to determine the efficacy and safety of cA2 treatment in providing continued reduction in signs and symptoms, reduction of disability, slowing of joint damage, promotion of disease remission and improvement in quality of life at 1 year following the onset of treatment.

View original record on NIH RePORTER →