Clinical Trial: Does Etanercept Influence Tweak Modulation of Inflammation During Inflammatory Rheumatisms (Psoriatic Arthritis and Rheumatoid Arthritis)?

Study Status: Completed
Recruit Status: Completed
Study Type: Interventional

Official Title: DOES ETANERCEPT INFLUENCE TWEAK MODULATION OF INFLAMMATION DURING INFLAMMATORY RHEUMATISMS (PSORIATIC ARTHRITIS AND RHEUMATOID ARTHRITIS)?

Brief Summary: TWEAK (TNF weakly inducer of apoptosis) is a type II-transmembrane protein, member of the TNF ligand superfamily that can be cleaved to function as a soluble cytokine. Depending on target cell type, TWEAK triggers multiple cellular responses ranging from modulation of inflammation to cell death when it binds to its main receptor, Fn 14. Our team has been the first to describe pro-inflammatory effects of TWEAK during central nervous system inflammation. Various data support the possibility that TWEAK produced by synovial macrophages may contribute to chronic synovitis in animal models and in humans. In psoriatic arthritis (PsoA), anti-TNF therapy has been successful concording with the key role of TNF in the pathogenesis of this disease and the generation by psoriatic patients of neutralizing anti-TNF autoantibodies referred as "beneficial autoimmunity to pro-inflammatory mediators". In 2010, Van Kuijk et al. have described a high expression of TWEAK in the inflammatory synovial of PsoA and rheumatoid arthritis (RA) patients before and after anti-TNF therapy. The role of TNF-alpha in the regulation of TWEAK expression remains unclear.

Detailed Summary:
Sponsor: Assistance Publique Hopitaux De Marseille

Current Primary Outcome: serum levels of soluble TWEAK [ Time Frame: 42 months ]

Original Primary Outcome: Same as current

Current Secondary Outcome:

Original Secondary Outcome:

Information By: Assistance Publique Hopitaux De Marseille

Dates:
Date Received: July 4, 2013
Date Started: September 2011
Date Completion:
Last Updated: September 9, 2015
Last Verified: September 2015