Serum adipokine levels in rheumatoid arthritis patients and their contributions to the resistance to treatment

Abstract

The aim of this study was to determine whether disease activity and the type of therapy differentially modulate serum adipokine levels in patients with rheumatoid arthritis (RA), and whether pre-therapy adipokine levels contribute to resistance to treatment. Fasting blood samples from 40RA patients were obtained at baseline and sixmonths following therapeutic treatment with disease-modifying antirheumatic drugs (DMARDs) and/or tumor necrosis factor (TNF)-α blockers. Serum levels of adiponectin, leptin, visfatin and resistin were measured by ELISA. Baseline adipokine levels did not exhibit a statistically significant difference when comparing patients with moderate and high disease activity, based on the disease activity score in 28joints (DAS28). Of all the adipokines, only adiponectin was significantly increased in patients responding to DMARDs and/or TNF-α blocker therapy, based on the American College of Rheumatology 20%improvement criteria (ACR20) at sixmonths (2,964±1,237 to 3,683±1,511ng/ml, P<0.01). However, adiponectin levels in non-responders did not significantly increase (3,192±2,090 to 3,222±1,150ng/ml). By contrast, there were no statistically significant changes in leptin, resistin or visfatin levels in either the responders or non-responders. Serum adipokine (adiponectin, leptin, visfatin, and resistin) levels in RA patients did not significantly change following therapy, with the exception of adiponectin. Adipokine levels may not contribute to therapeutic resistance to DMARDs and/or TNF-α blocking agents.