Anti-tumor necrosis factor therapy increases serum adiponectin levels with the improvement of endothelial dysfunction in patients with rheumatoid arthritis.

Lower adiponectin levels in circulation are shown to be associated with endothelial dysfunction, which is a crucial feature in the evolution of atherosclerosis. The aim of our study is to evaluate the effect of anti-tumor necrosis factor (TNF) therapy on adiponectin levels with endothelial function and arterial stiffness. Fifteen Japanese patients with rheumatoid arthritis (RA) received infusions with infliximab (3 mg/kg) at weeks 0, 2, and 6. Serum concentrations of adiponectin, endothelial function, and pulse wave velocity (PWV) were measured before each infusion. Endothelium-dependent vasodilatation and endothelium-independent vasodilatation were evaluated as forearm blood flow response to reactive and nitroglycerin-induced hyperemia using strain-gauge plethysmography. Endothelium-dependent vasodilatation was significantly improved at 2 weeks and 6 weeks by treatment with infliximab. PWV remained unchanged. Anti-TNF therapy significantly increased serum adiponectin levels at 2 weeks and 6 weeks. The adiponectin levels were positively correlated with the endothelium-dependent vasodilatation, and negatively with the disease activity score of 28 joints. Our study shows a short-term efficacy of infliximab on adiponectin levels and endothelial dysfunction of patients with RA, and provides additional evidence to support the regulatory role of TNF-alpha on the expression of adiponectin in vivo.