Endothelial dysfunction improves with Advanced glycation end-products inhibitor in Rheumatoid Arthritis

Abstract

Objective: Increased cardiovascular risk in rheumatoid arthritis (RA) provides a strong rationale for early therapeutical interventions. In view of the similarities between atherosclerosis and RA and the proven benefit of advanced glycation end products (AGEs) inhibitor in atherosclerotic vascular disease,1 the study aimed to delineate the impact of AGEs inhibitor (benfotiamine 50mg+ pyridoxamine 50mg + methylcobalamin 500µg, Vonder) on endothelial dysfunction (ED) in patients with RA. Methods: 24 RA patients received 12 weeks of treatment with oral AGEs inhibitor twice a day as an adjunct to existing stable antirheumatic drugs. ESR, CRP, nitrite, endothelium-dependent and independent vasodilatation of the brachial artery measured at baseline and after treatment. Results: FMD increased significantly (p<0.01) after treatment whereas there was no significant change in endothelium-independent vasodilation with nitroglycerin and baseline diameter. ESR, CRP and nitrite improved significantly (p<0.05) after treatment. Significant negative correlation was observed between FMD and nitrite at baseline and between FMD and CRP after treatment. Conclusion: AGEs inhibitor improves inflammation and ED in RA. The vasculoprotective effect of AGEs inhibitor in RA appears to be due to its anti-inflammatory effect.