Rheumatoid arthritis: a disturbance in copper homeostasis

Abstract

That understanding the mode of action of antirheumatic drugs could help understand the etiology of rheumatoid arthritis is complicated by their apparent different actions on different target cells. The point of view adopted here is that the primary defect in rheumatoid arthritis will be similarly altered by such drugs. The common reactivity of two of the most widely prescribed drugs, D-penicillamine and sodium aurothiomalate, toward albumin-bound copper is proposed as their primary site of action. Elevated serum concentration of this form of copper has previously been suggested to perturb synovial cell metabolism and trigger the disease.