Recent Advances in Study of Uric Acid Metabolism and Gout

Abstract

Increased understanding of the pathogenesis of acute gout has developed in the past few years. Investigators have indicated that an attack is precipitated by (1) deposition of sodium urate crystals, (2) development of an inflammatory reaction against these crystals, and (3) propagation of the inflammatory response by addition of more crystals to inflamed area.

The nature of the inborn metabolic errors of primary gout is still obscure. Studies point to a dual cause of the hyperuricemia. Until more evidence is accumulated, it seems useful to separate patients into two categories: those with overproduction and those with normal production of uric acid.