Hyperuricemia and gout: new insights into pathogenesis and treatment

Bull NYU Hosp Jt Dis. 2007;65(3):215-21.


Over the past decade, significant advances have been made regarding the pathogenesis, clinical implications, and treatment of hyperuricemia. While physicians have understood for at least a century that uric acid causes gout, we are now beginning to address the question of why hyperuricemia exists and the mechanisms by which uric acid acts to stimulate inflammation. This review focuses on (1) previously unknown biological roles of uric acid; (2) why the loss of the uricase gene and resultant hyperuricemia may have provided an evolutionary advantage to primates and, in particular, to humans; (3) the molecular effects of uric acid on inflammatory cells; and (4) novel antihyperuricemic agents currently under study.

Publication types

  • Review

MeSH terms

  • Adrenal Cortex Hormones / therapeutic use
  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
  • Colchicine / therapeutic use
  • Febuxostat
  • Gout / immunology*
  • Gout / prevention & control*
  • Gout Suppressants / therapeutic use*
  • Humans
  • Hyperuricemia / immunology*
  • Hyperuricemia / prevention & control*
  • Interleukin 1 Receptor Antagonist Protein / therapeutic use
  • Thiazoles / therapeutic use
  • Urate Oxidase / therapeutic use
  • Uric Acid / immunology*


  • Adrenal Cortex Hormones
  • Anti-Inflammatory Agents, Non-Steroidal
  • Gout Suppressants
  • Interleukin 1 Receptor Antagonist Protein
  • Thiazoles
  • Febuxostat
  • Uric Acid
  • Urate Oxidase
  • Colchicine