Hyperuricemia and cardiovascular disease risk

Expert Rev Cardiovasc Ther. 2014 Oct;12(10):1219-25. doi: 10.1586/14779072.2014.957675. Epub 2014 Sep 5.

Abstract

Uric acid (UA) is the final end product of purine catabolism and is formed from xanthines and hypoxanthines. Hyperuricemia can be secondary to either an exaggerated production of UA that follows high cellular turnover conditions or, most frequently, to a low renal excretion in patients with impaired renal function. Recent data suggest that serum UA (SUA) at high-normal level is associated with cardiovascular disease risk factors and cardiovascular disease, often being a predictor of incident events. Preliminary data suggest that the reduction of SUA level in subjects with normal-high SUA could prevent at least a part of target-organ damage related to high SUA, especially when xanthine oxidase is selectively inhibited.

Keywords: allopurinol; cardiovascular disease risk; epidemiology; febuxostat; pathophysiology; serum uric acid; xanthine-oxidase inhibitors.

Publication types

  • Review

MeSH terms

  • Cardiovascular Diseases / etiology*
  • Cardiovascular Diseases / prevention & control
  • Humans
  • Hyperuricemia / complications*
  • Hyperuricemia / drug therapy
  • Risk Factors
  • Uric Acid / blood*
  • Xanthine Oxidase / antagonists & inhibitors
  • Xanthine Oxidase / metabolism

Substances

  • Uric Acid
  • Xanthine Oxidase