Gout, urate-lowering drugs, and risk of cardiovascular disease: can we clinically trust in the adjusted real-life data?

Uric acid (UA) is the final product of purine metabolism and its increase in the circulating blood defines the presence of hyperuricaemia usually considered as a concentration of uric acid in serum above the threshold level of 7 mg/dL (416 μmol/L) in men and >6 mg/dL (357 μmol/L) in women.1 The typical consequence of elevated UA levels is the development of gout, a relatively common inflammatory arthritis affecting from 2% to 4% of the population with a significant increase in prevalence in patients with renal dysfunction as well as cardiac and metabolic diseases. In addition to its effects at the articular level, there is mixed evidence to support gout (and hyperuricaemia) as independent risk factors for cardiovascular disease (CVD).