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Diagnosis and management of gout

Gout is a common cause of acute arthritis. An ageing population, increasing obesity, and lifestyle changes will render it more common.1 Here I outline the epidemiology of gout, appraise the evidence base for its management, and suggest ways of managing idiopathic gout. Management of hyperuricaemia due to inborn errors of metabolism (for example, Lesch-Nyhan syndrome) and its prevention during cancer chemotherapy are not discussed here.

The material for this review draws heavily on my chapter on gout in Clinical Evidence and from my work on a recent systematic review of studies on the prevention and treatment of recurrent gout. To ensure that no relevant randomised controlled trials published since the systematic review had been overlooked, I ran a previous search strategy in PubMed and the Cochrane database of systematic reviews. I identified other relevant studies from my personal database of papers on gout, did forward and backward citation tracking from other key papers, and carried out new targeted searches of multiple electronic databases.

The clinical syndrome of gout arises from deposition of urate crystals in joints, where they cause an inflammatory response, and in soft tissues, where they do not. The classic symptom of gout affecting the big toe, podagra, literally a “foot catch,” has been recognised since antiquity. Crystal deposition occurs when serum becomes saturated with urate, the final breakdown product of purine metabolism. Most patients with idiopathic gout have a genetically reduced renal excretion of urate. This alone does not usually lead to hyperuricaemia. Many other factors affect serum urate concentration (box 1).

Typically, gout produces an acute monoarthritis of rapid onset, often waking patients from sleep. The most commonly affected joints are the great toe, foot, ankle, knee, wrist, finger, and elbow, possibly because urate is more likely to crystallise in cooler parts of the body. …