Introduction
Gout is a disorder of purine and urate metabolism in which persistently raised serum urate leads to deposition of monosodium urate crystals in joints, soft tissues and kidneys. Dietary prevention aims to limit the dietary load of purines, avoid foods and drinks that raise urate or trigger attacks, and support the weight, fluid and alcohol measures that reduce the risk of gout and its complications. Drug therapy is mentioned only where it links to diet.
Background: purine metabolism and urate
Purines (adenine and guanine) are broken down to uric acid, the final product of purine catabolism in humans, with xanthine oxidase as a key enzyme. Most urate comes from endogenous purine turnover; a smaller part comes from purines in food. About two-thirds of daily urate excretion is renal, and most of the filtered urate is reabsorbed. Urate is poorly soluble, so when serum levels are high, crystals form. Treatment targets usually aim for serum urate below about 360 µmol/L (6 mg/dL), and crystals tend to form at higher levels. The crystals activate inflammation, which produces acute gouty arthritis.