A high level of uric acid in the blood (hyperuricaemia) is usually present in gout with needle-like crystals of monosodium urate forming inside and around joints. It can affect any joint (and occasionally other tissues such as the ear) but typically occurs in a distal joint such as big toes, knees, ankles or fingers, with sudden flares, swelling, heat and reddening.[1,4]

While there is a strong linear relationship between gout and hyperuricaemia, this is not always the case. Many people may have hyperuricaemia but may be asymptomatic, and others may have gout but not hyperuricaemia.[5]

Hyperuricaemia can result from the kidneys not clearing urate from the blood stream, or from high intake of uric acid in the diet, crash dieting, stress, chronic illness or injury, and some medicines (see panel).[3,5,6]

But other factors are also involved such as overproduction of cells and agents such as cytokines including interleukins and tumour necrosis factor alpha in the inflammatory process. This may occur by activating inflammasomes (immune system receptors and sensors), as well as changed responses to serum uric acid levels in cell.[5,7]

There is a genetic component with up to half of patients having a family history of gout. More than 40 genes have been identified which affect serum uric acid (SUA) levels but the body producing excess uric acid is much less common a cause.[3,5,8]