What you need to know

·  An acute attack of gout is likely to require treatment with a NSAID (with gastroprotection for those at high risk of gastrointestinal complications) or colchicine.

·  In general, urate lowering therapy (ULT) is targeted to patients with recurrent attacks, tophi, urate arthropathy, or renal damage and to symptomatic patients with very high serum uric acid levels. Allopurinal is the first line option.

·  Shared decision making about ULT should include consideration of harms, benefits, and limitations of ULT, along with patient preferences, comorbidities, and concomitant drug treatments.

·  All patients taking ULT require regular monitoring of renal function and serum uric acid level to ensure that the dose is appropriate. For many people, allopurinol 300 mg daily will be insufficient to achieve target serum uric acid reductions.

·  Despite limited evidence, patients should be encouraged to manage their weight, increase exercise, and reduce alcohol consumption.

What are the main risk factors for gout?

The single most important risk factor is sustained hyperuricaemia, which can be caused by overproduction or underexcretion of urate. Pathological hyperuricaemia has been defined as the serum uric acid concentration (408 μmol/L) above which monosodium urate crystals form in vitro at physiological pH and temperature. For most people with gout, underexcretion is the main cause of hyperuricaemia. Other factors associated with the development of gout include drugs (such as diuretics, ciclosporin, and low dose aspirin), renal impairment, excessive consumption of red meat or seafood, fructose-sweetened drinks, and alcohol (in particular, beer and spirits).

How is it diagnosed?

Although the risk of developing gout increases with higher levels of serum uric acid, hyperuricaemia alone is not sufficient for diagnosis because most people with hyperuricaemia do not have gout.However, chronic hyperuricaemia is associated with recurrent flares and can lead to tophi, chronic gouty arthritis, and erosive arthritis.6 Although a definitive diagnosis of gout is made by the demonstration of monosodium urate crystals in synovial fluid, this is rarely undertaken in primary care.