Gout is a common inflammatory arthritis precipitated by an inflammatory reaction to urate crystals in the joint. Gout is increasingly being recognised as a disease primarily of urate overload with arthritis being a consequence of this pathological accumulation. It is associated with a number of important co-morbidities including chronic kidney disease, obesity, diabetes and cardiovascular disease. The prevalence of gout is increasing around the world. Significant progress has been made in determining the genetic basis for both gout and hyperuricaemia. Environmental risk factors for gout have been identified as certain foods, alcohol and several medications. There is, however, little evidence that changing these environmental risks improves gout on an individual level. Treatment of gout encompasses two strategies: firstly treatment of inflammatory arthritis with non-steroidal anti-inflammatories, corticosteroids, colchicine or interleukin-1 inhibitors. The second and most important strategy is urate lowering, to a target of 0.36 mmol/L (6 mg/dL) or potentially lower in those with tophi (collections of crystalline urate subcutaneously). Along with urate lowering, adequate and prolonged gout flare prophylaxis is required to prevent the precipitation of acute attacks. Newer urate lowering agents are in development and have the potential to significantly expand the potential treatment options. Education of patients regarding the importance of life long urate lowering therapy and prophylaxis of acute attacks is critical to treatment success as adherence with medication is low in chronic diseases in general but especially in gout.
Keywords: Chronic kidney disease; Diabetes mellitus; Diet; Gout; Hypertension; Urate.
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