Update on hyperuricaemia and gout with evidence based management guidelines

Gout is now the leading cause of inflammatory arthritis, affecting 1–2% of the population. The metabolic syndrome, cardiovascular risk factors, cardiovascular events and mortality are more common with gout. However, the role of uric acid as an independent risk factor is inconclusive. The identification of urate transporters has improved our understanding of urate homeostasis and identified targets for the development of newer drugs. Experience with ultrasound and dual energy computed tomography led to the detection of urate crystals in patients with asymptomatic hyperuricaemia. Several evidence-based management guidelines are now available. The dietary and lifestyle recommendations focus on general health and management of comorbidities. A low dose colchicine regimen is effective and better tolerated than the traditional use of higher doses in acute gout. Alternative measures for acute gout include non-steroidal anti-inflammatory drugs (NSAIDs) and corticosteroids. Allopurinol is the most widely used initial therapy; treatment is started with 100 mg or less per day, and titrated upwards to achieve a target level of 0.36 mmol/l (in patients with tophi, a lower target of 0.30 mmol/l is recommended). A new non-purine more potent xanthine oxidase inhibitor, febuxostat, is available (currently not registered in South Africa). Probenecid is the most widely used uricosuric agent. Prophylactic therapy with colchicine, NSAIDs or corticosteroids is used when urate lowering therapy is initiated. Although the cause of gout is known and effective treatment is available, gout is poorly managed worldwide with failure to achieve the target urate level