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Gout, which is caused by monosodium urate (MSU) deposition within joints in the presence of hyperuricaemia, is now the leading cause of inflammatory arthritis within developed countries.1 2 Despite recent observations that urate-lowering therapy (ULT) should be considered early to reduce disease chronicity, diagnosis is frequently delayed, leading to suboptimal clinical outcomes.2 3
The current American College of Rheumatology (ACR)/European League Against Rheumatism (EULAR) 2015 gout classification entry criterion requires the history of a prior episode of swelling, pain or tenderness of a peripheral joint/bursa before confirmation either through MSU crystal identification in synovial fluid or through achieving a score of >8 using a predefined scoring system of radiological, laboratory and clinical features. One such feature, a gout ‘episode’, is clearly defined both in terms of its intensity (joint erythema, tenderness, reduced/inhibited walking ability) and duration (time to maximal pain from onset <24 hour; resolution to baseline <14 days).4
Emerging evidence that the joints of asymptomatic hyperuricaemic individuals contain MSU deposits and that alternative presentations of foot pain occur in hyperuricaemia suggests that preclinical and clinical phases may occur prior to a first episodic gout attack.5 6 This case–control study evaluated urate deposition …
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