• A K Tausche.
• Medizinische Klinik III, Rheumatologie, Universitätsklinikum Carl Gustav Carus an der Technischen Universität Dresden, Fetscherstr. 74, 01309, Dresden, Deutschland. anne-kathrin.tausche@uniklinikum-dresden.de.
• Internist (Berl). 2021 May 1; 62 (5): 513-525.

AbstractGout is the most common inflammatory arthritis in men with a rising incidence worldwide. It is a metabolic disease caused by hyperuricemia. Common causes of hyperuricemia, in addition to hereditary reduced renal excretion of urate, include purine over-nutrition, aging, comorbidities and associated medications, some of which increase serum urate levels. The first gout flare represents the signal for deposited urate crystals. If hyperuricemia remains untreated, crystal deposition proceeds and can cause recurrent gout flares, joint destruction and tophi. There is evidence that silent inflammation is ongoing even during asymptomatic stages. Gout patients often exhibit other metabolic, renal and cardiovascular co-morbidities and have higher (cardiovascular) mortality. Therefore, guidelines call for consequent urate lowering strategies to bring serum urate levels to a target at least below 360 µmol/l. The following article summarizes the recent state of knowledge regarding the diagnosis and therapy of gout.

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