Abstract
Gout (lat. diathesis uraemica) is a metabolic and inflammatory disease associated with increased synthesis or reduced excretion of the uric acid. The aetiology and pathogenesis involve genetic predispositions (SLC2A9 gene polymorphism), environmental factors (effect of alcohol, an excess of purines, fructose, use of diuretics) and coexisting diseases (metabolic syndrome, diabetes, renal failure). The disease is six times fold more frequent in men than in women [1], [2]. Crystallisation of monosodium urate crystals in the synovial fluid and their deposition in joints and periarticular tissues results in damage of the cartilage, joint capsule, ligaments and tendons. In approximately 50–60 % of patients, formation of gouty nodules usually occurs around the joints. Deposition of monosodium urate in the tendons is not uncommon, but it usually has a form of infiltration (incrustation) of the tendon by urate crystals rather than a regular nodule with well-defined capsule.
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