Abstract
In most cases (98-99 %) primary hyperuricemia is caused by impaired renal excretion of uric acid. Overproduction of uric acid is rare. Secondary hyperuricemia has to be differentiated from primary forms. Clinical manifestations of hyperuricemia are acute inflammatory arthritis, tenosynovitis, bursitis, chronic arthropathy and accumulation of urate crystals in the form of tophaceous deposits. In addition renal complications can occur. Pathophysiology and diagnosis of gout were described. Treatment of gout has two goals: Treatment of the acute gout attack, to terminate pain and disability and treatment of hyperuricemia by lifestyle modification and with urate lowering drugs. A serum uric acid value below 6 mg/dl (360 µmol/L) should be achieved.
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