RRML - Gout, hyperuricemia and the metabolic syndrome

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Nr. 20(3)/2012

Gout, hyperuricemia and the metabolic syndrome

Mircea Cucuianu, Ioana Brudaşcă

Abstract:

Uric acid is a product of purine metabolism and hyperuricemia is considered to be the major etiological factor of gout. Actually, this metabolic arthritis is produced by the precipitation of monosodium urate monohydrate crystals within joints, triggering an inflammatory reaction. Hyperuricemia is offten associated with metabolic syndrome and may lead to vascular endothelial dysfunction, thereby contributing to cardiovascular and renal diseases. Mechanisms associating metabolic syndrome and hyperuricemia imply an accelerated hepatic purine synthesis, related to hyperinsulinemia and enzyme induction. A high fructose intake was incriminated in the associated increased incidence of metabolic syndrome and hyperuricemia. Insulin stimulated enhanced reabsorbtion of urate from the glomerular filtrate may also contribute to hyperuricemia, increasing the relative risk of death. Evidence was also provided that physiological concentration of uric acid would exert antioxidant effects, attenuating neuronal lesions caused by oxygen radicals, generated during an acute ischemic stroke and in cases of neurodegenerative disorders.

Keywords: gout,uric acid,metabolic syndrome,cardiovascular disease,antioxidant effects.

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Cucuianu M, Brudaşcă I. Gout, hyperuricemia and the metabolic syndrome. Rev Romana Med Lab. 2012;20(3):199-206