الفهرس 
introduction
: PATHOGENESIS OF HYPERURICEMIAOnly 14 pages are availabe for public view
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Abstract
Asymptomatic hyperuricemia is common and does not in itself constitute a disease. Almost 10% of adults are documented to have hyperuricemia at least once in their lifetime. The prevalence of gout rises with advancing age. Among men and women older than 80 years of age, the prevalence of the disorder is 9% and 6%, respectively. Although hyperuricemia is a major risk factor for the development of gout, acute gouty arthritis can occur in the presence of normal serum UA levels. Patients with asymptomatic hyperuricemia do not require treatment, but efforts should be made to lower their urate levels by encouraging them to make changes in diet or lifestyle. An epidemiological link between elevated serum UA level and cardiovascular risk has been recognized. Hyperuricemia in hypertensive subjects may represent an early indicator of hypertensive cardio renal disease. Data suggest that men with hyperuricaemia have a higher risk of death from all causes and that the increased mortality risk is due mainly to an elevated risk of death from cardiovascular disease. These findings indicate that aggressive management of cardiovascular risk factors is appropriate for individuals with gout. First step in treatment of hyperuricemia is lifestyle modification. Medical treatment of hyperuricemia includes xanthine oxidase inhibitors, uricase and uricosuric agents. Xanthine oxidase inhibitors include allopurinol the most commonly used, oxypurinol and febuxostat. Uricase (rasburicase) is another form of therapy which directly degrades UA. It is efficacious in reducing serum uric acid levels with associated diuresis more effectively and much faster than allopurinol, and to correct renal dysfunction more rapidly than allopurinol in patients with severe acute hyperuricemia as in tumor lysis syndrome.