Gout that occurs in children as a result of kidney disease caused by a genetic defect.
* Kidney failure * High blood uric acid level * Gouty arthritis * Gout
Although the exact cause of primary gout remains unknown, it appears to be linked to a genetic defect in purine metabolism, which causes elevated blood levels of uric acid (hyperuricemia) due to overproduction of uric acid, retention of uric acid, or both. In secondary gout, which develops during the course of another disease (such as obesity, diabetes mellitus, hypertension, sickle cell anemia, and renal disease), hyperuricemia results from the breakdown of nucleic acids. Myeloproliferative and lymphoproliferative diseases, psoriasis, and hemolytic anemia are the most common causes. Primary gout usually occurs in men and in postmenopausal women; secondary gout occurs in elderly people. Secondary gout can also follow drug therapy that interferes with uric acid excretion. Increased concentration of uric acid leads to urate deposits (tophi) in joints or tissues and consequent local necrosis or fibrosis. The risk is greater in men, postmenopausal women, and those who use alcohol.
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Correct management seeks to terminate an acute attack, reduce hyperuricemia, and prevent recurrence, complications, and the formation of renal calculi. Colchicine is effective in reducing pain, swelling, and inflammation; pain often subsides within 12 hours of treatment and is completely relieved in 48 hours. Treatment for the patient with acute gout consists of bed rest; immobilization and protection of the inflamed, painful joints; and local application of heat or cold, whichever works for the patient. Maximal doses of nonsteroidal anti-inflammatory drugs (NSAIDs) usually provide excellent relief for patients who can tolerate them; doses should be gradually reduced after several days.