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also result in overproduction of uric acid due to lysis and breakdown ofcellular matter.• Dietary purines play an unimportant role in the generation of hyperuricemiain the absence of some derangement in purine metabolism orelimination.• About two-thirds of the uric acid produced each day is excreted in theurine. The remainder is eliminated through the GI tract after enzymaticdegradation by colonic bacteria. A decline in the urinary excretion of uricacid to a level below the rate of production leads to hyperuricemia and anincreased miscible pool of sodium urate.• Drugs that decrease renal clearance of uric acid through modification offiltered load or one of the tubular transport processes include diuretics,nicotinic acid, salicylates (less than 2 g/day), ethanol, pyrazinamide,levodopa, ethambutol, cyclosporine, and cytotoxic drugs.• The average human produces 600 to 800 mg of uric acid daily and excretesless than 600 mg in urine. Individuals who excrete more than 600 mg afterbeing on a purine-free diet for 3 to 5 days are considered overproducers.Hyperuricemic individuals who excrete less than 600 mg of uric acid per24 hours on a purine-free diet are defined as underexcretors of uric acid.On a regular diet, excretion of more than 1,000 mg per 24 hours reflectsoverproduction; less than this is probably normal.• Deposition of urate crystals in synovial fluid results in an inflammatoryprocess involving chemical mediators that cause vasodilation, increasedvascular permeability, complement activation, and chemotactic activity forpolymorphonuclear leukocytes. Phagocytosis of urate crystals by leukocytesresults in rapid lysis of cells and a discharge of proteolytic enzymesinto the cytoplasm. The ensuing inflammatory reaction is associated withintense joint pain, erythema, warmth, and swelling.• Uric acid nephrolithiasis occurs in 10% to 25% of patients with gout.Predisposing factors include excessive urinary excretion of uric acid, acidicurine, and highly concentrated urine.• In acute uric acid nephropathy, acute renal failure occurs as a result ofblockage of urine flow secondary to massive precipitation of uric acidcrystals in the collecting ducts and ureters. This syndrome is a wellrecognizedcomplication in patients with myeloproliferative or lymphoproliferativedisorders and results from massive malignant cell turnover, particularlyafter initiation of chemotherapy. Chronic urate nephropathy is causedby the long-term deposition of urate crystals in the renal parenchyma.• Tophi (urate deposits) are uncommon in gouty subjects and are a latecomplication of hyperuricemia. The most common sites of tophaceousdeposits in patients with recurrent acute gouty arthritis are the base of thegreat toe, helix of the ear, olecranon bursae, Achilles tendon, knees, wrists,and hands
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