Abstract
AbstractAdvances in management of acute gouty arthritis, tophaceous gout and uric acid nephrolithiasis are briefly reviewed. With respect to pathogenesis, specific enzyme abnormalities have been demonstrated in rare monogenic cases but the presumptive polygenic and multifactorial pathogenesis in most cases of primary gout remains uncertain. The hypothesis favored here is that, possibly secondary to altered glutamate catabolism, glutamine apparently is overutilized for urate overproduction by the liver, underutilized for reduced renal ammonia formation. The kidneys, modulating urinary uric acid excretion, sustain the hyperuricemia.
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