Abstract
AN excessive endogenous synthesis of uric acid is present in a substantial portion of patients with gout1. The precise nature of the metabolic defect responsible for such excessive production is not known, but may be the result of a defective homœostatic mechanism for control of purine synthesis. Evidence for the existence of such a mechanism in the normal human has come from the observation2 that the simultaneous administration of 4-amino-5-imidazolecarboxamide suppresses de novo purine biosynthesis from glycine-15N. Factors affecting uric acid synthesis in the human are therefore of special interest in regard to the study of gout.
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