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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SEEGMILLER, J., GRAYZEL, A. & LIDDLE, L. Excessive Uric Acid Production in the Human induced by 2-Ethylamino-1,3,4-thiadiazole. Nature 183, 1463–1464 (1959). https://doi.org/10.1038/1831463a0
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DOI: https://doi.org/10.1038/1831463a0
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