WILLIAM N. KELLEY, M.D.; MARTIN L. GREENE, M.D.; FREDERICK M. ROSENBLOOM, M.D.; J. FRANK HENDERSON, PH.D.; J. E. SEEGMILLER, M.D.
Sophisticated biochemical studies in recent years have revealed that the regulation of intracellular metabolism is a logical, orderly, and intricate process. Control of enzyme activity, as well as the rate of enzyme synthesis and catabolism, provide regulatory mechanisms important to the economy of the cell. It has become apparent that some human disorders may indeed result from genetically determined alterations of these normal control mechanisms (1, 2).
A substantial proportion of gouty patients have a metabolic defect characterized by the synthesis of abnormally large quantities of uric acid that in turn is the result of an excessive rate of
KELLEY WN, GREENE ML, ROSENBLOOM FM, et al. Hypoxanthine-Guanine Phosphoribosyltransferase Deficiency in Gout. Ann Intern Med. 1969;70:155–206. doi: https://doi.org/10.7326/0003-4819-70-1-155
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Published: Ann Intern Med. 1969;70(1):155-206.
Encephalopathy, Gout, Neurology, Rheumatology.
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