JOSEPH J. BUNIM, M.D.; JOSEPH S. MCGUIRE JR., M.D.; THEODORE F. HILBISH, M.D.; LEONARD LASTER, M.D.; BERT N. LA DU JR., M.D.; J. EDWIN SEEGMILLER, M.D.
Dr. J. J. Bunim: Nearly 50 years ago, Garrod correctly concluded that failure to destroy homogentisic acid is a feature of the inborn error of metabolism characterizing alcaptonuria. It was also his belief that homogentisic acid is a normal intermediate compound in the oxidation of phenylalanine and tyrosine.1 The work to be presented today offers precise biochemical evidence for the validity of Garrod's insight.
The case of ochronosis and alcaptonuria that will be described embodies in a way the name of the Institute of Arthritis and Metabolic Diseases. The investigations conducted represent an integration of clinical and biochemical studies that
BUNIM JJ, MCGUIRE JS, HILBISH TF, et al. ALCAPTONURIA: CLINICAL STAFF CONFERENCE AT THE NATIONAL INSTITUTES OF HEALTH*. Ann Intern Med. 1957;47:1210–1224. doi: https://doi.org/10.7326/0003-4819-47-6-1210
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Published: Ann Intern Med. 1957;47(6):1210-1224.
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