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Glucose-6-Phosphate Dehydrogenase Deficiency: An Inborn Error of Metabolism of Medical and Biological Significance

ALVIN R. TARLOV, M.D.; GEORGE J. BREWER, M.D.; PAUL E. CARSON, M.D.; ALF S. ALVING, M.D.

Arch Intern Med. 1962;109(2):209-234.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

The potential danger of hemolysis from use of the 8-aminoquinoline antimalarial drug, pamaquine (Plasmoquine), has been known since 1926.¹ Earle,² in 1948, reported that pamaquine caused hemolysis in 5%-10% of American Negroes, but rarely in Caucasians. Similar observations were made in 1952 by Hockwald³ during an evaluation of the related, but less toxic drug, primaquine; it was further noted that the severity of hemolysis was determined by the amount of drug administered. In 1954, Dern⁴ discovered that the susceptibility to hemolysis by primaquine is due to an intrinsic abnormality of the erythrocyte. Dern, Beutler, and Alving⁵ reported that the hemolysis is self-limited in that clinical recovery occurs even if the daily dose of drug is continued. Many drugs can precipitate hemolysis.⁶ This hypersusceptibility to hemolysis by drugs is a genetically transmitted inborn error of metabolism.⁷ The first biochemical abnormality to characterize drug-sensitive cells, . . . [Full Text PDF of this Article]

Author Affiliations
CHICAGO

From the University of Chicago-Army Medical Research Unit, Department of Medicine.; Captain, Medical Corps, U.S. Army and Research Associate, Department of Medicine, University of Chicago (Drs. Tarlov and Brewer). Assistant Professor, Department of Medicine, University of Chicago (Dr. Carson). Professor of Medicine, University of Chicago (Dr. Alving).

Footnotes
Submitted for publication Aug. 24, 1961.

The previously unpublished studies of the authors included in this Review were supported by the Medical Research and Development Command, Office of the Surgeon General, Department of the Army, under contracts DA-49-007-MD-566 and DA-49-007-968 with the University of Chicago and were supplemented by grants from Burroughs Wellcome & Company, Winthrop Laboratories, and the Douglas Smith Foundation.

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