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,
TARLOV AR, BREWER GJ, CARSON PE, ALVING AS. Primaquine Sensitivity: Glucose-6-Phosphate Dehydrogenase Deficiency: An Inborn Error of Metabolism of Medical and Biological Significance. Arch Intern Med. 1962;109(2):209–234. doi:10.1001/archinte.1962.03620140081013
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