Abstract: The potential danger of hemolysis from use of the 8-aminoquinoline antimalarial drug, pamaquine (Plasmoquine), has been known since 1926.<sup>1</sup>Earle,<sup>2</sup>in 1948, reported that pamaquine caused hemolysis in 5%-10% of American Negroes, but rarely in Caucasians. Similar observations were made in 1952 by Hockwald<sup>3</sup>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, Dern<sup>4</sup>discovered that the susceptibility to hemolysis by primaquine is due to an intrinsic abnormality of the erythrocyte. Dern, Beutler, and Alving<sup>5</sup>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.<sup>6</sup>This hypersusceptibility to hemolysis by drugs is a genetically transmitted inborn error of metabolism.<sup>7</sup>The first biochemical abnormality to characterize drug-sensitive cells,
Publication Year: 1962
Publication Date: 1962-02-01
Language: en
Type: article
Indexed In: ['crossref', 'pubmed']
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Cited By Count: 270
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