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Research Article| Volume 70, ISSUE 1, P80-93, July 1967

Primaquine sensitivity in Caucasians: Hemolytic reactions induced by primaquine in G-6-PD deficient subjects

  • James N. George
    Affiliations
    From the Department of Hematology, Walter Reed Army Institute of Research and the Department of Medicine, Georgetown University School of Medicine Washington, D. C. U.S.A.
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  • David A. Sears
    Affiliations
    From the Department of Hematology, Walter Reed Army Institute of Research and the Department of Medicine, Georgetown University School of Medicine Washington, D. C. U.S.A.
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  • Paul R. McCurdy
    Affiliations
    From the Department of Hematology, Walter Reed Army Institute of Research and the Department of Medicine, Georgetown University School of Medicine Washington, D. C. U.S.A.
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  • Marcel E. Conrad
    Affiliations
    From the Department of Hematology, Walter Reed Army Institute of Research and the Department of Medicine, Georgetown University School of Medicine Washington, D. C. U.S.A.
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      Abstract

      The hemolytic reaction caused by the ingestion of the standard prophylactic antimalarial dose of primaquine was studied in 3 Caucasian males and 1 Negro male with G-6-PD deficiency. Each Caucasian subject came from an ethnic group in which primaquine sensitivity is uncommon (English, Sicilian, Ashkenazic Jewish). In contrast to the mild hemolytic reaction in the American Negro, destruction of about 20 per cent of circulating red cells occurred in each Caucasian subject. Hemolysis was similar in these individuals despite marked differences in clinical and laboratory studies. One subject had enzymatic studies similar to those observed in G-6-PD deficient Negroes; another had mild but significant hemolysis before the ingestion of primaquine; and the third failed to develop clinical jaundice because of accelerated plasma clearance of bilirubin. These studies suggest that the assay of G-6-PD in hemolysates and even the measurement of pentose phosphate shunt activity in intact red cells do not provide a basis for the prediction of the severity of primaquine sensitivity in vivo.
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