NANNIE K. M. DE LEEUW, M.D., M.SC., F.A.C.P.; LORNE SHAPIRO, M.D., F.R.C.P. (C), F.A.C.P.; LOUIS LOWENSTEIN, M.D., F.A.C.P.
Hemolytic Anemia may result from the administration of oxidant drugs, including primaquine, sulfonamides, nitrofurantoin, acetylsalicylic acid, and acetophenetidine (1-4). Recent publications have emphasized the close etiological relationship of erythrocyte glucose-6-phosphate dehydrogenase (G6PD) deficiency to this type of drug-induced hemolytic anemia (1-6). This deficiency is an inherited, sexlinked trait of incomplete dominance with variable expressivity (7, 8). It is associated with instability of reduced glutathione (GSH) in the red cell, and a slightly decreased red-cell life span (4) which is reduced further, by selective destruction of the older cells, when oxidant drugs are administered. It is believed that this red-cell defect
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DE LEEUW NKM, SHAPIRO L, LOWENSTEIN L. Drug-induced Hemolytic Anemia. Ann Intern Med. 1963;58:592–607. doi: 10.7326/0003-4819-58-4-592
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Published: Ann Intern Med. 1963;58(4):592-607.
Hematology/Oncology, Red Cell Disorders.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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