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FOR MANY YEARS hemolytic reactions have been recognized as hazards which accompany the administration of certain classes of therapeutic agents including sulfonamides, sulfones, benzene, and quinoline derivatives. Although some episodes of drug-induced hemolysis can be attributed to hypersensitivity, most reactions cannot be explained by an immune mechanism. In 1941 Emerson, Ham, and Castle suggested that some hemolytic drugs and chemical compounds, or their degradation products, functioned as oxidants in reversible oxidation-reduction systems in the erythrocytes and, thereby, caused methemoglobin formation, increased osmotic fragility, and hemolysis. Recently Jandl et al., showed, in vitro, that oxidant drugs capable of acting as redox intermediates oxidize hemoglobin, first reversibly to methemoglobin and eventually irreversibly to oxidation products resembling Heinz bodies; they postulated that administration of these drugs enhanced the oxidation of hemoglobin and other vital cellular components in vivo and, thus, interfered with cellular integrity.
In 1926 Cordes reported the occurrence of hemolytic anemia in
Kellermeyer RW, Tarlov AR, Brewer GJ, Carson PE, Alving AS. Hemolytic Effect of Therapeutic Drugs: Clinical Considerations of the Primaquine-Type Hemolysis. JAMA. 1962;180(5):388–394. doi:10.1001/jama.1962.03050180034008a
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