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The idea that certain ordinarily useful drugs may, on repetition of normal doses, cause unexpected, profound and sometimes fatal idiosyncrasy reactions of the blood cells and hemopoietic tissues is relatively new. Prior to 1930 the nearest approach to this concept of drug allergy as a cause of serious hematologic injury was to be found in the literature of arsphenamine.1The older views of hematologic injury from drugs were based for the most part on supposedly orthodox toxic reactions.2These included anemia from poisoning by lead, mercury, arsenic, phenylhydrazine, trinitrotoluene, benzene and radium and methemoglobinemia from potassium chlorate, antipyrine, acetanilid, acetophenetidin, aniline and nitrobenzene. Although these reactions were viewed as toxic, it was recognized that individual susceptibility to such special effects existed, and to this extent something akin to idiosyncrasy was implied. After 1930, centering about the mystery of that relatively new disease called agranulocytic angina, there developed knowledge
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Thomas Fitz-Hugh (1938) studied this question.
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