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RALPH NACHMAN, M.D.; JAMSHID JAVID, M.D.; STEPHEN KRAUSS, M.D.

Arch Intern Med. 1962;110(2):187-190.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Introduction

Two major mechanisms are generally implicated in drug-induced hemolytic anemia. (1) A genetically determined deficiency of erythrocyte glucose-6-phosphate dehydrogenase renders the red cell susceptible to the hemolytic action of certain ordinarily harmless drugs. This was first described in primaquine-induced anemia¹ and subsequently in anemia due to numerous other drugs.² (2) A drug-erythrocyte complex stimulates the production of antibodies which are capable of destroying the patient's erythrocytes in the presence of the drug. Stibophen (Fuadin)³ was the first drug reported to cause hemolysis by this haptenlike action. Other drugs similarly implicated include quindine,⁴ methylethylhydantoin ( Mesantoin),⁵ phenacetin,⁶ and aminosalicylic acid.⁶

Other agents such as sodium taurocholate and saponin can cause hemolysis⁷ apparently by a direct lytic action on the erythrocytes; this direct mechanism, however, is rarely of clinical significance.

The following is the first reported case of streptomycin-induced hemolytic anemia, the mechanism of . . . [Full Text PDF of this Article]

Author Affiliations
NEW YORK

Medical Division and the Department of Hematology, Laboratory Division, Montefiore Hospital.; Postdoctoral Research Fellow, Jane Coffin Childs Memorial Fund for Medical Research (Dr. Javid).

Footnotes
Submitted for publication Dec. 6, 1961.

This study was supported by Grant No. H5415 of the National Heart Institute, National Institutes of Health, U.S. Public Health Service.

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