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Martin Steinberg, MD; Mark J. Brauer, MD; Thomas F. Necheles, MD

Arch Intern Med. 1970;125(2):302-303.

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

In 1968, Necheles and co-workers described the first instances of hemolytic anemia associated with deficiency of erythrocyte glutathione peroxidase (GSH-Px).^1,2

Abnormalities of the pentose phosphate shunt leading to hemolytic anemia were first noted in 1956 when Carson and associates showed that erythrocytes of individuals susceptible to the hemolytic effects of primaquine were deficient in the enzyme glucose-6-phosphate dehydrogenase (G6PD).³ Since then, deficiencies of the other shunt enzymes, glutathione reductase ⁴ and 6-phosphogluconate dehydrogenase ⁵ and of glutathione⁶ have been described. These enzyme deficiencies may be associated at times with hemolytic anemia, which may occur spontaneously, or be precipitated by administration of oxidant drugs. In some instances, infection has been associated with the development of hemolytic anemia in individuals deficient in G6PD.^7,8

Previous reports include the presence of hemolytic disease in neonates with heterozygous GSH-PX deficiency ¹ and homozygous deficiency in an adult who had a hemolytic reaction after a transfusion . . . [Full Text PDF of this Article]

Author Affiliations
Boston

From the Blood Research Laboratory, New England Medical Center Hospitals; the Department of Pediatrics, Boston Floating Hospital; and the departments of medicine and pediatrics, Tufts University School of Medicine, Boston. Dr. Steinberg is a research fellow of the American Cancer Society. Dr. Necheles is an established investigator of the American Heart Association.

Footnotes
Received for publication, April 30, 1969; accepted July 16.

Reprint requests to 171 Harrison Ave, Boston 02111 (Dr. Steinberg).

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