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March 1967

Anemia During Acute Infections: Role of Glucose-6-Phosphate Dehydrogenase Deficiency in Negroes

Author Affiliations

Columbus, Ohio; Durham, NC

From the Division of Hematology and Oncology, The Ohio State University, Columbus (Dr. Mengel), and the Department of Medicine, Duke University, Durham (Drs. Metz and Yancey). Dr. Mengel is a John and Mary Markle Scholar in Academic Medicine. Dr. Metz is a Fellow in Hematology.

Arch Intern Med. 1967;119(3):287-290. doi:10.1001/archinte.1967.00290210119011

PHYSICIANS are often confronted with the problem of anemia occurring with various infectious diseases. Moderately severe anemia frequently develops during the course of chronic suppurative diseases,1-3 and presumably results primarily from depressed erythropoiesis. The less frequent anemia associated with acute infections usually has been assumed to result from elaboration of bacterial hemolysins, direct red blood cell (RBC) infestation, elevated titers of cold agglutinins, or transient hypersplenism.4

We had been impressed by the greater frequency of transient anemia during the course of acute bacterial infections in Negroes (30% to 40%) as compared to whites (5% to 10%) (in unpublished data). Furthermore, only rarely were any of the aforementioned mechanisms of anemia identified. In preliminary studies a few such patients were found to be deficient in the RBC enzyme glucose-6-phosphate dehydrogenase (G-6-PD). The present study was undertaken to determine if an association between G-6-PD deficiency and the occurrence of significant

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