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August 1965

Hereditary Hemolytic Anemia Due to Glucose-6-Phosphate Dehydrogenase Deficiency: Improvement Following Splenectomy and Folic Acid Therapy

Author Affiliations

From the Department of Medicine, Harbor General Hospital, Torrance, and UCLA Center for Health Sciences, Los Angeles. Attending Physician, Harbor General Hospital and Clinical Instructor in Medicine, UCLA Center for Health Sciences (Dr. Greenberg); Chief of Hematology, Harbor General Hospital, and Associate Professor of Medicine, UCLA Center for Health Sciences (Dr. Tanaka).

Am J Dis Child. 1965;110(2):206-209. doi:10.1001/archpedi.1965.02090030216023

DEFICIENCY of red cell glucose-6-phosphate dehydrogenase (G-6-PD) is not uncommon among Negroes or certain Caucasians of Mediterranean extraction.1 These individuals are not anemic but are subject to acute hemolytic crises after ingesting primaquine phosphate or other similar drugs possessing oxidative potential. However, chronic hemolytic disease due to G-6-PD deficiency is rare. Mohler and Crockett2 in 1964 tabulated 15 cases on reviewing the world literature and added three of their own. It has been found in Caucasians of British and Northern European extraction as well as in those originating in the geographic area where favism is prevalent.

Recently we have studied a young Caucasian boy of Mexican (Spanish) and Iraqi extraction with a chronic hemolytic anemia who was found to have a marked deficiency of erythrocyte G-6-PD. The following is his case report including studies of erythrocyte metabolism in the available family members. This case is of particular interest

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