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Acute Hemolytic Anemia Complicating Viral Hepatitis in Patients with Glucose-6-Phosphate Dehydrogenase Deficiency
- GERALD SALEN, M.D.;
- FRANZ GOLDSTEIN, M.D., F.A.C.P.;
- FARID HAURANI, M.D., F.A.C.P.; and
- C. WILMER WIRTS, M.D., F.A.C.P.
- Requests for reprints should be addressed to Franz Goldstein, M.D., F.A.C.P., 1025 Walnut St., Philadelphia, Pa. 19107.
Excerpt
Although shortened erythrocyte survival can frequently be demonstrated, severe anemia has rarely been noted during acute viral hepatitis (1-3). In the few reported cases of hemolytic anemia complicating hepatitis no mechanism explaining the increased red cell destruction has been established (4-6). Increased splenic pulp pressure (7) or elevated gamma globulin levels (8), observed in viral hepatitis, could not be related to the development of hemolysis (2, 4, 6). Burka, Weaver, and Marks (9) most recently suggested that erythrocyte glucose-6-phosphate dehydrogenase (G-6-PD) deficiency may predispose to the development of hemolytic anemia during viral hepatitis.
This report deals with three patients who
Acknowledgments
We are indebted to Dr. Allen J. Erslev for assistance in preparation of this manuscript.
Summario in Interlingua
Acute anemia hemolytic esseva observate in tres patientes con hepatitis a virus. Le diagnose de hepatitis esseva basate in le constatation del classic characteristicas clinic e laboratorial supportate per biopsias hepatic. Le syndrome hemolytic esseva characterisate per un declino rapide in le concentration de hemoglobina accompaniate de leucocytosis e reticulocytosis. Grados marcate de hyperbilirubinemia, foras de proportion con le altere anormalitates functional del hepate, esseva notate.
Nulle del usual mechanismos hemolytic poteva esser incriminate como le causa del accelerate destruction de erythrocytos durante le phase anemic. Post lor restablimento hematologic, le patientes habeva erythrocytos manifestante evidentia de carentia de dehydrogenase de glucosa-6-phosphato in le forma de anormal tests de stabilitate de glutathiona, anormal tests preliminari de dehydrogenase de glucosa-6-phosphato, e de basse valores in essayos quantitative de dehydrogenase de glucosa-6-phosphato. Le mechanismo que causa le destruction del erythrocytos pare esser simile a illo describite in anemia hemolytic post le administration de primaquina e assi pare includer un destruction oxydative del erythrocytos.
Le diagnose de carentia de dehydrogenase de glucosa-6-phosphato non poteva esser establite ante le occurrentia del restablimento hematologic viste que cellulas a carentia de dehydrogenase de glucosa-6-phosphato esseva destruite durante le acute stato hemolytic. Non-detection del causa de hemolyse durante le phase acute del destruction de erythrocytos deberea esser interpretate como signal pro le possibilitate del presentia de iste intrinsec defecto genetic del erythrocytos.
Article and Author Information
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From the Division of Gastroenterology and the Cardeza Foundation, Department of Medicine, Jefferson Medical College Hospital, Philadelphia, Pa.
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This study was supported in part by grants AM 08141-01 and CA 05554-04, U. S. Public Health Service, Washington, D. C.
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At the time of this study Gerald Salen, M.D., was a Postdoctoral Research Fellow in Gastroenterology, supported by fellowship F2 AM-28, 395-01 from the National Institutes of Arthritis and Metabolic Diseases, National Institutes of Health, Bethesda, Md.
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- Received August 11, 1966.
- Accepted August 31, 1966.
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