Reduced Chronic Hemolysis during High-Dose Vitamin E Administration in Mediterranean-Type Glucose-6-Phosphate Dehydrogenase Deficiency

Laurence Corash, Stephen Spielberg, Christos Bartsocas, Laurence Boxer, Reuven Steinherz, Michael Sheetz, Michael Egan, James Schlessleman, Joseph D. Schulman, Laurence Corash, Stephen Spielberg, Christos Bartsocas, Laurence Boxer, Reuven Steinherz, Michael Sheetz, Michael Egan, James Schlessleman, Joseph D. Schulman, Laurence Corash, Stephen SpielbergChristos Bartsocas, Laurence Boxer, Reuven Steinherz, Michael Sheetz, Michael Egan, James Schlessleman, Joseph D. Schulman, Laurence Corash, Stephen Spielberg, Christos Bartsocas, Laurence Boxer, Reuven Steinherz, Michael Sheetz, Michael Egan, James Schlessleman, Joseph D. Schulman, Laurence Corash, Stephen Spielberg, Christos Bartsocas, Laurence Boxer, Reuven Steinherz, Michael Sheetz, Michael Egan, James Schlessleman, Joseph D. Schulman

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Abstract

The observation that high-dose oral vitamin E supplementation (800 IU per day) improved red-cell survival in two rare disorders associated with increased red-cell susceptibility to oxidative stress prompted a similar trial in 23 patients with Mediterranean glucose-6-phosphate dehydrogenase (G6PD) deficiency. Three months of vitamin E administration resulted in decreased chronic hemolysis as evidenced by improved red-cell life span (P<0.025), with an improvement in red-cell half-life from 22.9±0.7 days to 25.1 ±0.6 days (mean ±S.E.M.), increased hemoglobin concentration (P<0.001), and decreased reticulocytosis (P<0.001) as compared with base-line values. Evaluation after one year of vitamin E administration demonstrated sustained improvement in all these indexes. Controlled clinical trials of vitamin E supplementation may be warranted to examine its efficacy in ameliorating acute hemolytic crises or in reducing morbidity from neonatal jaundice in this relatively common genetic disorder. (N Engl J Med. 1980; 303:416–20.) SINCE the observation by Rose and György1 that vitamin E can act as an antioxidant to protect red cells from lysis induced by oxidant stress, additional evidence of a biologic effect of the vitamin and of its role in pathologic processes secondary to a deficiency has been reported. Vitamin E can prevent lipid peroxidation and sulfhydryl group oxidation associated with oxidant-induced hemolysis in vitamin E-deficient rats.2 In human beings, vitamin E deficiency is also associated with increased red-cell susceptibility to oxidative stress, 3 which leads to shortened red-cell survival4,5 but can be corrected by supplemental vitamin E. Under experimental conditions in.

Original languageEnglish (US)
Pages (from-to)416-420
Number of pages5
JournalNew England Journal of Medicine
Volume303
Issue number8
DOIs
StatePublished - Aug 21 1980

ASJC Scopus subject areas

  • Medicine(all)

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    Corash, L., Spielberg, S., Bartsocas, C., Boxer, L., Steinherz, R., Sheetz, M., Egan, M., Schlessleman, J., Schulman, J. D., Corash, L., Spielberg, S., Bartsocas, C., Boxer, L., Steinherz, R., Sheetz, M., Egan, M., Schlessleman, J., Schulman, J. D., Corash, L., ... Schulman, J. D. (1980). Reduced Chronic Hemolysis during High-Dose Vitamin E Administration in Mediterranean-Type Glucose-6-Phosphate Dehydrogenase Deficiency. New England Journal of Medicine, 303(8), 416-420. https://doi.org/10.1056/NEJM198008213030802