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.
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