Vitamin E deficiency in β-thalassemia major: changes in hematological and biochemical parameters after a therapeutic trial with α-tocopherol

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Abstract
Serum α-tocopherol (vitamin E) levels less than 0.5 mg/100 ml were found in β-thalassemia major and intermedia. Vitamin E deficiency in thalassemia is not associated with malabsorption, but could be due to its consumption while neuthlizing oxidative damage in red blood cell (RBC) membrane and other tissues. A therapeutic trial with vitamin E was carried out in eight patients with β-thalassemia major with 750 to 1000 IU/day for an average period of 16 months. Serum vitamin E levels were determined consecutively in these patients and in seven untreated patients throughout that period. The treated patients showed: 1) A 4-fold increase in both serum and RBC vitamin E levels; 2) serum vitamin E dropped to the low pretreatment values after discontinuation of the therapeutic trial; 3) decrease in abnormally high malonyldialdehyde levels, which were generated after oxidant stress and indicate peroxidative damage to the lipid portion of the RBC membrane; 4) no changes in the low titratable sulfhydryl groups calculated per RBC membrane protein; 5) in three of seven patients prolonged RBC survival was found after administration of vitamin E for 12 months; 6) no significant changes were found in transfusion requirements between the treated and untreated groups followed for a period of 16 and 18 months, respectively. While there seem to be practical and theoretical indications to treat thalassemic patients with vitamin E, this by itself is incapable of correcting the variety of changes in RBC membrane components.