Hemolytic Anemia in Vitamin E Deficiency

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Abstract
Vitamin E deficiency in the premature infant is associated with a hemolytic anemia. This anemia responds to tocopherol and the response is characterized by a rise in the hemoglobin and a fall in the reticulocyte count. Treatment of premature infants from birth wih supplemental vitamin E reduces the severity of anemia and prevents the marked reticulocytosis commonly observed in these infants of low birth weight. Vitamin E deficiency in the rat results in the appearance of a mild compensated hemolytic process. This is accompanied by thrombocytosis. The erythrocytes demonstrate increased pentose phosphate pathway activity. Tocopherol appears to be poorly absorbed from a low-fat diet in the premature infant. In infants with vitamin E deficiency there appears to be an increase in the creatine-to-creatinine ratio, lower serum proteins, and an increased excretion of methylmalonic acid in the absence of vitamin B12 deficiency. The interrelationship of this potpourri of observations remains to be explained.