Vitamin E Deficiency

Published on 22/03/2015 by admin

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Chapter 49 Vitamin E Deficiency

Larry A. Greenbaum

Vitamin E is a fat-soluble vitamin and functions as an antioxidant, but its precise biochemical functions are not known. Vitamin E deficiency can cause hemolysis or neurologic manifestations and occurs in premature infants, in patients with malabsorption, and in an autosomal recessive disorder affecting vitamin E transport. Because of its role as an antioxidant, there is considerable research on the potential role of vitamin E supplementation in chronic illnesses.

Pathogenesis

The term vitamin E denotes a group of 8 compounds with similar structures and antioxidant activity. The most potent member of these compounds is α-tocopherol, which is also the main form in humans. The best dietary sources of vitamin E are vegetable oils, seeds, nuts, green leafy vegetables, and margarine (see Table 48-1).

The majority of vitamin E is located within cell membranes, where it prevents lipid peroxidation and the formation of free radicals. Other antioxidants, such as ascorbic acid, enhance the antioxidant activity of vitamin E. The importance of other functions of vitamin E is still being delineated.

Premature infants are particularly susceptible to vitamin E deficiency, because there is significant transfer of vitamin E during the last trimester of pregnancy. Vitamin E deficiency in premature infants causes thrombocytosis, edema, and hemolysis potentially causing anemia. The risk of symptomatic vitamin E deficiency was increased by the use of formulas for premature infants that had a high content of polyunsaturated fatty acids (PUFAs). These formulas led to a high content of PUFAs in red blood cell membranes, making them more susceptible to oxidative stress, which could be ameliorated by vitamin E. Oxidative stress was augmented by aggressive use of iron supplementation; iron increases the production of oxygen radicals. The incidence of hemolysis due to vitamin E deficiency in premature infants decreased secondary to the use of formulas with a lower content of polyunsaturated fatty acids, less-aggressive use of iron, and provision of adequate vitamin E.

Because vitamin E is plentiful in common foods, primary dietary deficiency is rare except in premature infants and in severe, generalized malnutrition. Vitamin E deficiency does occur in children with fat malabsorption secondary to the need for bile acid for vitamin E absorption. Although symptomatic disease is most common in children with cholestatic liver disease, it can occur in patients with cystic fibrosis, celiac disease, short-bowel syndrome, or Crohn disease. The autosomal recessive disorder abetalipoproteinemia (Chapter 80) causes fat malabsorption, and vitamin E deficiency is a common complication.

In ataxia with isolated vitamin E deficiency

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