Vitamin E deficiency
Vitamin E deficiency: Excerpt from Professional Guide to Diseases (Eighth Edition)
Vitamin E (tocopherol) appears to act primarily as an antioxidant, preventing intracellular oxidation of polyunsaturated fatty acids and other lipids. It protects body tissue from damage caused by unstable substances called free radicals, which can harm cells, tissues, and organs and are believed to be one of the causes of aging’s degenerative process. Vitamin E is also important in the formation of red blood cells (RBCs) and helps the body to use vitamin K. Vitamin E deficiency usually manifests as hemolytic anemia in low-birth-weight or premature neonates. With treatment, prognosis is good.
Causes and incidence
Vitamin E deficiency in infants usually results from consuming formulas high in polyunsaturated fatty acids that are fortified with iron but not vitamin E. Such formulas increase the need for antioxidant vitamin E because the iron supplement catalyzes the oxidation of RBC lipids. A neonate has low tissue concentrations of vitamin E to begin with because only a small amount passes through the placenta; the mother retains most of it. Because vitamin E is a fat-soluble vitamin, deficiency develops in conditions associated with fat malabsorption, such as kwashiorkor, celiac disease, or cystic fibrosis. These conditions may induce megaloblastic or hemolytic anemia and creatinuria, all of which are reversible with vitamin E administration.
Vitamin E deficiency is uncommon in adults but is possible in people whose diets are high in polyunsaturated fatty acids, which increase vitamin E requirements, and in people with vitamin E malabsorption, which impairs RBC survival.
Signs and symptoms
Vitamin E deficiency is difficult to recognize, but its early symptoms include edema and skin lesions in infants and muscle weakness or intermittent claudication in adults. In premature neonates, vitamin E deficiency produces hemolytic anemia, thrombocythemia, and erythematous papular skin eruption, followed by desquamation.
Diagnosis
Confirming diagnosis Dietary and medical histories suggest vitamin E deficiency. Serum alpha-tocopherol levels below 0.5 mg/dl in adults and below 0.2 mg/dl in infants confirm it. Creatinuria, increased creatine kinase levels, hemolytic anemia, and an elevated platelet count generally support the diagnosis.
Treatment
Replacement of vitamin E with a water-soluble supplement, either oral or parenteral, is the only appropriate treatment.
Special considerations
❑ As ordered, prevent deficiency by providing vitamin E supplements for low-birth-weight neonates receiving formulas not fortified with vitamin E and for adults with vitamin E malabsorption. Many commercial multivitamin supplements are easily absorbed by patients with vitamin E malabsorption.
❑ Inform new mothers who plan to breast-feed that human milk provides adequate vitamin E.
❑ Encourage adult patients to eat foods high in vitamin E; good sources include vegetable oils (corn, safflower, soybean, cottonseed); whole grains; dark green, leafy vegetables; nuts; and legumes. Tell them that heavy consumption of polyunsaturated fatty acids increases the need for vitamin E.
❑ If vitamin E deficiency is related to socioeconomic conditions, refer the patient to appropriate community agencies.
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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