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Vitamin E Deficiency

By

Larry E. Johnson

, MD, PhD, University of Arkansas for Medical Sciences

Last full review/revision Aug 2019| Content last modified Aug 2019
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Dietary vitamin E deficiency is common in developing countries; deficiency among adults in developed countries is uncommon and usually due to fat malabsorption. The main symptoms are hemolytic anemia and neurologic deficits. Diagnosis is based on measuring the ratio of plasma alpha-tocopherol to total plasma lipids; a low ratio suggests vitamin E deficiency. Treatment consists of oral vitamin E, given in high doses if there are neurologic deficits or if deficiency results from malabsorption.

Vitamin E deficiency causes fragility of red blood cells and degeneration of neurons, particularly peripheral axons and posterior column neurons.

Vitamin E is a group of compounds (including tocopherols and tocotrienols) that have similar biologic activities. The most biologically active is alpha-tocopherol, but beta-, gamma-, and delta-tocopherols, 4 tocotrienols, and several stereoisomers may also have important biologic activity. These compounds act as antioxidants, which prevent lipid peroxidation of polyunsaturated fatty acids in cellular membranes (see table Sources, Functions, and Effects of Vitamins). Dietary sources of vitamin E include vegetable oils and nuts.

Plasma tocopherol levels vary with total plasma lipid levels. Normally, the plasma alpha-tocopherol level is 5 to 20 mcg/mL (11.6 to 46.4 mcmol/L).

High-dose vitamin E supplements do not protect against cardiovascular disorders; whether supplements can protect against tardive dyskinesia is controversial. There is no convincing evidence that doses of up to 2000 units/day slow the progression of Alzheimer disease or decrease the risk of prostate cancer; one study suggested an increased risk of prostate cancer with vitamin E supplementation (1).

Although the amount of vitamin E in many fortified foods and supplements is given in units, current recommendations are to use mg.

(See also Overview of Vitamins.)

Reference

Etiology

In developing countries, the most common cause of vitamin E deficiency is

  • Inadequate intake of vitamin E

In developed countries, the most common causes are

A rare genetic form of vitamin E deficiency without fat malabsorption results from defective liver metabolism.

Symptoms and Signs

The main symptoms of vitamin E deficiency are mild hemolytic anemia and nonspecific neurologic deficits. Abetalipoproteinemia results in progressive neuropathy and retinopathy in the first 2 decades of life.

Vitamin E deficiency may contribute to retinopathy of prematurity (also called retrolental fibroplasia) in premature infants and to some cases of intraventricular and subependymal hemorrhage in neonates. Affected premature neonates have muscle weakness.

In children, chronic cholestatic hepatobiliary disease or cystic fibrosis causes neurologic deficits, including spinocerebellar ataxia with loss of deep tendon reflexes, truncal and limb ataxia, loss of vibration and position senses, ophthalmoplegia, muscle weakness, ptosis, and dysarthria.

In adults with malabsorption, vitamin E deficiency very rarely causes spinocerebellar ataxia because adults have large vitamin E stores in adipose tissue.

Diagnosis

  • Low alpha-tocopherol level or low ratio of serum alpha-tocopherol to serum lipids

Without a history of inadequate intake or a predisposing condition, vitamin E deficiency is unlikely. Confirmation usually requires measuring the vitamin level. Measuring red blood cell hemolysis in response to peroxide can suggest the diagnosis but is nonspecific. Hemolysis increases as vitamin E deficiency impairs red blood cell stability.

Measuring the serum alpha-tocopherol level is the most direct method of diagnosis. In adults, vitamin E deficiency is suggested if the alpha-tocopherol level is < 5 mcg/mL (<11.6 mcmol/L). Because abnormal lipid levels can affect vitamin E status, a low ratio of serum alpha-tocopherol to lipids (< 0.8 mg/g total lipid) is the most accurate indicator in adults with hyperlipidemia.

In children and adults with abetalipoproteinemia, serum alpha-tocopherol levels are usually undetectable.

Treatment

  • Supplemental alpha-tocopherol or mixed tocopherols (alpha-, beta-, and gamma-tocopherols)

If malabsorption causes clinically evident deficiency, alpha-tocopherol 15 to 25 mg/kg orally once a day should be given. Or mixed tocopherols (200 to 400 units) can be given. However, larger doses of alpha-tocopherol given by injection are required to treat neuropathy during its early stages or to overcome the defect of absorption and transport in abetalipoproteinemia.

Prevention

Although premature neonates may require supplementation, human milk and commercial formulas have enough vitamin E for full-term neonates.

Key Points

  • Vitamin E deficiency is usually caused by inadequate dietary intake in developing countries or by a disorder causing fat malabsorption in developed countries.

  • The deficiency causes mainly mild hemolytic anemia and nonspecific neurologic deficits.

  • In patients with inadequate intake or a predisposing condition plus compatible findings, measure the tocopherol level to confirm the diagnosis.

  • Treat with supplemental tocopherol.

Drugs Mentioned In This Article

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Selenium
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