Dietary vitamin E deficiency is common in countries with high rates of food insecurity; deficiency among adults in other 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 cancer or cardiovascular disorders, and the US Preventive Services Task Force recommends against taking vitamin E for such reasons (1); whether supplements can protect against tardive dyskinesia is controversial. There is no convincing evidence that doses of natural vitamin E up to 2000 international units [IU]/day (1340 mg alpha-tocopherol/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 (2).
Although the amount of vitamin E in many fortified foods and supplements is given in IU, current recommendations are to use milligrams alpha-tocopherol.
(See also Overview of Vitamins.)
Довідкові матеріали
1. Moyer VA; U.S. Preventive Services Task Force. Vitamin, mineral, and multivitamin supplements for the primary prevention of cardiovascular disease and cancer: U.S. Preventive services Task Force recommendation statement. Ann Intern Med. 2014;160(8):558-564. doi:10.7326/M14-0198
2. Klein EA, Thompson IM Jr, Tangen CM, et al: Vitamin E and the risk of prostate cancer: The Selenium and Vitamin E Cancer Prevention Trial (SELECT). JAMA 306(14):1549-56, 2011. doi: 10.1001/jama.2011.1437
Etiology of Vitamin E Deficiency
In countries with high rates of food insecurity, the most common cause of vitamin E deficiency is
Inadequate intake of vitamin E
In countries with low rates of food insecurity, the most common causes are
Disorders that cause fat malabsorption, including abetalipoproteinemia (Bassen-Kornzweig syndrome, due to genetic absence of apolipoprotein B), chronic cholestatic hepatobiliary disease, pancreatitis, short bowel syndrome, and cystic fibrosis
A rare genetic form of vitamin E deficiency without fat malabsorption results from defective liver metabolism.
Symptoms and Signs of Vitamin E Deficiency
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 preterm infants and to some cases of intraventricular and subependymal hemorrhage in neonates. Affected preterm neonates have muscle weakness.
In children, chronic cholestatic hepatobiliary disease or cystic fibrosis impairs fat and vitamin absorption, and deficiency 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 of Vitamin E Deficiency
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 of Vitamin E Deficiency
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 IU) 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 of Vitamin E Deficiency
Although preterm neonates may require supplementation, human milk and commercial formulas have enough vitamin E for full-term neonates.
Ключові моменти
Vitamin E deficiency is usually caused by inadequate dietary intake in countries with high rates of food insecurity or by a disorder causing fat malabsorption in countries with low rates of food insecurity.
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 alpha-tocopherol level to confirm the diagnosis.
Treat with supplemental tocopherol.
