Vitamin E Deficiency

Vitamin E deficiency is seen rarely in humans. However, there may be a risk of vitamin E deficiency in premature infants because the placenta does not transfer a-tocopherol to the fetus in adequate amounts. When it occurs in older children and adults, it is usually a result of lipoprotein deficiencies or a lipid malabsorption syndrome. These include patients with abetalipoproteinemia or homozygous hypobeta-lipoproteinemia, those with cholestatic disease, and patients receiving total parenteral nutrition. There is also an extremely rare disorder in which primary vitamin E deficiency occurs in the absence of lipid malabsorption. This disorder is a rare autosomal recessive neurodegenerative disease caused by mutations in the gene for a-TTP. This disorder is known as ataxia with vitamin E deficiency (AVED). Patients with AVED have extraordinary low plasma vitamin E concentrations (<5 mgml-1) and have an onset between 4 and 18 years, with progressive development of peripheral neuropathy, spinocere-bellar ataxia, dysarthria, the absence of deep tendon reflexes, and vibratory and proprioceptive sensory loss. Patients with an a-TTP defect have enhanced urinary excretion of a-CEHC despite having much lower plasma a-tocopherol concentrations than healthy subjects. Therapeutic and prophylactic vitamin E supplementation (up to 2000 mg day2 1) prevents the onset of the disease before irreversible neurological damage develops.

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