Human Vitamin E Deficiency

Vitamin E deficiency was first described in children with fat malabsorption syndromes, principally abe-talipoproteinemia, cystic fibrosis, and cholestatic liver disease. Subsequently, humans with severe vitamin E deficiency with no known defect in lipid or lipoprotein metabolism were described to have a defect in the a-TTP gene.

Erythrocyte fragility, hemolysis, and anemia were described as vitamin E deficiency symptoms in various animals fed diets devoid of vitamin E. Additionally, studies in experimental animals have shown that a deficiency of both selenium (a required component of glutathione peroxidases) and vitamin E causes a more rapid and severe onset of debilitating deficiency symptoms. Hypothetically, a deficiency of both vitamins E and C should also cause more severe antioxidant deficiency symptoms, but most animals make their own vitamin C, so this interaction has not been unequivocally demonstrated in humans or animals.

In contrast to experimental vitamin E deficiency in rodents, in humans the major vitamin E deficiency symptom is a peripheral neuropathy characterized by the degeneration of the large caliber axons in the sensory neurons.

Vitamin E deficiency occurs only rarely in humans and almost never as a result of inadequate vitamin E intakes, therefore, interactions with other nutrients have not been well studied. There have been reports of vitamin E deficiency symptoms in persons with protein-calorie malnutrition. Vitamin E deficiency does occur as a result of genetic abnormalities in a-TTP and as a result of various fat malabsorption syndromes. Vitamin E supplementation halts the progression of the neurologic abnormalities caused by inadequate nerve tissue a-tocopherol and, in some cases, has reversed them.

Patients with these disorders require daily phar-macologic vitamin E doses for life to overcome the mechanisms leading to deficiency. Generally, patients with 'ataxia with vitamin E deficiency' are advised to consume 1000 mg RRR-a-tocopherol per day in divided doses, patients with abetalipopro-teinemia 100 mg per kg body weight, and cystic fibrosis sufferers 400 mg day-1. However, patients with fat malabsorption due to impaired biliary secretion generally do not absorb orally administered vitamin E. These patients are treated with special forms of vitamin E, such as a-tocopheryl polyethylene glycol succinate, that spontaneously form micelles, obviating the need for bile acids.

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