M. Feki et al., Vitamin E deficiency: pathogenic, clinical, histopathological and electrical features and principal causes, ANN MED IN, 152(6), 2001, pp. 392-397
Vitamin E deficiency is frequently observed in human pathology. In most cas
es, deficiency is moderate and asymptomatic. Severe deficiency is rare and
presents as a progressive neurological syndrome including cerebellar ataxia
and posterior cord injury. Neuropathological and electrophysiological feat
ures confirm spinocerebellar degeneration. The pathophysiology of vitamin E
deficiency nervous dysfunction is still unknown. Oxidative alterations due
to the tack of the main lipid-soluble antioxidant could be involved. A few
causes of vitamin E deficiency are recognized (malnutrition, impaired lipi
d absorption, specific anomaly of hepatic or intestinal secretion of vitami
n E, excessive endogenous consumption), but diseases associated with vitami
n E deficiency are numerous and divers. Symptomatic severe deficiency is co
nstantly observed in ataxia with vitamin E deficiency and abetalipoproteine
mia. Intestinal, hepatobiliary, and pancreatic diseases are often associate
d with more or less marked deficiency. Other pathological circumstances suc
h as malnutrition, alcoholism, hemolytic anemia, renal failure and hemodial
ysis could be associated with moderated and asymptomatic vitamin E deficien
cy.
Oral or regular administration of high-dose vitamin E is required for patie
nts with symptomatic severe deficiency. An adapted supplementation is recom
mended for patients with a marginal vitamin E status.