Serious neurological abnormalities due to vitamin-E deficiency

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http://www.soe.nl/ore/res7engl.htm#neurologicalSerious neurological

abnormalities due to vitamin-E deficiencyBattisti et al. describe the case of a

patient, suffering from coeliac disease, in which this intestinal disorder was

accompanied by a disturbance in the vitamin-E absorption, which resulted in

serious neurological abnormalities.

By administering parenteral megadoses of vitamin E during a prolonged period,

the deficiency of this nutritional antioxidant could be corrected, and

remarkable results were attained as to the neurological symptoms.

Nerve fiber loss

The patient was a man who, at the age of 56, began to suffer from intestinal

problems, which in time were complicated further by the emergence of various

neurological symptoms, consisting predominantly of cerebellar impairment and

peripheral neuropathy. A nerve biopsy revealed, among other things, a severe

loss of nerve fibers and also demonstrated the presence of lipofuscin.

Lipofuscin, a substance which is formed when polyunsaturated fatty acids, due to

a lack of vitamin E, are insufficiently protected from lipid peroxidation, was

also found in skin and muscle biopsies.

 

Furthermore, a most apparent vitamin-E deficiency was recorded, to such an

extent that not a trace of this antioxidant could be detected in the serum. Oral

administration of a megadose (2 grams) of vitamin E did not appear to have any

effect on the serum level.

 

High vitamin-E dosage

When after jejunal biopsy coeliac disease was diagnosed, the patient was treated

with a gluten-free diet. Also a high vitamin-E dosage (900 mg daily) was

administered intramuscularly. After 6 months, a slight clinical improvement was

observed which progressed constantly and ultimately resulted in a considerable

improvement of the neurological picture.

 

The vitamin E in the blood returned to its normal level and the intestinal

absorption disorder was restored to such a degree that the serum vitamin-E

concentration was maintained, even after treatment switched to the oral

supplementation of a daily dosage of 900 mg. Further illustrative proof of the

improvement of the antioxidative defense mechanism, obtained with vitamin-E

therapy, was that in a second skin biopsy no lipofuscin could be found.

 

(Disappearance of skin lipofuscin storage and marked clinical improvement in

adult onset coeliac disease and severe vitamin E deficiency after chronic

vitamin E megatherapy; Battisti C et al. (Institute of Neurological Sciences,

University of Siena, Italië); Journal of Submicroscopic Cytology & Pathology,

28(3):339-344, 1996 July)

 

 

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