Correction of vitamin E deficiency in children with chronic cholestasis. II. Effect on gastrointestinal and hepatic function

✍ Scribed by Ronald J. Sokol; James E. Heubi; Catherine McGraw; William F. Balistreri

• Publisher: John Wiley and Sons
• Year: 1986
• Tongue: English
• Weight: 712 KB
• Volume: 6
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.1840060607

✦ Synopsis

Although secondary vitamin E deficiency causes a reversible neurologic disorder in children with chronic cholestasis, the effect of this deficiency state on other organ systems is unknown. We studied the effects of vitamin E therapy on selected gastrointestinal and hepatic functions in five children with chronic cholestasis and well-documented biochemical and neurologic evidence of vitamin E deficiency. After 2 to 3 years of oral or parenteral vitamin E therapy, there was no improvement in fecal fat losses, severity of vitamin E malabsorption (as measured by an oral vitamin E tolerance test) or total serum fatty acid concentrations. Serial analyses of liver function blood tests demonstrated a marked decline in fasting serum cholylglycine concentrations during 18 to 31 months of vitamin E therapy, while other liver function tests showed no consistent changes. We conclude that vitamin E deficiency does not appear to alter intestinal absorption of fat or vitamin E; however, vitamin E deficiency may further impair already compromised hepatic function during pathologic conditions such as cholestasis.

Vitamin E (a-tocopherol) functions as the major membrane-localized cellular antioxidant, protecting membrane phospholipids from peroxidative damage initiated by free radicals (1). Changes in the structure and functional properties of cellular membranes leading to tissue injury have been reported in experimental animal models