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

Authors

  • Ronald J. Sokol M.D.,

    Corresponding author
    1. Divisions of Gastroenterology and Nutrition, and the Clinical Research Center, Children's Hospital Research Foundation, Cincinnati, Ohio 45229
    • Section of Pediatric Gastroenterology and Nutrition, Department of Pediatrics, University of Colorado School of Medicine, Box C228, 4200 East Ninth Avenue, Denver, Colorado 80262
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    • Dr. Sokol received a postdoctoral fellowship grant from the American Liver Foundation during this study.

  • James E. Heubi,

    1. Divisions of Gastroenterology and Nutrition, and the Clinical Research Center, Children's Hospital Research Foundation, Cincinnati, Ohio 45229
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  • Catherine McGraw,

    1. Divisions of Gastroenterology and Nutrition, and the Clinical Research Center, Children's Hospital Research Foundation, Cincinnati, Ohio 45229
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  • William F. Balistreri

    1. Divisions of Gastroenterology and Nutrition, and the Clinical Research Center, Children's Hospital Research Foundation, Cincinnati, Ohio 45229
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  • This work was presented in part at the American Association for the Study of Liver Diseases Annual Meeting in November, 1983 and at the American College of Nutrition Annual Meeting in September, 1984 and published in abstract form (Hepatology 1983; 3:848 and J. Am. Coll. Nutr. 1984; 3:236).

Abstract

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.

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