Related Experiment Videos
Correction of vitamin E deficiency in children with chronic cholestasis. II. Effect on gastrointestinal and hepatic
Insights
Vitamin E deficiency in children with cholestasis does not affect fat absorption but may worsen liver function. Vitamin E therapy did not improve gastrointestinal or hepatic issues in this study.
Area of Science:
- Pediatric Gastroenterology
- Hepatology
- Nutritional Science
Background:
- Secondary vitamin E deficiency is linked to neurological issues in children with chronic cholestasis.
- The impact of vitamin E deficiency on other organ systems in this population is not well understood.
Purpose of the Study:
- To investigate the effects of vitamin E therapy on gastrointestinal and hepatic functions in children with chronic cholestasis and vitamin E deficiency.
Main Methods:
- Five children with chronic cholestasis and vitamin E deficiency received vitamin E therapy (oral or parenteral) for 2-3 years.
- Evaluated fecal fat losses, vitamin E malabsorption via oral tolerance tests, serum fatty acid levels, and serial liver function tests.
Main Results:
- Vitamin E therapy did not improve fecal fat losses, vitamin E malabsorption, or serum fatty acid levels.
- Fasting serum cholylglycine concentrations significantly declined during vitamin E therapy.
- Other liver function tests showed no consistent changes.
Conclusions:
- Vitamin E deficiency does not appear to impair intestinal fat or vitamin E absorption.
- Vitamin E deficiency may exacerbate compromised hepatic function in conditions like cholestasis.
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.