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Related Experiment Videos

Early hepatobiliary dysfunction during total parenteral nutrition: an experimental study

J B Das1, C M Cosentino, M F Levy

  • 1Division of Pediatric Surgery, Children's Memorial Hospital, Chicago, IL 60614.

Journal of Pediatric Surgery
|January 1, 1993
PubMed
Summary

Total parenteral nutrition (TPN) can cause liver issues. This study in rabbits shows early TPN impairs bile secretion and leads to gallbladder sludge, potentially causing liver damage in infants.

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Area of Science:

  • Hepatology
  • Gastroenterology
  • Pediatric Nutrition

Background:

  • Liver disease is a known complication of total parenteral nutrition (TPN), but its causes are not fully understood.
  • Early detection of hepatobiliary dysfunction is crucial for managing TPN-associated liver injury.

Purpose of the Study:

  • To investigate the early changes in hepatobiliary function in young rabbits receiving total parenteral nutrition.
  • To identify the initial pathophysiological events leading to liver disease in TPN-dependent individuals.

Main Methods:

  • Young rabbits were nourished exclusively via TPN for 3, 5, and 15 days, with controls on standard chow.
  • Hepatobiliary function was assessed by measuring basal bile flow, serum bile acids, cholesterol, and the biliary secretion of sulfobromophthalein (BSP) and ursodeoxycholic acid (UDCA).

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  • Gallbladder bile volume and bile acid content were analyzed after 15 days of TPN.

    • Main Results:

    • TPN led to decreased basal bile flow, elevated serum bile acids and cholesterol.
    • Impaired biliary sulfobromophthalein (BSP) secretion was observed after 5 days of TPN.
    • After 15 days, reduced maximal bile acid secretory rate, decreased bile flow post-UDCA challenge, and increased gallbladder bile volume and bile acid content were noted.

    Conclusions:

    • TPN in rabbits causes bile secretory failure and gallbladder sludge, mimicking clinical TPN complications.
    • Enteral fasting and intravenous nutrient delivery interrupt enterohepatic circulation, leading to bile acid sequestration.
    • These findings suggest early bile secretory dysfunction and gallbladder sludge are precursors to cholestasis and liver damage in TPN-dependent neonates.