Total parenteral nutrition in infancy: effect on the liver and suggested pathogenesis

Gut
|March 1, 1983
PubMed

Insights

Prolonged parenteral nutrition in preterm infants can cause cholestasis, a liver condition, due to absent gut hormones. Liver cell damage may occur upon reintroducing enteral nutrition.

Area of Science:

  • Neonatal Medicine
  • Pediatric Gastroenterology
  • Hepatology

Background:

  • Prolonged parenteral nutrition (PN) is essential for preterm infants lacking gut function.
  • Jaundice is a potential complication in infants receiving long-term PN.
  • The exact mechanisms causing liver issues during PN are not fully understood.

Purpose of the Study:

  • To investigate the cause of conjugated hyperbilirubinemia (jaundice) in preterm infants on prolonged PN.
  • To determine if PN directly causes liver injury or if other factors are involved.
  • To explore the impact of enteral nutrition resumption on liver health.

Main Methods:

  • Biochemical analysis of liver function.
  • Histological examination of liver tissue.
  • Electron-microscopic evaluation of liver cells.
  • Investigation included seven jaundiced preterm infants receiving prolonged PN.

Main Results:

  • Infants exhibited conjugated hyperbilirubinemia indicative of cholestasis without significant primary liver cell injury.
  • Findings suggest cholestasis results from suppressed gut-hormone production due to absent enteral nutrition.
  • Necropsy and animal studies support the hypothesis of suppressed trophic/secretory hormones.
  • Liver cell damage was suggested by biochemical and electron-microscopic findings upon resuming enteral nutrition.

Conclusions:

  • Cholestasis in preterm infants on prolonged PN is likely due to absent enteral stimulation of gut hormones.
  • Direct toxic effects of PN on the liver appear unlikely.
  • Liver cell injury may be a consequence of reintroducing enteral nutrition after a period of absence.

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