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Total parenteral nutrition in infancy: effect on the liver and suggested pathogenesis
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.
Abstract:
Biochemical, histological, and electron-microscopic investigation of seven preterm infants who became jaundiced after prolonged total parenteral nutrition showed conjugated hyperbilirubinaemia apparently due to cholestasis without significant primary liver cell injury. In the absence of evidence indicating a direct toxic effect on the liver of this form of nutrition the necropsy findings in one child and analogy with the effects of total parenteral nutrition in animals suggest that the cholestasis is the result of suppression of trophic and/or secretion-stimulating hormone(s) normally produced by the gut, due to absent enteral nutrition. Biochemical and electron-microscopic findings suggest that liver cell damage occurs after resumption of enteral nutrition.
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