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Total parenteral nutrition-related liver disease
1Pediatric Liver Center, University of Colorado School of Medicine, Denver 80218-1088, USA. sokol.ronald@tchden.org
Insights
Parenteral nutrition in infants can cause liver issues like cholestasis. Oxidative stress and gut bacteria are key factors, but early feeding and new therapies may help prevent this parenteral nutrition-associated liver disease.
Area of Science:
- Neonatal Medicine
- Gastroenterology
- Hepatology
Background:
- Parenteral nutrition (PN) is crucial for infant morbidity reduction but is linked to significant cholestasis and liver dysfunction.
- Parenteral nutrition-associated liver disease (PNALD) affects a high proportion of infants receiving long-term PN.
- Understanding the pathogenesis of PNALD is critical for improving infant outcomes.
Purpose of the Study:
- To outline contributing factors in the etiopathogenesis of PNALD.
- To propose a unifying theory for the pathogenesis of PNALD.
- To review current and novel therapeutic strategies for PNALD.
Main Methods:
- Review of existing literature on PNALD.
- Analysis of factors contributing to cholestasis and liver injury during PN.
- Synthesis of a unifying theory on PNALD pathogenesis.
Main Results:
- Oxidant stress is a major factor in PNALD.
- Bacterial cell wall products from injured intestines stimulate Kupffer cells, contributing to liver injury.
- Early introduction of enteral feedings is associated with improved outcomes.
Conclusions:
- Oxidant stress and gut-derived bacterial products are central to PNALD pathogenesis.
- Novel therapies including antibiotics, probiotics, ursodeoxycholic acid, and cholecystokinin are being explored.
- Further understanding of PNALD mechanisms will drive new preventative and treatment strategies.
Abstract:
Administration of parenteral nutrition to the small infant has decreased morbidity but is associated with the development of cholestasis and liver dysfunction in a high proportion of infants. In this review, contributing factors of the etiopathogenesis of parenteral nutrition-associated liver disease will be outlined, forming the basis for a unifying theory of its pathogenesis. It is proposed that oxidant stress and stimulation of hepatic Kupffer cells by bacterial cell wall products absorbed from the injured intestine are major factors leading to cholestasis and liver injury during prolonged parenteral nutrition. Improved outcome in patients has been related to the early introduction of feedings. New proposed therapeutic modalities have included antibiotics and probiotics to prevent bacterial overgrowth of the small intestine, enterally-administered ursodeoxycholic acid and intravenous cholecystokinin. Improved understanding of the fundamental mechanisms producing liver injury and fibrosis during parenteral nutrition will lead to new preventative and treatment measures in the future.