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[Cholestasis in total parenteral nutrition. A review]
Insights
Intrahepatic cholestasis, a common complication of total parenteral nutrition in infants, may be indicated by elevated serum bile acids. Its multifactorial causes include lack of oral feeding and potential amino acid toxicity.
Area of Science:
- Pediatric Gastroenterology
- Hepatology
- Neonatal Nutrition
Context:
- Intrahepatic cholestasis frequently complicates total parenteral nutrition in infants, affecting 10-50% of cases.
- This condition remains a significant clinical challenge in neonatal care.
- Early detection is crucial for managing potential liver damage.
Purpose:
- To review the incidence, histological features, and multifactorial etiology of intrahepatic cholestasis in infants receiving total parenteral nutrition.
- To highlight serum bile acids as a sensitive biomarker for early cholestasis detection.
- To discuss key contributing factors in the development of this complication.
Summary:
- Intrahepatic cholestasis is a common complication of total parenteral nutrition (TPN) in infants, with reported frequencies of 10-50%.
- Elevated serum bile acids are a sensitive indicator of developing cholestasis.
- Histological findings include inflammatory portal reactions, fibrosis, and bile duct proliferation.
- Multifactorial causes include lack of oral alimentation, fetal bile acid pathways, amino acid toxicity, hypoalbuminemia, sepsis, and substrate excess.
Impact:
- Provides a comprehensive overview of a critical neonatal complication.
- Emphasizes the importance of monitoring serum bile acids for early diagnosis.
- Informs clinical practice regarding the management and prevention of TPN-induced cholestasis in infants.
Abstract:
Intrahepatic cholestasis is a frequent, however, unresolved complication of total parenteral nutrition in infancy. A frequency of 10-50% is reported. The concentration of serum bile acids seems to be a sensitive indicator for a beginning cholestasis. As typical histological alterations of the liver are considered: inflammatory portal reaction, fibrosis and proliferation of bile ducts. As important components of the obviously multifactorial etiology are considered: lacking oral alimentation, fetal bile acid synthetic pathways, amino acid toxicity, hypoalbuminemia, sepsis and substrate excess.