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Total parenteral nutrition-associated cholestasis in infants: clinical and liver histologic studies
1Department of Pediatrics, National Taiwan University Hospital, Taipei, R.O.C.
Insights
Total parenteral nutrition-associated cholestasis (TPN-C) in infants is often reversible. Younger preterm infants on TPN may experience more severe liver changes.
Area of Science:
- Neonatology
- Pediatric Gastroenterology
- Hepatology
Background:
- Infant cholestasis is a significant concern, particularly in those receiving total parenteral nutrition (TPN).
- Understanding the clinical and pathological features of TPN-associated cholestasis (TPN-C) is crucial for effective management.
Purpose of the Study:
- To evaluate the clinicopathologic characteristics of TPN-associated cholestasis in infants.
- To identify risk factors and outcomes associated with TPN-C.
Main Methods:
- Retrospective clinicopathologic study of 15 infants who received TPN.
- Analysis of clinical data, including gestational age, birth weight, duration of TPN, and bilirubin levels.
- Review of liver biopsy or autopsy findings.
Main Results:
- TPN-C onset occurred 2-9 weeks after TPN initiation, with earlier onset in preterm infants (<32 weeks).
- Histologic findings included cholestasis, inflammation, fibrosis, and bile ductular proliferation.
- Sixty percent of infants survived, with normalized liver function within 14 weeks after TPN cessation.
Conclusions:
- Infant TPN-associated cholestasis is generally reversible.
- Younger preterm infants are more susceptible to prolonged TPN courses and more severe liver pathology.
- Prompt recognition and management are key to favorable outcomes in TPN-C.
Abstract:
To evaluate total parenteral nutrition-associated cholestasis (TPN-C) in infants, a retrospective clinicopathologic study was conducted of 15 infants who had received TPN. The mean gestational age and birth weight were 32.1 weeks (26-40 weeks) and 1807 g (840-5840 g) respectively. Two-thirds of the patients were kept on TPN for more than 60 days. The onset of rising direct bilirubin ranged 2-9 weeks (mean 4.5 +/- 2.4) after TPN therapy. Preterm babies less than 32 weeks of age had an earlier rise of direct bilirubin and AST. Bile sludge of the gallbladder was observed in only one case, and none had gallstone. The main histologic findings of liver biopsy or autopsy were cholestasis (intracellular and canalicular), periportal inflammation, fibrosis and bile ductular proliferation. Sixty percent of these survived, the remaining 40% died of complications unrelated to TPN-C. The liver function profile became normalized within a mean of 14.0 +/- 9.4 (8-34) weeks after discontinuation of TPN in the survival cases. It was concluded that infant TPN-associated cholestasis was mostly reversible, but that the younger preterm babies were susceptible to a prolonged TPN course with more marked clinical and pathological changes.