Cholestasis in late metabolic acidosis of prematurely born infants

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Updated: Oct 21, 2026

Isolation of Neonatal Extrahepatic Cholangiocytes
07:54

Isolation of Neonatal Extrahepatic Cholangiocytes

Published on: June 5, 2014

H Senger1, G Boehm, K Beyreiss

  • 1Department of Pediatrics, Karl-Marx University Leipzig, GDR.

Journal of Clinical Chemistry and Clinical Biochemistry. Zeitschrift Fur Klinische Chemie Und Klinische Biochemie
|July 1, 1987
PubMed

Insights

Metabolic acidosis in premature infants disrupts bile acid and tyrosine levels, leading to impaired fat digestion. Treatment normalized these levels, improving infant health.

Area of Science:

  • Biochemistry
  • Pediatric Gastroenterology
  • Neonatology

Background:

  • Premature infants are susceptible to metabolic acidosis.
  • Metabolic acidosis can affect various physiological processes, including digestion and nutrient absorption.

Purpose of the Study:

  • To investigate the impact of late metabolic acidosis on bile acid and tyrosine metabolism in premature infants.
  • To assess the effects of metabolic acidosis on digestive enzyme activity and fat excretion.
  • To evaluate the recovery of these parameters after acidosis resolution.

Main Methods:

  • Serum bile acids and tyrosine were measured in infants with and without metabolic acidosis.
  • Duodenal juice analysis included bile acid concentration and lipase/trypsin activity.
  • Fecal fat excretion was quantified.
  • Duodenal studies were repeated in a subset of patients after acidosis correction.

Main Results:

  • Infants with metabolic acidosis exhibited significantly higher serum bile acids and tyrosine.
  • Decreased duodenal bile acids, lipase, and trypsin activity were observed during acidosis.
  • Increased fecal fat excretion was associated with metabolic acidosis.
  • Duodenal parameters normalized within a week after acidosis resolution.

Conclusions:

  • Late metabolic acidosis in premature infants is linked to cholestasis and altered amino acid transport.
  • Digestive enzyme deficiencies and impaired fat absorption are consequences of metabolic acidosis.
  • Correction of metabolic acidosis leads to the recovery of gastrointestinal function.

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