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Bile acid-induced lung injury in newborn infants: a bronchoalveolar lavage fluid study
Enrico Zecca1, Daniele De Luca, Silvia Baroni
1Division of Neonatology, Department of Pediatrics, University Hospital A. Gemelli, Catholic University of the Sacred Heart, Rome, Italy. enrizecca@rm.unicatt.it
Insights
Bile acids are found in the lungs of newborns with respiratory distress syndrome born to mothers with intrahepatic cholestasis of pregnancy. This suggests bile acids contribute to neonatal lung injury.
Area of Science:
- Neonatal medicine
- Pulmonology
- Gastroenterology
Background:
- Neonatal respiratory distress syndrome (RDS) is linked to intrahepatic cholestasis of pregnancy (ICP).
- Bile acids are implicated in neonatal bile acid pneumonia, a potential complication of ICP.
Purpose of the Study:
- To detect bile acids in the bronchoalveolar lavage fluid (BALF) of neonates with RDS born from ICP pregnancies.
- To explore the role of bile acids in acute lung injury within this population.
Main Methods:
- A prospective study comparing 10 neonates with RDS from ICP pregnancies to two control groups (20 RDS without ICP, 20 no lung disease).
- Measurement of bile acids and pH in BALF and serum within 24 hours of birth.
Main Results:
- Bile acids were present in the BALF of all neonates in the ICP group; absent in controls.
- No significant difference in BALF pH among the groups.
- Significantly elevated serum bile acid levels in the ICP group compared to controls.
Conclusions:
- Bile acids are detectable in the BALF of newborns with RDS from ICP pregnancies.
- Elevated serum bile acids suggest circulation-to-lung transfer.
- Findings support bile acids as a cause of bile acid pneumonia in neonates.
Objectives:
Neonatal respiratory distress syndrome is associated with intrahepatic cholestasis of pregnancy, and bile acids may play a major role in neonatal bile acid pneumonia. Our aim was to demonstrate the bile acid presence in the bronchoalveolar lavage fluid of neonates affected by respiratory distress syndrome who were born from intrahepatic cholestasis of pregnancy and to investigate bile acid mechanisms of action in acute lung injury.
Methods:
In this prospective study, we enrolled 10 neonates delivered from intrahepatic cholestasis of pregnancy, affected by respiratory distress syndrome requiring mechanical ventilation (intrahepatic cholestasis of pregnancy group) and 2 control groups. The first group consisted of 20 infants with respiratory distress syndrome delivered from pregnancies without any sign of intrahepatic cholestasis of pregnancy (respiratory-distress-syndrome group), and the second group included 20 neonates with no lung disease who were ventilated for extrapulmonary reasons (no-lung-disease group). We measured bile acid and pH in the bronchoalveolar lavage fluid and serum bile acid levels in the first 24 hours of life.
Results:
Bile acids were measurable in the bronchoalveolar lavage fluid of all of the infants in the intrahepatic cholestasis of pregnancy group but were absent in the 2 control groups. Bronchoalveolar lavage fluid pH was not different among the 3 groups. Infants in the intrahepatic-cholestasis-of-pregnancy group had significantly higher serum bile acid levels compared with those in both of the control groups.
Conclusions:
Bile acids are detectable in the bronchoalveolar lavage fluid of newborns from intrahepatic cholestasis of pregnancy affected by respiratory distress syndrome. Elevated serum bile acid levels in these infants allow us to hypothesize that bile acid reaches the lung after an uptake from the circulation. These findings strongly support a role for bile acid in causing bile acid pneumonia.
