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Maternal bile acid transporter deficiency promotes neonatal demise. | LitMetric

AI Article Synopsis

  • Intrahepatic cholestasis of pregnancy (ICP) affects 0.4 to 5% of pregnancies and is linked to poor neonatal outcomes, including death due to respiratory issues shortly after birth.
  • Maternal cholestasis leads to elevated pulmonary bile acids in newborns, which disrupts surfactant structure and causes pulmonary hypoxia.
  • Reducing maternal bile acid levels can improve neonatal survival, suggesting potential treatment targets to prevent respiratory failure in affected infants.

Article Abstract

Intrahepatic cholestasis of pregnancy (ICP) is associated with adverse neonatal survival and is estimated to impact between 0.4 and 5% of pregnancies worldwide. Here we show that maternal cholestasis (due to Abcb11 deficiency) produces neonatal death among all offspring within 24 h of birth due to atelectasis-producing pulmonary hypoxia, which recapitulates the neonatal respiratory distress of human ICP. Neonates of Abcb11-deficient mothers have elevated pulmonary bile acids and altered pulmonary surfactant structure. Maternal absence of Nr1i2 superimposed on Abcb11 deficiency strongly reduces maternal serum bile acid concentrations and increases neonatal survival. We identify pulmonary bile acids as a key factor in the disruption of the structure of pulmonary surfactant in neonates of ICP. These findings have important implications for neonatal respiratory failure, especially when maternal bile acids are elevated during pregnancy, and highlight potential pathways and targets amenable to therapeutic intervention to ameliorate this condition.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4598356PMC
http://dx.doi.org/10.1038/ncomms9186DOI Listing

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