Histological demonstration of BSEP/ABCB11 inhibition in transient neonatal cholestasis: a case report

BMC Pediatr. 2020 Jul 9;20(1):340. doi: 10.1186/s12887-020-02201-x.

Abstract

Background: Idiopathic or transient neonatal cholestasis (TNC) represents a group of cholestatic disorders with unidentified origin and remains a diagnosis of exclusion. Dysfunction of hepatobiliary transporters mediating excretion of biliary constituents from hepatocytes may play a central role in the pathogenesis of cholestasis. Despite variants of bile salt (BS) export pump (BSEP/ABCB11) have already been described in TNC, the pathogenic role of BSEP dysfunction in TNC remained so far elusive.

Case presentation: We report on a newly-identified heterozygous ABCB11 missense variant (c.1345G > A, p.Glu449Lys) which was associated with prolonged cholestasis in a term infant after a complicated neonatal period. Moreover, we show for the first time almost completely abolished BSEP expression on the hepatocellular membrane in TNC.

Conclusion: This report demonstrates for the first time a close association between the prolonged cholestasis in infancy and impaired BSEP expression on the hepatocyte canalicular membrane in a heterozygous carrier of newly-identified ABCB11 variant.

Keywords: BSEP deficiency; Transient neonatal cholestasis.

Publication types

  • Case Reports

MeSH terms

  • ATP Binding Cassette Transporter, Subfamily B, Member 11 / genetics
  • Cholestasis* / genetics
  • Hepatocytes
  • Humans
  • Infant
  • Infant, Newborn
  • Liver Diseases*
  • Mutation, Missense

Substances

  • ABCB11 protein, human
  • ATP Binding Cassette Transporter, Subfamily B, Member 11