BMC Pediatrics (May 2022)

Associations between UGT1A1 and SLCO1B1 polymorphisms and susceptibility to neonatal hyperbilirubinemia in Thai population

  • Chalirmporn Atasilp,
  • Janjira Kanjanapipak,
  • Jaratdao Vichayaprasertkul,
  • Pimonpan Jinda,
  • Rawiporn Tiyasirichokchai,
  • Pornpen Srisawasdi,
  • Chatchay Prempunpong,
  • Monpat Chamnanphon,
  • Apichaya Puangpetch,
  • Natchaya Vanwong,
  • Suwit Klongthalay,
  • Thawinee Jantararoungtong,
  • Chonlaphat Sukasem

DOI
https://doi.org/10.1186/s12887-022-03311-4
Journal volume & issue
Vol. 22, no. 1
pp. 1 – 8

Abstract

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Abstract Hyperbilirubinemia is the main mechanism that causes neonatal jaundice, and genetics is one of the risk factors of hyperbilirubinemia. Therefore, this study aims to explore the correlation between two genes, UGT1A1 and SLCO1B1, and hyperbilirubinemia in Thai neonates. One hundred thirty seven neonates were recruited from Division of Clinical Chemistry, Ramathibodi Hospital. UGT1A1*28 and *6 were determined by pyrosequencing whereas, SLCO1B1 388A > G and 521 T > C genetic variants were determined by TaqMan® real-time polymerase chain reaction. Neonates carrying with homozygous (AA) and heterozygous (GA) variants in UGT1A1*6 were significantly related to hyperbilirubinemia development compared with wild type (GG; P C variant provide protection for Thai neonatal hyperbilirubinemia (P = 0.041). There are no significant differences in UGT1A1*28 and SLCO1B1 388A > G for the different severity of hyperbilirubinemia. The combined UGT1A1*28 and *6 polymorphism is a strong risk factor for the development of severe hyperbilirubinemia in Thai neonates. Therefore, we suggest neonates with this gene should be closely observed to avoid higher severities of bilirubin.

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