ArticleBMC pediatrics2022
Associations between UGT1A1 and SLCO1B1 polymorphisms and susceptibility to neonatal hyperbilirubinemia in Thai population.
Article in BMC pediatrics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- Association of SLCO1B1 genetic variants with neonatal hyperbilirubinemia: a consolidated analysis of 36 studies.BMC pediatrics · 2025Pooled it
- OATP1B3 c.699G>A Predicts a 6.3-Fold Increased Risk of Hyperbilirubinemia During OPrD Therapy for HCV.Current issues in molecular biology · 2026Article
- Variants in UGT1A1 and SLCO1B1 increase the risk of neonatal hyperbilirubinemia: a case-control study in subtropical China.Frontiers in pediatrics · 2026Article
- Advances in laboratory diagnosis of neonatal hyperbilirubinemia and peculiarities in plateau regions: a review of evidence.Frontiers in pediatrics · 2026Review
- The Association Between Genetic Polymorphisms ofPharmaceutics · 2025Article
- UGT1A1 and BLVRA allele and genotype variants in neonatal patients with hyperbilirubinemia in southern China.Scientific reports · 2024Article
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Authors and funding
13 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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 < 0.001). To the combined of UGT1A1, total bilirubin levels in homozygous variant were higher significantly than heterozygous variant and wild type (P = 0.002, P = 0.003, respectively). Moreover, SLCO1B1 combination was significant differences between the hyperbilirubinemia and the control group (P = 0.041). SLCO1B1 521 T > 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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