Abstract
BackgroundTo evaluate the association between the genetic polymorphism of the solute carrier organic anion transporter family member 1B1 (SLCO1B1, also known as organic anion transport polypeptide C) and hyperbilirubinemia in Chinese neonates.Methods183 infants with hyperbilirubinemia and 192 control subjects from the Fifth People’s Hospital of Shenzhen were recruited. Polymerase chain reaction, restriction fragment length polymorphisms and agarose gel electrophoresis techniques were used to detect genetic variants of SLCO1B1.ResultsThe study revealed that SLCO1B1 388 G > A occurred significantly more frequently in neonates with hyperbilirubinemia than in controls (RR = 1.50; 95% CI: 1.13–2.00). There were no significant differences in SLCO1B1 521 T > C between the hyperbilirubinemia and the control group (RR, 1.00; 95% CI, 0.72–1.40). No carriage of the C to A substitution at nucleotide 463 was detected.ConclusionThe SLCO1B1 388 G > A variant is associated with neonatal hyperbilirubinemia in Chinese neonates.
Highlights
To evaluate the association between the genetic polymorphism of the solute carrier organic anion transporter family member 1B1 (SLCO1B1, known as organic anion transport polypeptide C) and hyperbilirubinemia in Chinese neonates
We found that the UDP-glucuronosyltransferase 1A1 (UGT1A1) 211G > A mutation is associated with neonatal hyperbilirubinemia in Asians [6]
We hypothesized that the SLCO1B1 mutation may be one of the risk factors for neonatal hyperbilirubinemia, which possibly accounts for the variability in prevalence rates in the Chinese neonates
Summary
To evaluate the association between the genetic polymorphism of the solute carrier organic anion transporter family member 1B1 (SLCO1B1, known as organic anion transport polypeptide C) and hyperbilirubinemia in Chinese neonates. We found that the UGT1A1 211G > A mutation is associated with neonatal hyperbilirubinemia in Asians [6]. Studies have suggested that variations of 388 G > A, 521 T > C, 463 C > A of the SLCO1B1 gene may predispose subjects to neonatal hyperbilirubinemia by limiting hepatic bilirubin uptake [7]. We conducted a case-control study of three variants (388 G > A, 521 T > C, 463 C > A) of SLCO1B1 and investigated their association with neonatal hyperbilirubinemia in the Chinese neonates
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