This meta-analysis confirms that UGT1A1Gly71Arg polymorphism significantly increases the risk of neonatal hyperbilirubinemia in Asian population, but results from the Caucasians were conflicting and further well-designed epidemiological studies are, therefore, required to more adequately assess this correlation.
No association was observed between UGT1A1*28 gene polymorphisms and NHBI in allele model (TA7 versus TA6, OR (95% CI) = 2.13 (0.81-5.62), <i>p</i> = 0.13), codominance models (TA7/6 versus TA6/6, OR (95% CI) = 2.94 (0.90-9.57), <i>p</i> = 0.07; TA7/7 versus TA6/6, OR (95% CI) = 2.08 (0.37-11.52), <i>p</i> = 0.40), recessive model (TA7/7 versus TA6/6 + TA7/6, OR (95% CI) = 1.44 (0.41-5.14), <i>p</i> = 0.57) and dominant model (TA7/7 + TA7/6 versus TA6/6, OR (95% CI) = 2.92 (0.84-10.12), <i>p</i> = 0.09).
The genotype of Gilbert syndrome, the UGT1A1*28 allele, causes markedly reduced activity of this enzyme, but its association with neonatal hyperbilirubinemia is uncertain and its relationship with extreme hyperbilirubinemia has not been studied.
Short (GT)n repeats of HO-1 gene, c.211G>A variant of UGT1A1 gene, and excessive weight loss were independent risk factors for neonatal hyperbilirubinemia.
We previously reported that 211G>A (G71R) mutation of the UGT1A1 gene is prevalent in East Asians and is associated with the development of neonatal hyperbilirubinemia.
We studied mice in which the original Ugt1 locus was disrupted and replaced with the human UGT1 locus (hUGT1 mice); these mice spontaneously develop neonatal hyperbilirubinemia and BIND.
The uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1) gene polymorphism was shown to contribute to the development of neonatal hyperbilirubinemia.