HYPERBILIRUBNEMIA : Prolonged Unconjugated Hyperbilirubinemia in Breast-fed Male Infants with a Mutation of Uridine Diphosphate-Glucuronosyl Transferase.

Chang PF, Lin YC, Liu K, Yeh SJ, Ni YH.

J Pediatr. 2009 Aug 13. [Epub ahead of print] PMID: 19683255 [PubMed – as supplied by publisher]

Chang PF, Lin YC, Liu K, Yeh SJ, Ni YH.

From the Department of Pediatrics (P.-F.C., Y.-C.L., K.L., S.-J.Y.), Far Eastern Memorial Hospital, Pan-Chiao, Taipei, Taiwan; and National Taiwan University Children’s Hospital (Y.-H.N.), Taipei, Taiwan.

OBJECTIVE: To test the hypothesis that a mutation in uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1) gene of breast-fed infants is a contributory factor to prolonged unconjugated hyperbilirubinemia. STUDY DESIGN: Of 125 breast-fed term infants, 35 infants had prolonged unconjugated hyperbilirubinemia; another 90 breast-fed neonates without prolonged jaundice were control infants. The polymerase chain reaction-restriction fragment length polymorphism method was used to detect the known variant sites (promoter area, nucleotides 211, 686, 1091, and 1456) of the UGT1A1 gene. RESULTS: Of 35 breast-fed infants with prolonged unconjugated hyperbilirubinemia, 29 had at least 1 mutation of the UGT1A1 gene. Variation at nucleotide 211 was most common. The percentages of the neonates carrying the variant nucleotide 211 were significantly different between the prolonged hyperbilirubinemia group and control neonates. Male breast-fed infants had a higher risk than female infants for prolonged hyperbilirubinemia. CONCLUSIONS: Male breast-fed neonates with a variant nucleotide 211 in UGT1A1 have a high risk for developing prolonged hyperbilirubinemia.

 

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