Neonatal hyperbilirubinemia and Gilbert's syndrome
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N. Laforgia
Abstract
The role of Gilbert's syndrome (GS) in neonatal hyperbilirubinemia, characterized by bilirubin levels higher than 223 μMol/L during the first seven days of life, has been investigated, evaluating the frequency of GS genotype (A(TA)7TAA polymorphism in the promoter of the gene encoding UGT1). The frequency of GS was significantly higher in the hyperbilirubinemic group, even though neither the peak of bilirubin, nor the day on which the highest value was found, differed according to genotype. The normalization of bilirubin levels was slower in neonates with GS. These results confirm the idea that GS is one of the factors contributing to neonatal hyperbilirubinemia, but that other factors play a role in determining neonatal jaundice. The slower decrease of bilirubin levels in A(TA)7TAA homozygous neonates confirms that GS is an important factor in determining a prolonged neonatal jaundice.
Copyright © 2002 by Walter de Gruyter GmbH & Co. KG
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Articles in the same Issue
- Vitamin A supplementation ameliorates butyric acid-induced intestinal mucosal injury in newborn rats
- Effect of amino acids on glucose tolerance and hyperkalemia in very low birth weight infants
- Steroidogenesis patterns in common trisomies
- A weighted risk index for antenatal prediction of perinatal outcome
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- HPA-1 carrier status and thrombocytopenia in preterm infants with a birth weight below 1500 grams
- Sacrococcygeal teratoma. Outcome and management. An analysis of 17 cases
- Treatment of severe cholestasis in neonatal Dubin-Johnson syndrome with ursodeoxycholic acid
- Urinary bladder perforation in a very low birth weight infant. A case report
- Book review
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