Yadollah Zahedpasha1, Mousa Ahmadpour2, Haleh Akhavan Niaki3, Ehsan Alaee4. 1. Faculty, Paediatric Research Center, Amirkola Children Hospital, Department of Paediatric, School of Medicine, Babol University of Medical Sciences , Babol, Iran . 2. Faculty, Paediatric Research Center, Amirkola Pediatrics Hospital, Department of Paediatric, School of Medicine, Babol University of Medical Sciences Babol, Iran . 3. Faculty, Cellular and Molecular Biology Research Center (CMBRC) of Babol University of Medical Sciences , Iran . 4. Neonatologist, Neonatal and Children's Health Research Center, Golestan University of Medical Sciences , Gorgan, Iran .
Abstract
BACKGROUND AND AIM: The pathogenesis of neonatal hyperbilirubinemia hasn't been completely defined in Gloucose-6-Phosphate Dehydrogenase (G6PD) deficient newborns. The aim of this study was to detect the relationship between Gilbert's syndrome and hyperbilirubinemia in Gloucose-6-Phosphate Dehydrogenase (G6PD) deficient neonates. MATERIALS AND METHODS: This case-control study was conducted in Amirkola pediatrics teaching hospital, Babol, Iran. A total number of one hundred four infants were included in the study (51 infants with neonatal jaundice and Gloucose-6-Phosphate Dehydrogenase (G6PD) deficiency admitted to phototherapy or transfusion were selected as the case group and 53 infants with Gloucose-6-Phosphate Dehydrogenase (G6PD) deficiency admitted for other reasons than jaundice were selected as the control group). Exclusion criteria were ABO or Rh incompatibility or other reasons that made Coombs test positive, sepsis, hepatosplenomegaly, metabolic diseases, medical treatment and phototherapy. The promoter and coding regions of Uridine diphosphate Glucuronosyl Transferase 1A1 (UGT1A1) of genomic DNA were amplified by polymerase chain reaction (PCR) isolated from leukocytes. We used chi-square test and t-test to compare cases and controls. RESULTS: Distribution of Gilbert genome was not significantly different between the two groups; among cases, 33.3% were homozygote, 35.3% heterozygote, and 31.4% normal. Among controls, 22.6% were homozygote, 34% heterozygote, and 43.4% normal (p-value=xxx). Hyperbilirubinemia family history didn't differ significantly between these two groups. CONCLUSIONS: We showed that in Gloucose-6-Phosphate Dehydrogenase (G6PD) deficient neonates, there was no significant association between Gilbert's syndrome (promoter polymorphism) and hyperbilirubinemia.
BACKGROUND AND AIM: The pathogenesis of neonatal hyperbilirubinemia hasn't been completely defined in Gloucose-6-Phosphate Dehydrogenase (G6PD) deficient newborns. The aim of this study was to detect the relationship between Gilbert's syndrome and hyperbilirubinemia in Gloucose-6-Phosphate Dehydrogenase (G6PD) deficient neonates. MATERIALS AND METHODS: This case-control study was conducted in Amirkola pediatrics teaching hospital, Babol, Iran. A total number of one hundred four infants were included in the study (51 infants with neonatal jaundice and Gloucose-6-Phosphate Dehydrogenase(G6PD) deficiency admitted to phototherapy or transfusion were selected as the case group and 53 infants with Gloucose-6-Phosphate Dehydrogenase(G6PD) deficiency admitted for other reasons than jaundice were selected as the control group). Exclusion criteria were ABO or Rh incompatibility or other reasons that made Coombs test positive, sepsis, hepatosplenomegaly, metabolic diseases, medical treatment and phototherapy. The promoter and coding regions of Uridine diphosphate Glucuronosyl Transferase 1A1 (UGT1A1) of genomic DNA were amplified by polymerase chain reaction (PCR) isolated from leukocytes. We used chi-square test and t-test to compare cases and controls. RESULTS: Distribution of Gilbert genome was not significantly different between the two groups; among cases, 33.3% were homozygote, 35.3% heterozygote, and 31.4% normal. Among controls, 22.6% were homozygote, 34% heterozygote, and 43.4% normal (p-value=xxx). Hyperbilirubinemia family history didn't differ significantly between these two groups. CONCLUSIONS: We showed that in Gloucose-6-Phosphate Dehydrogenase (G6PD) deficient neonates, there was no significant association between Gilbert's syndrome (promoter polymorphism) and hyperbilirubinemia.
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Authors: K Akaba; T Kimura; A Sasaki; S Tanabe; T Ikegami; M Hashimoto; H Umeda; H Yoshida; K Umetsu; H Chiba; I Yuasa; K Hayasaka Journal: Biochem Mol Biol Int Date: 1998-09
Authors: Neil A Hanchard; Jennifer Skierka; Amy Weaver; Brad S Karon; Dietrich Matern; Walter Cook; Dennis J O'Kane Journal: BMC Med Genet Date: 2011-04-22 Impact factor: 2.103