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首页> 外文期刊>Journal of Clinical and Diagnostic Research >Relation Between Neonatal Icter And Gilbert Syndrome in Gloucose-6-Phosphate Dehydrogenase Deficient Subjects
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Relation Between Neonatal Icter And Gilbert Syndrome in Gloucose-6-Phosphate Dehydrogenase Deficient Subjects

机译：葡糖-6磷酸脱氢酶缺乏症患者新生儿黄疸与吉尔伯特综合征的关系

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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.
机译：背景与目的：缺乏葡萄糖6磷酸脱氢酶（G6PD）的新生儿尚未完全确定新生儿高胆红素血症的发病机理。这项研究的目的是检测缺乏葡萄糖6磷酸脱氢酶（G6PD）的新生儿的吉尔伯特综合征和高胆红素血症之间的关系。材料与方法：本病例对照研究在伊朗巴博尔Amirkola儿科教学医院进行。 。该研究共纳入104例婴儿（其中选择了接受光疗或输血的51例新生儿黄疸和6磷酸葡糖脱氢酶（G6PD）缺乏症的婴儿作为病例组，53例6磷酸葡糖的婴儿。以黄疸以外的其他原因入院的脱氢酶（G6PD）缺乏症为对照组。排除标准是ABO或Rh不相容或其他使Coombs测试呈阳性，败血症，肝脾肿大，代谢性疾病，药物治疗和光疗的原因。通过从白细胞分离的聚合酶链反应（PCR）扩增基因组DNA的尿苷二磷酸葡萄糖苷葡萄糖苷基转移酶1A1（UGT1A1）的启动子和编码区。结果：两组之间的Gilbert基因组分布无显着差异。在这些病例中，纯合子为33.3％，杂合子为35.3％，正常为31.4％。在对照组中，纯合子为22.6％，杂合子为34％，正常为43.4％（p值= xxx）。两组之间的高胆红素血症家族史无显着差异。结论：我们显示，在葡萄糖6磷酸脱氢酶（G6PD）缺陷型新生儿中，吉尔伯特综合征（启动子多态性）与高胆红素血症之间无显着关联。

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