Please use this identifier to cite or link to this item: https://hdl.handle.net/11499/9200
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dc.contributor.authorHalis, Hülya-
dc.contributor.authorErgin, Hacer-
dc.contributor.authorKöseler, Aylin-
dc.contributor.authorAtalay, Erol Ömer-
dc.date.accessioned2019-08-16T12:58:54Z-
dc.date.available2019-08-16T12:58:54Z-
dc.date.issued2017-
dc.identifier.issn1476-7058-
dc.identifier.urihttps://hdl.handle.net/11499/9200-
dc.identifier.urihttps://doi.org/10.1080/14767058.2016.1261105-
dc.description.abstractObjective: In the present study, we investigated the effects of promoter polymorphism and an exon-1 mutation (G71R) in the UGT1A1 gene in neonates with unexplained hyperbilirubinemia and direct Coombs-negative [DC(-)] ABO incompatibility. Methods: Two-hundred term neonates in their first week of life and without additional icterogenic factors were included in the study. Neonates with a serum total bilirubin (STB) level ?17 mg/dL constituted the hyperbilirubinemia group (n = 100), while the control group comprised healthy neonates with a STB level <12.9 mg/dL (n = 100). The cases were further subdivided into unexplained hyperbilirubinemia (n = 50), ABO(+) hyperbilirubinemia (n = 50), ABO(-) control (n = 50), and ABO(+) control (n = 50) groups on the basis of the presence or absence of DC(-) ABO incompatibility. DNA was isolated from peripheral blood and amplified by PCR, and UGT1A1 gene promoter and exon-1 were sequenced to verify sequence alterations. Results: The frequency of TA6/6, TA6/7, TA7/7, and GGA/GGA, GGA/AGA, AGA/AGA genotypes was found to be 63.5%, 21%, 15.5%, and 91.5%, 8%, 0.5%, respectively. While both heterozygous and homozygous TA7 polymorphism increased risk of hyperbilirubinemia in the ABO(+) hyperbilirubinemia group (heterozygous OR 16.76, 95% CI:3.52-79.70, p < 0.0001; homozygous OR 6.81, 95% CI:1.98-23:42, p = 0.002), only heterozygous TA7 polymorphism increased jaundice risk (OR 5.0895% CI:76-14.65, p = 0.003) in unexplained hyperbilirubinemia. But, the coexistence of G71R mutation and promoter polymorphism or G71R mutation and DC(-) ABO incompatibility did not increase the severity of hyperbilirubinemia (p > 0.05). Conclusions: UGT1A1 gene promoter polymorphism and G71R mutation are possible risk factors for Turkish neonates with DC(-) ABO incompatibility and unexplained hyperbilirubinemia. © 2017 Informa UK Limited, trading as Taylor & Francis Group.en_US
dc.language.isoenen_US
dc.publisherTaylor and Francis Ltden_US
dc.relation.ispartofJournal of Maternal-Fetal and Neonatal Medicineen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectExon-1 mutationen_US
dc.subjectHyperbilirubinemiaen_US
dc.subjectPromoter polymorphismen_US
dc.subjectadenineen_US
dc.subjectbilirubinen_US
dc.subjectDNAen_US
dc.subjectglucuronosyltransferase 1A1en_US
dc.subjectguanineen_US
dc.subjectglucuronosyltransferaseen_US
dc.subjectUGT1A1 enzymeen_US
dc.subjectArticleen_US
dc.subjectbilirubin blood levelen_US
dc.subjectblood group ABO incompatibilityen_US
dc.subjectcontrolled studyen_US
dc.subjectdisease severityen_US
dc.subjectDNA polymorphismen_US
dc.subjectexonen_US
dc.subjectfemaleen_US
dc.subjectgene frequencyen_US
dc.subjectgene functionen_US
dc.subjectgene mutationen_US
dc.subjectgene sequenceen_US
dc.subjectgenotypeen_US
dc.subjectgestational ageen_US
dc.subjectheterozygoteen_US
dc.subjecthomozygoteen_US
dc.subjecthumanen_US
dc.subjectmajor clinical studyen_US
dc.subjectmaleen_US
dc.subjectneonatal hyperbilirubinemiaen_US
dc.subjectnewbornen_US
dc.subjectnewborn jaundiceen_US
dc.subjectpolymerase chain reactionen_US
dc.subjectpriority journalen_US
dc.subjectpromoter regionen_US
dc.subjectTurk (people)en_US
dc.subjectUGT1A1 geneen_US
dc.subjectblooden_US
dc.subjectblood group ABO systemen_US
dc.subjectblood group incompatibilityen_US
dc.subjectcase control studyen_US
dc.subjectgenetic polymorphismen_US
dc.subjectgenetic predispositionen_US
dc.subjectgeneticsen_US
dc.subjectimmunologyen_US
dc.subjectmutationen_US
dc.subjectpregnancyen_US
dc.subjectABO Blood-Group Systemen_US
dc.subjectBlood Group Incompatibilityen_US
dc.subjectCase-Control Studiesen_US
dc.subjectExonsen_US
dc.subjectFemaleen_US
dc.subjectGenetic Predisposition to Diseaseen_US
dc.subjectGestational Ageen_US
dc.subjectGlucuronosyltransferaseen_US
dc.subjectHumansen_US
dc.subjectHyperbilirubinemia, Neonatalen_US
dc.subjectInfant, Newbornen_US
dc.subjectJaundice, Neonatalen_US
dc.subjectMaleen_US
dc.subjectMutationen_US
dc.subjectPolymorphism, Geneticen_US
dc.subjectPregnancyen_US
dc.subjectPromoter Regions, Geneticen_US
dc.subjectTurkeyen_US
dc.titleThe role of UGT1A1 promoter polymorphism and exon-1 mutations in neonatal jaundiceen_US
dc.typeArticleen_US
dc.identifier.volume30en_US
dc.identifier.issue22en_US
dc.identifier.startpage2658-
dc.identifier.startpage2658en_US
dc.identifier.endpage2664en_US
dc.authorid0000-0003-4832-0436-
dc.authorid36835035474-
dc.authorid0000-0001-6272-9380-
dc.identifier.doi10.1080/14767058.2016.1261105-
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.identifier.pmid27842454en_US
dc.identifier.scopus2-s2.0-85011798892en_US
dc.identifier.wosWOS:000417425800003en_US
dc.identifier.scopusqualityQ2-
dc.ownerPamukkale University-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeArticle-
item.fulltextNo Fulltext-
item.languageiso639-1en-
item.grantfulltextnone-
item.cerifentitytypePublications-
crisitem.author.dept14.02. Internal Medicine-
crisitem.author.dept14.02. Internal Medicine-
crisitem.author.dept14.03. Basic Medical Sciences-
crisitem.author.dept14.03. Basic Medical Sciences-
Appears in Collections:PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Tıp Fakültesi Koleksiyonu
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection
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