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Glutathione S-Transferase Gene Polymorphisms in Neonatal Hyperbilirubinemia

BackgroundGlutathione S-transferases (GSTs) are a polymorphic superfamily of multifunctional enzymes known to play an important role in the detoxification of several substances. GSTM1 and GSTT1 are present in the liver in relatively high levels. Polymorphisms of the GSTM1 and GSTT1 genes may affect...

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Bibliographic Details
Published in:Journal of investigative medicine 2012-01, Vol.60 (1), p.18-22
Main Authors: Abdel Ghany, Eman Abdel Ghany, Hussain, Nouran Fahmy, Botros, Shahira Kamal Anis
Format: Article
Language:English
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Summary:BackgroundGlutathione S-transferases (GSTs) are a polymorphic superfamily of multifunctional enzymes known to play an important role in the detoxification of several substances. GSTM1 and GSTT1 are present in the liver in relatively high levels. Polymorphisms of the GSTM1 and GSTT1 genes may affect ligandin functions that are important in bilirubin transportation.ObjectiveThe aim of this study was to investigate the role of GSTM1 and GSTT1 gene polymorphisms as risk factors for neonatal jaundice.MethodsThis study was conducted on 72 neonates with pathologic hyperbilirubinemia (bilirubin >15 mg/dL) and 112 neonates with bilirubin level less than 15 mg/dL as a control group. GSTM1 and GSTT1 genotypes were assessed by multiplex polymerase chain reaction.Results GSTM1 null genotype was significantly higher in the patient compared with control groups (P = 0.005; odds ratio = 2.43; 95% confidence interval, 1.29–4.55) and was significantly associated with higher bilirubin levels compared with the wild genotype (P < 0.001). There was no statistically significant difference in the GSTT1 genotypes between the patient and the control groups. In the patient group, total bilirubin levels did not vary significantly among the null and wild GSTT1 genotypes (P = 0.108).ConclusionsNeonates with the GSTM1 null genotype are at high risk to develop pathologic hyperbilirubinemia and may have higher bilirubin levels.
ISSN:1081-5589
1708-8267
DOI:10.2310/JIM.0b013e318235479a