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Journal of the Korean Society of Neonatology 2007;14(1):46-52.
Published online May 1, 2007.
UDP-glucuronosyltransferase 1A1 Gene Polymorphism in Severe Neonatal Hyperbilirubinemia.
Je Deok Jeon, Heui Seung Jo, Seong Gyu Lee, Sung Hwan Byun, Joong Suk Yeo, Yeon Hwa Ahn, Soo Hee Chang, Se Young Kim, Jong Woon Choi
1Department of Pediatrics, Bundang Jesaeng General Hospital, Sungnam, Korea. jo@dmc.or.kr
2Department of Laboratory Medicine, Bundang Jesaeng General Hospital, Sungnam, Korea.
UDP-glucuronosyltransferase 1A1 유전자 촉진자 부위의 다형성이 출생 초기의 심한 신생아 황달에 미치는 영향
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2
Abstract
PURPOSE
TATA box mutation/polymorphism in the promoter region of the bilirubin uridinediphosphoglucuronate glucuronosyltransferase 1A1 (UGT-1A1) gene is known to be an etiology of hyperbilirubinemia. This study examined if a TATA box mutation/polymorphism in UGT-1A1 gene promoter could be associated with the development of severe early neonatal jaundice in Korean infants.
METHODS
Thirty-nine neonatal jaundice patients and 40 controlled infants were analyzed for UGT-1A1 promoter genotypes by using DNA sequencing.
RESULTS
The homozygote for (TA)7TAA mutation was not found in this study. Comparison of the prevalence of UGT-1A1 promoter (TA)7TAA heterozygotes revealed no difference between the group with jaundice and the controlled group (15.4% vs. 10%). The peak bilirubin level was higher and the onset of jaundice was earlier in the jaundice group with (TA)7TAA heterozygote compared to the jaundice group without (TA)7TAA heterozygote (23.2+/-1.0 mg/dL vs. 19.7+/-2.4 mg/dL, P=0.004, 5.0+/-1.5 days vs. 8.3+/-4.1 days, P= 0.057).
CONCLUSION
The results of this study showed that TATA box polymorphism in UGT-1A1 gene promoter did not increase the prevalence of severe early neonatal jaundice in Korean infants.
Key Words: Uridinediphosphoglucuronate glucuronosyltransferase 1A1 (UGT-1A1) gene, Promoter, Mutation, Neonatal jaundice


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