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Vol. 89. Issue 5.
Pages 434-443 (September - October 2013)
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Vol. 89. Issue 5.
Pages 434-443 (September - October 2013)
ARTIGO DE REVISÃO
Open Access
The impact of SLCO1B1 genetic polymorphisms on neonatal hyperbilirubinemia: a systematic review with meta-analysis
Impacto dos polimorfismos genéticos SLCO1B1 sobre a hiperbilirrubinemia neonatal: revisão sistemática com metanálise
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Jiebo Liua,
Corresponding author
jiebol@126.com

Corresponding author.
, Jun Longb, Shaofang Zhangb, Xiaoyan Fangb, Yuyuan Luob
a Doutor, Departamento de Pediatria, The Fifth People's Hospital of Shenzhen, Shenzhen, China
b Médico, Departamento de Pediatra, The Fifth People's Hospital of Shenzhen, Shenzhen, China
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Article information
Abstract
Objective

To determine whether three variants (388 G>A, 521 T>C, and 463 C>A) of the solute carrier organic anion transporter family member 1B1 (SLCO1B1) are associated with neonatal hyperbilirubinemia.

Data source

The China National Knowledge Infrastructure and MEDLINE databases were searched. The systematic review with meta-analysis included genetic studies which assessed the association between neonatal hyperbilirubinemia and 388 G>A, 521 T>C, and 463 C>A variants of SLCO1B1 between January of 1980 and December of 2012. Data selection and extraction were performed independently by two reviewers.

Summary of the findings

Ten articles were included in the study. The results revealed that SLCO1B1 388 G>A is associated with an increased risk of neonatal hyperbilirubinemia (OR, 1.39; 95% CI, 1.07–1.82) in Chinese neonates, but not in white, Thai, Latin American, or Malaysian neonates. The SLCO1B1 521 T>C mutation showed a low risk of neonatal hyperbilirubinemia in Chinese neonates, while no significant associations were found in Brazilian, white, Asian, Thai, and Malaysian neonates. There were no significant differences in SLCO1B1 463 C>A between the hyperbilirubinemia and the control group.

Conclusion

This study demonstrated that the 388 G>A mutation of the SLCO1B1 gene is a risk factor for developing neonatal hyperbilirubinemia in Chinese neonates, but not in white, Thai, Brazilian, or Malaysian populations; the SLCO1B1 521 T>C mutation provides protection for neonatal hyperbilirubinemia in Chinese neonates, but not in white, Thai, Brazilian, or Malaysian populations.

Keywords:
Genetic polymorphisms
Neonatal hyperbilirubinemia
Organic anion transport polypeptide C
Meta-analysis
Resumo
Objetivo

Determinar se três variantes (388 G>A, 521 T>C, 463 C>A) do membro 1B1da família de transportadores de ânions orgânicos portadores de solutos (SLCO1B1) se associam à hiperbilirrubinemia neonatal.

Fonte de dados

Foi realizada busca na Infraestrutura do Conhecimento Nacional da China e em MEDLINE. A revisão sistemática com metanálise incluiu estudos genéticos que avaliaram a associação entre hiperbilirrubinemia neonatal e as variantes 388 G>A, 521 T>C, 463 C>A de SLCO1B1 entre janeiro de 1980 e dezembro de 2012. Foi realizada seleção e extração de dados por dois analistas, de forma independente.

Sumário dos achados

Foram incluídos dez artigos no estudo. Os resultados revelaram que SLCO1B1 388 G>A se associa a um aumento do risco de hiperbilirrubinemia neonatal (OR< 1,39; IC 95%: 1,07 a 1,82) em recém-nascidos chineses, mas não em recém-nascidos caucasianos, tailandeses, latino-americanos ou malaios. A mutação SLCO1B1 521 T>C mostrou baixo risco de hiperbilirrubinemia neonatal em recém-nascido chineses, e não foram encontradas associações importantes no Brasil nem em recém-nascidos caucasia- nos, asiáticos, tailandeses e malaios. Não houve diferenças significativas da SLCO1B1 463 C>A entre o grupo com hiperbilirrubinemia e o grupo controle.

Conclusão

O estudo mostrou que a mutação 388 G>A do gene SLCO1B1 é fator de risco para desenvolver hiperbilirrubinemia neonatal em recém-nascidos chineses, mas não em populações caucasianas, tailandesas, brasileiras ou malaias; a mutação SLCO1B1 521 T>C fornece proteção de hiperbilirrubinemia neonatal em recém-nascidos chineses, mas não nas populações caucasianas, tailandesas, brasileiras ou malaias.

Palavras chave:
Polimorfismos genéticos
Hiperbilirrubinemia neonatal
Polipeptídeo C de transporte de ânions orgânicos
Metanálise
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Referências
[1]
B.J. Lauer, N.D. Spector.
Hyperbilirubinemia in the newborn.
Pediatr Rev., 32 (2011), pp. 341-349
[2]
N.N. Hameed, A.M. Na’ Ma, R. Vilms, V.K. Bhutani.
Severe neonatal hyperbilirubinemia and adverse short-term consequences in Baghdad, Iraq.
Neonatology., 100 (2011), pp. 57-63
[3]
Subspecialty Group of Neonatology; Society of Pediatrics; Chinese Medical Association. Clinical characteristics of bilirubin encephalopathy in Chinese newborn infants – a national multicenter survey. Zhonghua Er Ke Za Zhi. 2012;50:331-5.
[4]
M.J. Maisels.
Risk assessment and follow-up are the keys to preventing severe hyperbilirubinemia.
J Pediatr (Rio J)., 87 (2011), pp. 275-276
[5]
R. Gamaleldin, I. Iskander, I. Seoud, H. Aboraya, A. Aravkin, P.D. Sampson, et al.
Risk factors for neurotoxicity in newborns with severe neonatal hyperbilirubinemia.
Pediatrics., 128 (2011), pp. e925-e931
[6]
L. Vitek, J.D. Ostrow.
Bilirubin chemistry and metabolism; harmful and protective aspects.
Curr Pharm Des., 15 (2009), pp. 2869-2883
[7]
J. Long, S. Zhang, X. Fang, Y. Luo, J. Liu.
Neonatal hyperbilirubinemia and Gly71Arg mutation of UGT1A1 gene: a Chinese case-control study followed by systematic review of existing evidence.
Acta Paediatr., 100 (2011), pp. 966-971
[8]
J.F. Watchko, Z. Lin.
Exploring the genetic architecture of neonatal hyperbilirubinemia.
Semin Fetal Neonatal Med., 15 (2010), pp. 169-175
[9]
R.G. Tirona, B.F. Leake, G. Merino, R.B. Kim.
Polymorphisms in OATP-C: identification of multiple allelic variants associated with altered transport activity among European- and African- Americans.
J Biol Chem., 276 (2001), pp. 35669-35675
[10]
S. Setia, A. Villaveces, P. Dhillon, B.A. Mueller.
Neonatal jaundice in Asian, white, and mixed-race infants.
Arch Pediatr Adolesc Med., 156 (2002), pp. 276-279
[11]
P.F. Chang, Y.C. Lin, K. Liu, S.J. Yeh, Y.H. Ni.
Risk of hyperbilirubinemia in breast-fed infants.
J Pediatr., 159 (2011), pp. 561-565
[12]
H.X. Zhang, X. Zhao, Z. Yang, C.Y. Peng, R. Long, G.N. Li, et al.
OATP 1B1 T521C/A388G is an important polymorphism gene related to neonatal hyperbilirubinemia.
Chin J Pediatr., 48 (2010), pp. 650-655
[13]
G.Y. Tian, F.S. Xu, F.X. Zhu, F.X. Lan, Y. Han.
The association of mutations of UDP-glucuronosyl transferase 1A1 gene and organic anion transporter 2 gene with neonatal jaundice.
Chin J Neonatology., 22 (2007), pp. 193-196
[14]
M. Jiang, Y.J. Wang, J. Luo, C.Y. Yang, X.F. Yang, Y. Ma, et al.
UGT1A1 and OATP2 gene mutations in neonates from northern China with hyperbilirubinemia.
Chin J Neonatology., 27 (2012), pp. 369-372
[15]
M.J. Huang, K.E. Kua, H.C. Teng, K.S. Tang, H.W. Weng, C.S. Huang.
Risk factors for severe hyperbilirubinemia in neonates.
Pediatr Res., 56 (2004), pp. 682-689
[16]
F.L. Wong, N.Y. Boo, O. Ainoon, M.K. Wang.
Variants of organic anion transporter polypeptide 2 gene are not risk factors associated with severe neonatal hyperbilirubinemia.
Malays J Pathol., 31 (2009), pp. 99-104
[17]
S. Prachukthum, P. Nunnarumit, P. Pienvichit, A. Chuansumrit, D. Songdej, S. Kajanachumpol, et al.
Genetic polymorphisms in Thai neonates with hyperbilirubinemia.
Acta Paediatr., 98 (2009), pp. 1106-1110
[18]
J.F. Watchko, Z. Lin, R.H. Clark, A.S. Kelleher, M.W. Walker, A.R. Spitzer.
Complex multifactorial nature of significant hyperbilirubinemia in neonates.
Pediatrics., 124 (2009), pp. e868-e877
[19]
G. Büyükkale, G. Turker, M. Kasap, G. Akpınar, E. Arısoy, A. Günlemez, et al.
Neonatal hyperbilirubinemia and organic anion transporting polypeptide-2 gene mutations.
Am J Perinatol., 28 (2011), pp. 619-626
[20]
L. Alencastro de Azevedo, T. Reverbel da Silveira, C.G. Carvalho, S. Martins de Castro, R. Giugliani, U. Matte.
UGT1A1, SLCO1B1, and SLCO1B3 polymorphisms vs. neonatal hyperbilirubinemia: is there an association?.
Pediatr Res., 72 (2012), pp. 169-173
[21]
Y. Kameyama, K. Yamashita, K. Kobayashi, M. Hosokawa, K. Chiba.
Functional characterization of SLCO1B1 (OATP-C) variants, SLCO1B1*5, SLCO1B1*15 and SLCO1B1*15+C1007G, by using transient expression systems of HeLa and HEK293 cells.
Pharmacogenet Genomics., 15 (2005), pp. 513-522
[22]
S.D. Campbell, S.M. de Morais, J.J. Xu.
Inhibition of human organic anion transporting polypeptide OATP 1B1 as a mechanism of drug-induced hyperbilirubinemia.
Chem Biol Interact., 150 (2004), pp. 179-187
[23]
W. Zhang, Y.J. He, Z. Gan, L. Fan, Q. Li, A. Wang, et al.
OATP1B1 polymorphism is a major determinant of serum bilirubin level but not associated with rifampicin-mediated bilirubin elevation.
Clin Exp Pharmacol Physiol., 34 (2007), pp. 1240-1244
[24]
C. Michalski, Y. Cui, A.T. Nies, A.K. Nuessler, P. Neuhaus, U.M. Zanger, et al.
A naturally occurring mutation in the SLC21A6 gene causing impaired membrane localization of the hepatocyte uptake transporter.
J Biol Chem., 277 (2002), pp. 43058-43063

Como citar este artigo: Liu J, Long J, Zhang S, Fang X, Luo Y. The impact of SLCO1B1 genetic polymorphisms on neonatal hyperbilirubinemia: a systematic review with meta-analysis. J Pediatr (Rio J). 2013;89:434–43.

Copyright © 2013. Brasileira de Pediatria
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