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The influence of polymorphic GSTM1 gene on the increased susceptibility of non-viral hepatic cirrhosis: evidence from observational studies

It is reported that glutathione S-transferase mu (GSTM1) polymorphism is associated with non-viral hepatic cirrhosis (HC). However, some studies showed different views. Therefore, in this paper, a meta-analysis was conducted to get a more comprehensive understanding of GSTM1 polymorphisms in non-vir...

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Autores principales: Gu, Ye, Zhao, Jing, Ao, Li, Ma, Jianning, Bao, Kena, Liu, Min, Huang, Weiping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6011196/
https://www.ncbi.nlm.nih.gov/pubmed/29921322
http://dx.doi.org/10.1186/s40001-018-0331-z
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author Gu, Ye
Zhao, Jing
Ao, Li
Ma, Jianning
Bao, Kena
Liu, Min
Huang, Weiping
author_facet Gu, Ye
Zhao, Jing
Ao, Li
Ma, Jianning
Bao, Kena
Liu, Min
Huang, Weiping
author_sort Gu, Ye
collection PubMed
description It is reported that glutathione S-transferase mu (GSTM1) polymorphism is associated with non-viral hepatic cirrhosis (HC). However, some studies showed different views. Therefore, in this paper, a meta-analysis was conducted to get a more comprehensive understanding of GSTM1 polymorphisms in non-viral HC susceptibility. The results showed that GSTM1 null was associated with the increased risk of non-viral HC (OR = 1.337, 95% CI 1.112–1.804, p = 0.005). Subgroup analysis of cirrhosis type revealed that GSTM1 null was a prominent risk factor for alcoholic HC (OR = 1.416, 95% CI 1.112–1.804, p = 0.005). Meanwhile, subgroup analysis of population indicated that the significant differences only existed in Asian population (OR = 1.719, 95% CI 1.212–2.438, p = 0.002). In hospital-based studies, patients with GSTM1 null were more likely in risk of HC (OR = 1.426, 95% CI 1.092–1.863, p = 0.009). Subgroup analysis using genotyping method showed a significant association between GSTM1 null genotype and HC occurrence in the studies employing the multiple PCR genotyping method (OR = 1.559, 95% CI 1.171–2.076, p = 0.002). Based on the results of this analysis, it was concluded that GSTM1 null genotype could increase the susceptibility of non-viral hepatic cirrhosis. In addition, alcohol intake, Asian ethnicity, sample source from hospital and multiple PCR genotyping method may also influence the susceptibility of hepatic cirrhosis.
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spelling pubmed-60111962018-06-27 The influence of polymorphic GSTM1 gene on the increased susceptibility of non-viral hepatic cirrhosis: evidence from observational studies Gu, Ye Zhao, Jing Ao, Li Ma, Jianning Bao, Kena Liu, Min Huang, Weiping Eur J Med Res Review It is reported that glutathione S-transferase mu (GSTM1) polymorphism is associated with non-viral hepatic cirrhosis (HC). However, some studies showed different views. Therefore, in this paper, a meta-analysis was conducted to get a more comprehensive understanding of GSTM1 polymorphisms in non-viral HC susceptibility. The results showed that GSTM1 null was associated with the increased risk of non-viral HC (OR = 1.337, 95% CI 1.112–1.804, p = 0.005). Subgroup analysis of cirrhosis type revealed that GSTM1 null was a prominent risk factor for alcoholic HC (OR = 1.416, 95% CI 1.112–1.804, p = 0.005). Meanwhile, subgroup analysis of population indicated that the significant differences only existed in Asian population (OR = 1.719, 95% CI 1.212–2.438, p = 0.002). In hospital-based studies, patients with GSTM1 null were more likely in risk of HC (OR = 1.426, 95% CI 1.092–1.863, p = 0.009). Subgroup analysis using genotyping method showed a significant association between GSTM1 null genotype and HC occurrence in the studies employing the multiple PCR genotyping method (OR = 1.559, 95% CI 1.171–2.076, p = 0.002). Based on the results of this analysis, it was concluded that GSTM1 null genotype could increase the susceptibility of non-viral hepatic cirrhosis. In addition, alcohol intake, Asian ethnicity, sample source from hospital and multiple PCR genotyping method may also influence the susceptibility of hepatic cirrhosis. BioMed Central 2018-06-19 /pmc/articles/PMC6011196/ /pubmed/29921322 http://dx.doi.org/10.1186/s40001-018-0331-z Text en © The Author(s) 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Review
Gu, Ye
Zhao, Jing
Ao, Li
Ma, Jianning
Bao, Kena
Liu, Min
Huang, Weiping
The influence of polymorphic GSTM1 gene on the increased susceptibility of non-viral hepatic cirrhosis: evidence from observational studies
title The influence of polymorphic GSTM1 gene on the increased susceptibility of non-viral hepatic cirrhosis: evidence from observational studies
title_full The influence of polymorphic GSTM1 gene on the increased susceptibility of non-viral hepatic cirrhosis: evidence from observational studies
title_fullStr The influence of polymorphic GSTM1 gene on the increased susceptibility of non-viral hepatic cirrhosis: evidence from observational studies
title_full_unstemmed The influence of polymorphic GSTM1 gene on the increased susceptibility of non-viral hepatic cirrhosis: evidence from observational studies
title_short The influence of polymorphic GSTM1 gene on the increased susceptibility of non-viral hepatic cirrhosis: evidence from observational studies
title_sort influence of polymorphic gstm1 gene on the increased susceptibility of non-viral hepatic cirrhosis: evidence from observational studies
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6011196/
https://www.ncbi.nlm.nih.gov/pubmed/29921322
http://dx.doi.org/10.1186/s40001-018-0331-z
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