乙醇脱氢酶 1C 基因多态性与酒精性肝硬化易感性的 Meta 分析
| 作者: |
1何晶晶,
1张岭漪,
2张亚武,
2张有成
1 兰州大学第二医院 肝病科，甘肃 兰州 730030 2 兰州大学第二医院 普通外科，甘肃 兰州 730030 |
| 通讯: |
张有成
Email: hanxw2016@126.com |
| DOI: | 10.3978/.2018.07.011 |
| 基金: | 甘肃省兰州市科技计划资助项目（2012-1-29）。 |
摘要
目的：采用 Meta 分析的方法定量评价乙醇脱氢酶 1C（ADH1C）基因多态性与酒精性肝硬化（ALC）易感性的关系。
方法：计算机检索多个国内外数据库，搜索相关的病例对照研究，检索时间截止 2017 年 10 月。采用Stata 12.0 软件进行统计分析。
结果：共纳入 14 篇病例对照研究，其中病例组 1 457 例，对照组 2 715 例。全组分析结果显示，在等位基因模型（OR=1.17，95% CI=1.02~1.34，P=0.013）、 杂合子模型（OR=1.39，95% CI=1.16~1.66， P=0.035）、 纯合子模型（OR=1.27，95% CI=1.02~1.58，P=0.036） 及显性模型（OR=1.37，95% CI= 1.16~1.63，P=0.027）中 ALC 的发病风险明显升高，而在隐性模型（OR=1.19，95% CI=0.98~1.44， P=0.052）中 ALC 发病风险无明显变化。亚组分析结果显示，亚洲人群在等位基因模型（OR=1.43，95% CI= 1.07~1.90，P=0.037）、杂合子模型（OR=1.53，95% CI=1.14~2.04，P=0.034）、纯合子模型（OR=1.52， 95% CI=1.05~2.18，P=0.036）、显性模型（OR=1.52，95% CI=1.14~2.03，P=0.039）及隐性模型（OR=1.51， 95% CI=1.08~2.11，P=0.016）中 ALC 发病风险均升高，而高加索人群仅在杂合子模型（OR=1.31， 95% CI=1.04~1.64，P=0.038） 及显性模型（OR=1.30，95% CI=1.05~1.60，P=0.022） 中 ALC 发病风险升高。
结论：ADH1C 基因多态性与 ALC 的易感性密切相关，携带突变杂合子、突变纯合子基因型及突变等位基因型的人群罹患 ALC 的风险可能增加。
关键词：
肝硬化，酒精性；醇脱氢酶；多态性，单核苷酸；Meta 分析
方法：计算机检索多个国内外数据库，搜索相关的病例对照研究，检索时间截止 2017 年 10 月。采用Stata 12.0 软件进行统计分析。
结果：共纳入 14 篇病例对照研究，其中病例组 1 457 例，对照组 2 715 例。全组分析结果显示，在等位基因模型（OR=1.17，95% CI=1.02~1.34，P=0.013）、 杂合子模型（OR=1.39，95% CI=1.16~1.66， P=0.035）、 纯合子模型（OR=1.27，95% CI=1.02~1.58，P=0.036） 及显性模型（OR=1.37，95% CI= 1.16~1.63，P=0.027）中 ALC 的发病风险明显升高，而在隐性模型（OR=1.19，95% CI=0.98~1.44， P=0.052）中 ALC 发病风险无明显变化。亚组分析结果显示，亚洲人群在等位基因模型（OR=1.43，95% CI= 1.07~1.90，P=0.037）、杂合子模型（OR=1.53，95% CI=1.14~2.04，P=0.034）、纯合子模型（OR=1.52， 95% CI=1.05~2.18，P=0.036）、显性模型（OR=1.52，95% CI=1.14~2.03，P=0.039）及隐性模型（OR=1.51， 95% CI=1.08~2.11，P=0.016）中 ALC 发病风险均升高，而高加索人群仅在杂合子模型（OR=1.31， 95% CI=1.04~1.64，P=0.038） 及显性模型（OR=1.30，95% CI=1.05~1.60，P=0.022） 中 ALC 发病风险升高。
结论：ADH1C 基因多态性与 ALC 的易感性密切相关，携带突变杂合子、突变纯合子基因型及突变等位基因型的人群罹患 ALC 的风险可能增加。
Meta-analysis of relationship between alcohol dehydrogenase 1C polymorphisms and susceptibility to alcoholic liver cirrhosis
CorrespondingAuthor:Youcheng ZHANG Email: hanxw2016@126.com
Abstract
Objective: To assess the relations of alcohol dehydrogenase 1C (ADH1C) gene polymorphisms with the susceptibility to alcoholic liver cirrhosis (ALC) through Meta-analysis.
Methods: The relevant case-control studies were retrieved by searching several national and international databases from their inception to October 2017. Statistical analyses were performed by using Stata 12.0 software.
Results: A total of 14 case-control studies were included, involving 1 457 patients in case group and 2 715 subjects in control group. Results of the entire group showed that the risk of ALC was significantly increased in allele model (OR=1.17, 95% CI=1.02–1.34, P=0.013), heterozygous model (OR=1.39, 95% CI=1.16–1.66, P=0.035), homozygous model (OR=1.27, 95%CI=1.02–1.58, P=0.036) and dominant model (OR=1.37, 95% CI=1.16–1.63, P=0.027), but had no significant change in recessive model (OR=1.19, 95% CI=0.98–1.44, P=0.052). Results of subgroup analysis showed that the risk of ALC among Asian populations was increased in allele model (OR=1.43, 95% CI=1.07–1.90, P=0.037), heterozygous model (OR=1.53, 95%CI=1.14–2.04, P=0.034), homozygous model (OR=1.52, 95% CI=1.05–2.18, P= 0.036), dominant model (OR=1.52, 95% CI=1.14–2.03, P=0.039) and recessive model (OR=1.51, 95% CI=1.08–2.11, P=0.016), while an increased risk of ALC was only found in heterozygous model (OR=1.31, 95% CI=1.04–1.64, P=0.038) and dominant model (OR=1.30, 95% CI=1.05–1.60, P=0.022) among Caucasian populations.
Conclusion: ADH1C gene polymorphism is closely related to ALC susceptibility, and those with heterozygous mutation, homozygous mutation and mutant allele genotype may have increased risk of ALC.
Keywords：
Liver Cirrhosis
Alcoholic; Alcohol Dehydrogenase; Polymorphism
Single Nucleotide; Meta-Analysis
Methods: The relevant case-control studies were retrieved by searching several national and international databases from their inception to October 2017. Statistical analyses were performed by using Stata 12.0 software.
Results: A total of 14 case-control studies were included, involving 1 457 patients in case group and 2 715 subjects in control group. Results of the entire group showed that the risk of ALC was significantly increased in allele model (OR=1.17, 95% CI=1.02–1.34, P=0.013), heterozygous model (OR=1.39, 95% CI=1.16–1.66, P=0.035), homozygous model (OR=1.27, 95%CI=1.02–1.58, P=0.036) and dominant model (OR=1.37, 95% CI=1.16–1.63, P=0.027), but had no significant change in recessive model (OR=1.19, 95% CI=0.98–1.44, P=0.052). Results of subgroup analysis showed that the risk of ALC among Asian populations was increased in allele model (OR=1.43, 95% CI=1.07–1.90, P=0.037), heterozygous model (OR=1.53, 95%CI=1.14–2.04, P=0.034), homozygous model (OR=1.52, 95% CI=1.05–2.18, P= 0.036), dominant model (OR=1.52, 95% CI=1.14–2.03, P=0.039) and recessive model (OR=1.51, 95% CI=1.08–2.11, P=0.016), while an increased risk of ALC was only found in heterozygous model (OR=1.31, 95% CI=1.04–1.64, P=0.038) and dominant model (OR=1.30, 95% CI=1.05–1.60, P=0.022) among Caucasian populations.
Conclusion: ADH1C gene polymorphism is closely related to ALC susceptibility, and those with heterozygous mutation, homozygous mutation and mutant allele genotype may have increased risk of ALC.