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Apolipoprotein A1 polymorphisms and risk of coronary artery disease: a meta-analysis

INTRODUCTION: It has been reported that APOA1 –75G/A polymorphism might be associated with susceptibility to coronary artery disease (CAD). Owing to mixed and inconclusive results, we conducted a meta-analysis to systematically summarize and clarify the association between APOA1-75G/A polymorphism a...

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Detalles Bibliográficos
Autores principales: Xu, Lang-Biao, Zhou, Ya-Feng, Yao, Jia-Lu, Sun, Si-Jia, Rui, Qing, Yang, Xiang-Jun, Li, Xiao-Bo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5510497/
https://www.ncbi.nlm.nih.gov/pubmed/28721149
http://dx.doi.org/10.5114/aoms.2017.65233
Descripción
Sumario:INTRODUCTION: It has been reported that APOA1 –75G/A polymorphism might be associated with susceptibility to coronary artery disease (CAD). Owing to mixed and inconclusive results, we conducted a meta-analysis to systematically summarize and clarify the association between APOA1-75G/A polymorphism and the risk of CAD. MATERIAL AND METHODS: A systematic search of studies on the association of single nucleotide polymorphisms (SNP) with susceptibility to CAD was conducted. A total of 9 case-control studies (1864 cases and 1196 controls) on the APOA1-75G/A polymorphism were included. RESULTS: We observed no statistically significant association between APOA1 –75G/A polymorphism and risk of CAD under the dominant genetic model (AA + AG vs. GG: OR = 1.03, 95% CI: 0.65–1.66), allelic contrast (A vs. G: OR = 0.88, 95% CI: 0.58–1.32), heterozygote model (AG vs. GG: OR = 1.24, 95% CI: 0.81–1.89) or homozygote model (AA vs. GG: OR = 0.52, 95% CI: 0.26–1.05). Significant heterogeneity between individual studies appears in all five models, but a strong association under the recessive genetic model (AA vs. AG + GG: OR = 0.51, 95% CI: 0.28–0.92). In the subgroup analysis by Hardy-Weinberg equilibrium (HWE; the presence or absence of HWE in controls), significantly decreased CAD risk and no significant heterogeneity were observed among controls consistent with HWE. Overall, the APOA1 A allele is one of the protective factors of CAD. A stronger association between APOA1-75G/A polymorphisms and CAD risk was present in the studies consistent with HWE. CONCLUSIONS: The minor allele of the APOA1-75G/A polymorphism is a protective factor for CAD, especially in the studies consistent with HWE.