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Association of LPP and TAGAP Polymorphisms with Celiac Disease Risk: A Meta-Analysis

Background: Lipoma preferred partner (LPP) and T-cell activation Rho GTPase activating protein (TAGAP) polymorphisms might influence the susceptibility to celiac disease. Therefore, we performed a meta-analysis by identifying relevant studies to estimate the risks of these polymorphisms on celiac di...

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Detalles Bibliográficos
Autores principales: Huang, Shi-Qi, Zhang, Na, Zhou, Zi-Xing, Huang, Chui-Can, Zeng, Cheng-Li, Xiao, Di, Guo, Cong-Cong, Han, Ya-Jing, Ye, Xiao-Hong, Ye, Xing-Guang, Ou, Mei-Ling, Zhang, Bao-Huan, Liu, Yang, Zeng, Eddy Y., Yang, Guang, Jing, Chun-Xia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5334725/
https://www.ncbi.nlm.nih.gov/pubmed/28208589
http://dx.doi.org/10.3390/ijerph14020171
Descripción
Sumario:Background: Lipoma preferred partner (LPP) and T-cell activation Rho GTPase activating protein (TAGAP) polymorphisms might influence the susceptibility to celiac disease. Therefore, we performed a meta-analysis by identifying relevant studies to estimate the risks of these polymorphisms on celiac disease. Methods: The PubMed, Web of Science and Embase databases were searched (up to October 2016) for LPP rs1464510 and TAGAP rs1738074 polymorphisms. Results: This meta-analysis included the same 7 studies for LPP rs1464510 and TAGAP rs1738074. The minor risk A allele at both rs1464510 and rs1738074 carried risks (odds ratios) of 1.26 (95% CI: 1.22–1.30) and 1.17 (95% CI: 1.14–1.21), respectively, which contributed to increased risks in all celiac disease patients by 10.72% and 6.59%, respectively. The estimated lambdas were 0.512 and 0.496, respectively, suggesting that a co-dominant model would be suitable for both gene effects. Conclusions: This meta-analysis provides robust estimates that polymorphisms in LPP and TAGAP genes are potential risk factors for celiac disease in European and American. Prospective studies and more genome-wide association studies (GWAS) are needed to confirm these findings, and some corresponding molecular biology experiments should be carried out to clarify the pathogenic mechanisms of celiac disease.