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Correlation of angiotensin I-converting enzyme gene insertion/deletion polymorphism with rheumatic heart disease: a meta-analysis
Rheumatic heart disease (RHD) is a serious cardiovascular disorder worldwide. Several articles have reported the effect of angiotensin I-converting enzyme gene insertion/deletion (ACE I/D) polymorphism in RHD risk. However, the results still remain inconsistent. The objective of the present study wa...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Portland Press Ltd.
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5293560/ https://www.ncbi.nlm.nih.gov/pubmed/27758878 http://dx.doi.org/10.1042/BSR20160151 |
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author | Tian, Yulong Ge, Zhongchun Xing, Yuliang Sun, Yan Ying, Jie |
author_facet | Tian, Yulong Ge, Zhongchun Xing, Yuliang Sun, Yan Ying, Jie |
author_sort | Tian, Yulong |
collection | PubMed |
description | Rheumatic heart disease (RHD) is a serious cardiovascular disorder worldwide. Several articles have reported the effect of angiotensin I-converting enzyme gene insertion/deletion (ACE I/D) polymorphism in RHD risk. However, the results still remain inconsistent. The objective of the present study was to assess more precise estimations of the relationship between ACE I/D variant and RHD susceptibility. Relevant case–control studies published between January 2000 and 2016 were searched in the electronic databases. The odds ratio (OR) with its 95% confidence interval (CI) was employed to calculate the strength of the effect. A total of nine articles were retrieved, including 1333 RHD patients and 1212 healthy controls. Overall, our result did not detect a significant association between ACE I/D polymorphism and RHD risk under each genetic model (P > 0.05). Subgroup analysis by ethnicity showed no positive relationship in Asians as well (P > 0.05). With respect to the severity of RHD, our result found that the frequency differences between mitral valve lesion (MVL), combined valve lesion (CVL) and healthy controls were not significantly different. Furthermore, no significant association was found between female, male RHD patients and the controls regarding to the ACE I/D polymorphism. In conclusion, our result indicated that ACE I/D polymorphism might not be a risk factor for RHD progression based on the existing research results. Additional well-designed studies with larger samples are still needed to confirm these findings. |
format | Online Article Text |
id | pubmed-5293560 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Portland Press Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-52935602017-02-14 Correlation of angiotensin I-converting enzyme gene insertion/deletion polymorphism with rheumatic heart disease: a meta-analysis Tian, Yulong Ge, Zhongchun Xing, Yuliang Sun, Yan Ying, Jie Biosci Rep Original Papers Rheumatic heart disease (RHD) is a serious cardiovascular disorder worldwide. Several articles have reported the effect of angiotensin I-converting enzyme gene insertion/deletion (ACE I/D) polymorphism in RHD risk. However, the results still remain inconsistent. The objective of the present study was to assess more precise estimations of the relationship between ACE I/D variant and RHD susceptibility. Relevant case–control studies published between January 2000 and 2016 were searched in the electronic databases. The odds ratio (OR) with its 95% confidence interval (CI) was employed to calculate the strength of the effect. A total of nine articles were retrieved, including 1333 RHD patients and 1212 healthy controls. Overall, our result did not detect a significant association between ACE I/D polymorphism and RHD risk under each genetic model (P > 0.05). Subgroup analysis by ethnicity showed no positive relationship in Asians as well (P > 0.05). With respect to the severity of RHD, our result found that the frequency differences between mitral valve lesion (MVL), combined valve lesion (CVL) and healthy controls were not significantly different. Furthermore, no significant association was found between female, male RHD patients and the controls regarding to the ACE I/D polymorphism. In conclusion, our result indicated that ACE I/D polymorphism might not be a risk factor for RHD progression based on the existing research results. Additional well-designed studies with larger samples are still needed to confirm these findings. Portland Press Ltd. 2016-11-22 /pmc/articles/PMC5293560/ /pubmed/27758878 http://dx.doi.org/10.1042/BSR20160151 Text en © 2016 The Author(s) http://creativecommons.org/licenses/by/4.0/ This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution Licence 4.0 (CC BY) (http://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Original Papers Tian, Yulong Ge, Zhongchun Xing, Yuliang Sun, Yan Ying, Jie Correlation of angiotensin I-converting enzyme gene insertion/deletion polymorphism with rheumatic heart disease: a meta-analysis |
title | Correlation of angiotensin I-converting enzyme gene insertion/deletion polymorphism with rheumatic heart disease: a meta-analysis |
title_full | Correlation of angiotensin I-converting enzyme gene insertion/deletion polymorphism with rheumatic heart disease: a meta-analysis |
title_fullStr | Correlation of angiotensin I-converting enzyme gene insertion/deletion polymorphism with rheumatic heart disease: a meta-analysis |
title_full_unstemmed | Correlation of angiotensin I-converting enzyme gene insertion/deletion polymorphism with rheumatic heart disease: a meta-analysis |
title_short | Correlation of angiotensin I-converting enzyme gene insertion/deletion polymorphism with rheumatic heart disease: a meta-analysis |
title_sort | correlation of angiotensin i-converting enzyme gene insertion/deletion polymorphism with rheumatic heart disease: a meta-analysis |
topic | Original Papers |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5293560/ https://www.ncbi.nlm.nih.gov/pubmed/27758878 http://dx.doi.org/10.1042/BSR20160151 |
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