Genetic Polymorphism of Angiotensin-Converting Enzyme and Chronic Obstructive Pulmonary Disease Risk: An Updated Meta-Analysis.

Sang Wook Kang,Jinju Kim,Joo-Ho Chung,Kwan-Il Kim,Hee-Jae Jung,Su Kang Kim,Ju Yeon Ban

doi:10.1155/2016/7636123

Abstract

The relationship between polymorphism of the angiotensin I converting enzyme (ACE) gene and chronic obstructive pulmonary disease (COPD) has been examined in many previous studies. However, their results were controversial. Therefore, we performed a meta-analysis to evaluate the relationship between the ACE gene and the risk of COPD. Fourteen case-control studies were included in this meta-analysis. The pooled p value, odds ratio (OR), and 95% confidence interval (95% CI) were used to investigate the strength of the association. The meta-analysis was performed using comprehensive meta-analysis software. Our meta-analysis results revealed that ACE polymorphisms were not related to the risk of COPD (p > 0.05 in each model). In further analyses based on ethnicity, we observed an association between insertion/deletion polymorphism of the ACE gene and risk of COPD in the Asian population (codominant 2, OR = 3.126, 95% CI = 1.919–5.093, p < 0.001; recessive, OR = 3.326, 95% CI = 2.190–5.050, p < 0.001) but not in the Caucasian population (p > 0.05 in each model). In conclusion, the present meta-analysis indicated that the insertion/deletion polymorphism of the ACE gene may be associated with susceptibility to COPD in the Asian population but not in the Caucasian population. However, the results of the present meta-analysis need to be confirmed in a larger sample.

Highlights

chronic obstructive pulmonary disease (COPD) is a serious disease which is characterized by destruction of the lung parenchyma and inflammation of the peripheral airways [1]
Insertion/ deletion polymorphism of the angiotensin I converting enzyme (ACE) gene did not show any significant association with susceptibility to COPD in each model, respectively (p > 0.05, Table 2)
ACE insertion/deletion polymorphism is associated with serum ACE levels [20] and D allele is related to increased formation of angiotensin II [38]

Summary

Introduction

COPD is a serious disease which is characterized by destruction of the lung parenchyma and inflammation of the peripheral airways [1]. The Global Burden of Disease (GBD) study reported that COPD was the sixth leading cause of death in 1990 and the fourth leading cause of death in 2000 [4]. Cigarette smoking is known to be the major cause of COPD, but some COPD cases cannot be explained by smoking alone [6]. Environmental exposure such as occupational exposures [7] and indoor biomass fuel burning [8] is closely related to the development of COPD. Many previous studies have reported the association between genetic factors and COPD susceptibility. Previous family and twin studies have shown the role of genetic factors in COPD susceptibility [9]. Some authors have used genetic polymorphisms to explain the genetic contribution to the development of COPD, and several candidate genes such as proteinase-activated receptor-1 [10], plasminogen activator inhibitor-1 [11], and β2-adrenergic receptor [12] were reported to have an association with COPD susceptibility

Methods

Results

Conclusion