The insertion/deletion (I/D) polymorphism in the angiotensin‐converting enzyme gene and erectile dysfunction risk: a meta‐analysis

Summary Erectile dysfunction (ED) is increasingly recognized as a public health problem. Several studies have reported the influence of the insertion/deletion (I/D) polymorphism in the Angiotensin‐converting enzyme (ACE) gene on ED susceptibility, but the results remain controversial. To derive a mo...

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Veröffentlicht in:Andrology (Oxford) 2013-03, Vol.1 (2), p.274-280
Hauptverfasser: Zhang, T., Li, W. L., He, X. F., Wu, Z. Y., Liu, L. H., He, S. H., Wei, A. Y.
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Sprache:eng
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Zusammenfassung:Summary Erectile dysfunction (ED) is increasingly recognized as a public health problem. Several studies have reported the influence of the insertion/deletion (I/D) polymorphism in the Angiotensin‐converting enzyme (ACE) gene on ED susceptibility, but the results remain controversial. To derive a more precise estimation of the relationship, a meta‐analysis was conducted using data published previously by other groups. A total of six case‐control studies, including 1039 cases and 927 controls, were selected. The pooled odds ratios (ORs) and respective 95% confidence intervals (CIs) were calculated by comparing the carriers of D‐allele with the wild homozygotes (ID + DD vs. II). Comparisons of other genetic models were also performed (ID + II vs. DD, DD vs. II, DI vs. II and D vs. I). In the overall analysis, no significant association between the polymorphism and ED risk was observed (OR=1.07, 95% CI = 0.84 − 1.37, p = 0.575 for ID + DD vs. II). In the subgroup analysis by ethnic, no significant association was detected among Asian, Latino and European for the comparison of ID + DD vs. II (Asian: OR=1.27, 95% CI = 0.89 − 1.81; Latino: OR=0.76, 95% CI = 0.46 − 1.27; European: OR=1.06, 95% CI = 0.67 − 1.66). Results from other comparative genetic models also indicated the lack of associations between this polymorphism and ED risk. In conclusion, this meta‐analysis indicates that the ACE I/D polymorphism might not contribute to the risk of ED.
ISSN:2047-2919
2047-2927
DOI:10.1111/j.2047-2927.2012.00029.x