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

Andrology. 2013 Mar;1(2):274-80. doi: 10.1111/j.2047-2927.2012.00029.x. Epub 2012 Nov 29.

Abstract

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.

Publication types

  • Meta-Analysis
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Case-Control Studies
  • Erectile Dysfunction / genetics*
  • Genetic Association Studies
  • Genetic Predisposition to Disease*
  • Humans
  • INDEL Mutation / genetics*
  • Male
  • Mutagenesis, Insertional
  • Odds Ratio
  • Peptidyl-Dipeptidase A / genetics*
  • Risk
  • Sequence Deletion

Substances

  • Peptidyl-Dipeptidase A