Assessment of insertion/deletion polymorphism of the angiotensin-converting enzyme gene in abdominal aortic aneurysm and inguinal hernia

Vascular. 2013 Feb;21(1):1-5. doi: 10.1258/vasc.2011.oa0322. Epub 2012 Jan 23.

Abstract

The aim of the paper is to determine whether the angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism is associated with abdominal aortic aneurysm (AAA) and inguinal hernia. A case-control study was conducted in 264 subjects: 65 patients with AAA, 91 patients with inguinal hernia, 19 patients with both AAA and hernia, and 89 controls were investigated for the ACE I/D polymorphism. Genotype analysis was performed using a polymerase chain reaction technique. Significant differences in the genotype between the patient groups and controls were identified (aneurysm versus control, P = 0.011; aneurysm plus hernia versus control, P = 0.022; hernia versus control, P = 0.001), whereas no differences were found within patient groups. Patients with AAA and/or hernia had an increased prevalence of I/D heterozygosity, which persisted even after adjusting for differences in confounding clinical variables (aneurysm versus control, OR 0.3, 95% CI 0.2-0.8, P = 0.005; aneurysm plus hernia versus control, OR 0.3, 95% CI 0.1-0.9, P = 0.040; hernia versus control, OR 0.4, 95% CI 0.2-0.7, P = 0.004). In conclusion, an association between the heterozygote ACE I/D state and the presence of AAA and/or hernia was identified. The role of the ACE I/D polymorphism in aneurysm and hernia needs further investigation.

Publication types

  • Multicenter Study

MeSH terms

  • Aged
  • Analysis of Variance
  • Aortic Aneurysm, Abdominal / enzymology
  • Aortic Aneurysm, Abdominal / genetics*
  • Case-Control Studies
  • Chi-Square Distribution
  • Gene Frequency
  • Genetic Predisposition to Disease
  • Greece
  • Hernia, Inguinal / enzymology
  • Hernia, Inguinal / genetics*
  • Heterozygote
  • Humans
  • Logistic Models
  • Male
  • Middle Aged
  • Odds Ratio
  • Phenotype
  • Polymerase Chain Reaction
  • Polymorphism, Genetic*
  • Risk Factors