No association between the angiotensin-converting-enzyme gene insertion/deletion polymorphism and the occurrence of macroangiopathy in patients with diabetes mellitus type 2

Horm Metab Res. 2003 Jan;35(1):43-7. doi: 10.1055/s-2003-38390.

Abstract

Previous studies have reported an association between the ACE-I/D-polymorphism and coronary heart disease (CHD) in patients with diabetes mellitus. However, ACE inhibitor treatment, which could have compensated for negative effects of the D/D form of the ACE gene polymorphism, was not considered in the studies. We investigated the influence of the ACE-I/D polymorphism and the ACE inhibitor treatment in patients with diabetes mellitus on the occurrence of CHD by multiple-regression analysis. Distribution of the ACE gene I/D-polymorphism was investigated in 691 patients with diabetes mellitus prospectively characterised for the presence/absence of coronary heart disease. The distribution of DD; ID; II genotypes was 105 vs. 202 vs. 102 (25.7 % vs. 49.4 % vs. 24.9) in the CHD + group and 55 vs. 160 vs. 67 (19.5 % vs. 56.7 % vs. 23.8 %) in the CHD - group, respectively (p = 0.1). A multiple logistic regression analysis introducing the typical risk factors for CHD (age, gender, smoking, BMI > 26 kg/m 2, LDL elevation, HbA1c > 7 %) could not identify the ACE gene I/D-polymorphism as an independent risk factor for CHD (p = 0.87). Our data therefore suggest that the ACE gene I/D polymorphism is not associated with the occurrence of diabetic macroangiopathy in patients with or without treatment of ACE inhibitors.

Publication types

  • Clinical Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Alleles
  • Cardiovascular Diseases / epidemiology
  • Cardiovascular Diseases / genetics
  • Diabetes Mellitus, Type 2 / genetics*
  • Diabetic Angiopathies / genetics*
  • Female
  • Gene Deletion
  • Gene Frequency
  • Genotype
  • Humans
  • Logistic Models
  • Male
  • Middle Aged
  • Mutation / genetics*
  • Peptidyl-Dipeptidase A / genetics*
  • Phenotype
  • Polymorphism, Genetic / genetics
  • Prospective Studies
  • Risk Factors

Substances

  • Peptidyl-Dipeptidase A