Angiotensin-converting enzyme insertion/deletion polymorphism and risk and outcome of pneumonia

Chest. 2008 Jan;133(1):220-5. doi: 10.1378/chest.07-1400. Epub 2007 Oct 1.

Abstract

Background: Recent studies have suggested involvement of the angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism in the susceptibility to and severity of community-acquired pneumonia (CAP) in Asian populations. We have explored the hypothesis that the ACE I/D polymorphism affects the risk and outcome of CAP in a Dutch white population.

Methods: This is a hospital-based prospective observational study including patients with CAP admitted between October 2004 and August 2006. All patients were genotyped, and pneumonia severity and clinical outcome were compared between patients with II, ID, and DD genotypes of the ACE gene. Pneumonia severity was assessed on day of hospital admission and consecutively on days 2, 3, 5, and 10 of hospital stay using the acute physiology score (APS). Outcomes evaluated were duration of hospital stay, ICU admittance, and in-hospital and 28-day mortality rates. To study the association between ACE genotype and risk of pneumonia, the distribution of the ACE I/D polymorphism was compared with healthy control subjects from the same geographic region.

Results: In total, 200 patients with pneumonia and 200 control subjects were included in the study. Mean age of the patients was 63 years. APS scores were not different between the genotype groups on any of the days, and all clinical outcomes (duration of hospital stay, ICU admittance, in-hospital and 28-day mortality rates) were comparable between the three genotype groups. The ACE I/D genotype distribution was identical for patients and control subjects (p = 0.973).

Conclusions: The ACE I/D polymorphism is not associated with risk and outcome of CAP in the Dutch white population.

MeSH terms

  • Aged
  • Female
  • Genotype
  • Humans
  • Male
  • Middle Aged
  • Netherlands
  • Peptidyl-Dipeptidase A / genetics*
  • Pneumonia / genetics*
  • Polymorphism, Genetic*
  • Prospective Studies
  • Risk Factors

Substances

  • Peptidyl-Dipeptidase A