title: Impact of I/D polymorphism of ACE gene on risk of development and course of chronic obstructive pulmonary disease.
abstract: BACKGROUND
  Chronic obstructive pulmonary disease (COPD) affects more than 10% of the world's population over 40 years of age. The main exogenous risk factor is cigarette smoking; however, only 20% of smokers develop COPD, indicating that some other factors, e.g. genetic, may play an important role in the disease pathogenesis. Recent research indicates that ACE (angiotensin-converting enzyme) may be a susceptibility gene for asthma or COPD. The aim of our study was to determine the influence of I/D (insertion/deletion) polymorphism of the ACE gene (AluYa5, rs4646994) on the risk and course of COPD.
  
  
  METHODS
  We investigated ACE I/D polymorphism in 206 COPD and 165 healthy Caucasian subjects.
  
  
  RESULTS
  In the generalized linear model (GLZ) analysis of the influence of selected factors on presence of COPD we found a significant independent effect for male sex (repeatedly increases the risk of COPD, OR = 7.7, p = 0.049), as well as smoking or lower body mass index, but only in combination with older age (OR = 0.96, p = 0.003 and OR = 1.005, p = 0.04 respectively). Interestingly, analysis of factors which may influence the risk of a higher number of exacerbations demonstrated that occurrence of DD genotype, but only in men, is associated with a lower risk (OR = 0.7, p = 0.03) of this complication.
  
  
  CONCLUSIONS
  We suggest that ACE may not be a susceptibility gene for the origin of COPD but a disease-modifying gene. Since the impact of I/D polymorphism of the ACE gene on COPD risk is moderate or negligible, other molecular changes, that will help predict the development of this disease, should still be sought.
authors.affiliation: Department of Human Physiology, Medical University of Lublin, Lublin, Poland; Department of Oncology, Medical University of Lublin, Lublin, Poland.
authors.forename: Radosław
authors.initials: R
authors.lastname: Mlak
authors.affiliation: Department of Human Physiology, Medical University of Lublin, Lublin, Poland; Department of Oncology, Medical University of Lublin, Lublin, Poland.
authors.forename: Iwona
authors.initials: I
authors.lastname: Homa-Mlak
authors.affiliation: Department of Oncology, Medical University of Lublin, Lublin, Poland.
authors.forename: Tomasz
authors.initials: T
authors.lastname: Powrózek
authors.affiliation: Department of Oncology, Medical University of Lublin, Lublin, Poland.
authors.forename: Barbara
authors.initials: B
authors.lastname: Mackiewicz
authors.affiliation: Department of Oncology, Medical University of Lublin, Lublin, Poland.
authors.forename: Marek
authors.initials: M
authors.lastname: Michnar
authors.affiliation: Department of Oncology, Medical University of Lublin, Lublin, Poland.
authors.forename: Paweł
authors.initials: P
authors.lastname: Krawczyk
authors.affiliation: Department of Laboratory Diagnostics, Medical University of Lublin, Lublin, Poland.
authors.forename: Marcin
authors.initials: M
authors.lastname: Dziedzic
authors.affiliation: Department of Internal Medicine, Pulmonology and Allergology, Medical University of Warsaw, Warsaw, Poland.
authors.forename: Renata
authors.initials: R
authors.lastname: Rubinsztajn
authors.affiliation: Department of Internal Medicine, Pulmonology and Allergology, Medical University of Warsaw, Warsaw, Poland.
authors.forename: Ryszarda
authors.initials: R
authors.lastname: Chazan
authors.affiliation: Department of Oncology, Medical University of Lublin, Lublin, Poland.
authors.forename: Janusz
authors.initials: J
authors.lastname: Milanowski
authors.affiliation: Department of Human Physiology, Medical University of Lublin, Lublin, Poland.
authors.forename: Teresa
authors.initials: T
authors.lastname: Małecka-Massalska
keywords: ACE polymorphism; chronic obstructive pulmonary disease; exacerbation; renin-angiotensin-aldosterone system