Angiotensin-converting enzyme I/D polymorphism in chronic obstructive pulmonary disease

<p>Abstract</p> <p>Study objective</p> <p>The etiology of chronic obstructive lung disease (COPD) is unclear. It is supposed to be the product of an exogenous antigenic stimulus, such as tobacco smoke, and an endogenous genetic susceptibility. The angiotensin-converting...

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Main Authors: Pabst S, Theis B, Gillissen A, Lennarz M, Tuleta I, Nickenig G, Skowasch D, Grohé C
Format: Article
Language:English
Published: BMC 2009-12-01
Series:European Journal of Medical Research
Subjects:
Online Access:http://www.eurjmedres.com/content/14/S4/177
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spelling doaj-3e984b73dcac4651b3f550cdd75cdd772020-11-25T00:24:59ZengBMCEuropean Journal of Medical Research2047-783X2009-12-0114Suppl 417718110.1186/2047-783X-14-S4-177Angiotensin-converting enzyme I/D polymorphism in chronic obstructive pulmonary diseasePabst STheis BGillissen ALennarz MTuleta INickenig GSkowasch DGrohé C<p>Abstract</p> <p>Study objective</p> <p>The etiology of chronic obstructive lung disease (COPD) is unclear. It is supposed to be the product of an exogenous antigenic stimulus, such as tobacco smoke, and an endogenous genetic susceptibility. The angiotensin-converting enzyme (ACE) gene contains a polymorphism based on the presence (insertion [I]) or absence (deletion [D]) of a 287-bp nonsense domain, resulting in three different genotypes (II, ID and DD). The aim of the study was to find out whether the ACE gene polymorphism can determine the course of COPD.</p> <p>Patients and design</p> <p>We genotyped 152 Caucasian patients with COPD and 158 healthy controls for the ACE (I/D) polymorphism. We divided the COPD group into one group of 64 patients with a stable course of disease, defined as less than three hospitalizations over the last three years due to COPD, and another group of 88 patients with an instable course with more than three hospitalizations.</p> <p>Results</p> <p>The I-allele was significantly associated with an increased risk for COPD in a dominant model (OR 1.67 (95% CI 1.00 to 2.78), p = 0.048), but not in a recessive or co-dominant model. Moreover, the I-allele of ACE (I/D) was significantly increased in patients with a stable course of COPD (p = 0.012) compared with controls. In a dominant model (II/ID v DD) we found an even stronger association between the I-allele and a stable course of COPD (OR 3.24 (95% CI 1.44 to 7.31), p = 0.003).</p> <p>Conclusion</p> <p>These data suggest that the presence of an ACE I-allele determines a stable course of COPD.</p> http://www.eurjmedres.com/content/14/S4/177COPDangiotensin converting enzyme (ACE)genetics
collection DOAJ
language English
format Article
sources DOAJ
author Pabst S
Theis B
Gillissen A
Lennarz M
Tuleta I
Nickenig G
Skowasch D
Grohé C
spellingShingle Pabst S
Theis B
Gillissen A
Lennarz M
Tuleta I
Nickenig G
Skowasch D
Grohé C
Angiotensin-converting enzyme I/D polymorphism in chronic obstructive pulmonary disease
European Journal of Medical Research
COPD
angiotensin converting enzyme (ACE)
genetics
author_facet Pabst S
Theis B
Gillissen A
Lennarz M
Tuleta I
Nickenig G
Skowasch D
Grohé C
author_sort Pabst S
title Angiotensin-converting enzyme I/D polymorphism in chronic obstructive pulmonary disease
title_short Angiotensin-converting enzyme I/D polymorphism in chronic obstructive pulmonary disease
title_full Angiotensin-converting enzyme I/D polymorphism in chronic obstructive pulmonary disease
title_fullStr Angiotensin-converting enzyme I/D polymorphism in chronic obstructive pulmonary disease
title_full_unstemmed Angiotensin-converting enzyme I/D polymorphism in chronic obstructive pulmonary disease
title_sort angiotensin-converting enzyme i/d polymorphism in chronic obstructive pulmonary disease
publisher BMC
series European Journal of Medical Research
issn 2047-783X
publishDate 2009-12-01
description <p>Abstract</p> <p>Study objective</p> <p>The etiology of chronic obstructive lung disease (COPD) is unclear. It is supposed to be the product of an exogenous antigenic stimulus, such as tobacco smoke, and an endogenous genetic susceptibility. The angiotensin-converting enzyme (ACE) gene contains a polymorphism based on the presence (insertion [I]) or absence (deletion [D]) of a 287-bp nonsense domain, resulting in three different genotypes (II, ID and DD). The aim of the study was to find out whether the ACE gene polymorphism can determine the course of COPD.</p> <p>Patients and design</p> <p>We genotyped 152 Caucasian patients with COPD and 158 healthy controls for the ACE (I/D) polymorphism. We divided the COPD group into one group of 64 patients with a stable course of disease, defined as less than three hospitalizations over the last three years due to COPD, and another group of 88 patients with an instable course with more than three hospitalizations.</p> <p>Results</p> <p>The I-allele was significantly associated with an increased risk for COPD in a dominant model (OR 1.67 (95% CI 1.00 to 2.78), p = 0.048), but not in a recessive or co-dominant model. Moreover, the I-allele of ACE (I/D) was significantly increased in patients with a stable course of COPD (p = 0.012) compared with controls. In a dominant model (II/ID v DD) we found an even stronger association between the I-allele and a stable course of COPD (OR 3.24 (95% CI 1.44 to 7.31), p = 0.003).</p> <p>Conclusion</p> <p>These data suggest that the presence of an ACE I-allele determines a stable course of COPD.</p>
topic COPD
angiotensin converting enzyme (ACE)
genetics
url http://www.eurjmedres.com/content/14/S4/177
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