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Angiotensin-converting-enzyme gene polymorphisms, smoking and chronic obstructive pulmonary disease

Authors Xavier Busquets, Niall G MacFarlane, Damià Heine-Suñer, Montse Morlá, Laura Torres-Juan, et al

Published 15 October 2007 Volume 2007:2(3) Pages 329—334

Xavier Busquets1, Niall G MacFarlane2, Damià Heine-Suñer3, Montse Morlá1, Laura Torres-Juan3, Amanda Iglesias1, Jeronia Lladó1, Jaume Sauleda4, Alvar GN Agustí1,4

1IUNICS-Unitat d’Investigació, 2Institute of Biochemical and Life Sciences, University of Glasgow, Scotland, UK; 3Secció de Genetica and 4Servei de Pneumologia, Hospital Universitari Son Dureta, Fundacio Caubet-Cimera, Palma de Mallorca, Spain

Abstract: While tobacco smoking is the main risk factor for chronic obstructive pulmonary disease (COPD) only a fraction of smokers go on to develop the disease. We investigated the relationship between the insertion (I) – deletion (D) polymorphisms in the Angiotensin converting enzyme (ACE) gene and the risk of developing COPD in smokers by determining the distribution of the ACE genotypes (DD, ID and II) in 151 life-long male smokers. 74 of the smokers had developed COPD (62 ± 2 years; FEV1 44 ± 6 % reference) whereas the rest retained normal lung function (56 ± 2 yrs; FEV1 95 ± 3 % reference). In addition, we genotyped 159 males recruited randomly from the general population. The prevalence of the DD genotype was highest (p = 0.01) in the smokers that developed COPD and its presence was associated with a 2-fold increase in the risk for COPD (OR 2.2; IC95% 1.1 to 5.5). Surprisingly, the 151 individuals in the smoking population did not demonstrate Hardy-Weinberg equilibrium unlike the 159 recruited from the general population. Our results suggest that ACE polymorphisms are associated with both the smoking history of an individual and their risk of developing COPD.

Keywords: chronic bronchitis, COPD, dopamine, drug addiction, emphysema

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