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. 2007;2(3):329-34.

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

Xavier Busquets  1 , Niall G MacFarlane, Damià Heine-Suñer, Montse Morlá, Laura Torres-Juan, Amanda Iglesias, Jeronia Lladó, Jaume Sauleda, Alvar G N Agustí
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Angiotensin-converting-enzyme gene polymorphisms, smoking and chronic obstructive pulmonary disease

Xavier Busquets et al. Int J Chron Obstruct Pulmon Dis. 2007.

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.

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Figures

Figure 1
Figure 1
Determination of DD, ID, and II genotypes by PCR. Panel a shows a representative experiment using the method described by Rigat et al (1992). PCR products are a 190 bp fragment (D genotype) and a 490 bp fragment (I genotype). Heterozygotes (ID) have both the 190 bp and 490 bp fragments. Panel b shows a representative experiment using the method described by Evans et al (1994). PCR products are a 84 bp (D genotype) and a 65 bp (I genotype). Heterozygotes (ID) have both the 84 bp and 65 bp fragments.
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