Common intronic D variant of ACE gene is associated with endothelial dysfunction in COPD

Pathogenesis of chronic obstructive lung disease (COPD) includes primary inflammatory events, multiple vascular reactions, remodeling of bronchial and vascular walls.

The aim of present single-center study was to assess relations between angiotensin-converting enzyme (ACE) gene and prevalence of clinical symptoms characteristic to COPD.

The study involved sixty-three male patients with COPD (44-86 years old, a mean of 60.4 years). COPD diagnostics was performed according to common criteria, including evaluation of systolic pressure in pulmonary artery (SPPA) and endothelial disfunction (ED). Genotyping of ACE I/D was performed by means of gene-specific PCR.

1. Allele distribution of studied gene alleles among COPD patients did not differ from control age-matched group. 2. Detectable endothelial dysfunction in COPD patients was shown to correlate with high-producer D allele of ACE gene, at an odds ratio of 6.632 (CI = 1.67-26.31; chi2 = 8.39, p = 0.004). Moreover, detectable ED correlated with numbers of COPD exacerbations per year.

These findings suggest possible association of the functional ACE D allele with altered vascular responses that may modulate development of distinct COPD symptoms. The results are obtained in a limited clinical cohort, and deserve repeated trials in other groups of COPD patients.