Longer Telomere Length in COPD Patients with α(1)-Antitrypsin Deficiency Independent of Lung Function

Oxidative stress is involved in the pathogenesis of airway obstruction in α(1)-antitrypsin deficient patients. This may result in a shortening of telomere length, resulting in cellular senescence. To test whether telomere length differs in α(1)-antitrypsin deficient patients compared with controls, we measured telomere length in DNA from peripheral blood cells of 217 α(1)-antitrypsin deficient patients and 217 control COPD patients. We also tested for differences in telomere length between DNA from blood and DNA from lung tissue in a subset of 51 controls. We found that telomere length in the blood was significantly longer in α(1)-antitrypsin deficient COPD patients compared with control COPD patients (p = 1×10(−29)). Telomere length was not related to lung function in α(1)-antitrypsin deficient patients (p = 0.3122) or in COPD controls (p = 0.1430). Although mean telomere length was significantly shorter in the blood when compared with the lungs (p = 0.0078), telomere length was correlated between the two tissue types (p = 0.0122). Our results indicate that telomere length is better preserved in α(1)-antitrypsin deficient COPD patients than in non-deficient patients. In addition, measurement of telomere length in the blood may be a suitable surrogate for measurement in the lung.