Chest computed tomography: is it ready for major studies of chronic obstructive pulmonary disease?

Publisher Website
Google Scholar
Abstract
How can the rate of progression be monitored? Using tools derived from usual COPD to monitor α1-AT-COPD might not be correct. These diseases share pathophysiological similarities but there are also important differences. α1-AT-COPD is mostly due to the rapid development of PLE predominantly in the lower lobes; airflow obstruction and hyperinflation are mainly due to emphysema and losses of elastic recoil. In usual COPD, airflow limitation is largely secondary to airway damage and remodelling and emphysema (mainly centrilobular emphysema (CLE)) predominates in the upper lobes with a heterogeneous distribution in the lung. The extent of CLE is quite variable for a given level of airflow limitation. Moreover, Sanders et al. 1 and Santis et al. 2 found that 68–80% of smokers showed emphysema by high-resolution computed tomography (HRCT) in the presence of normal lung function tests. These facts highlight the complexity of COPD and the relative independence and at the same time interdependence of airway remodelling and emphysema in their contribution to the development of COPD.