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• W2108641738 abstract "Chronic obstructive pulmonary disease (COPD) requires for diagnosis the presence of chronic airflow limitation and emphysema or chronic bronchitis. In the USA, the disease causes >100,000 deaths annually, it is the fourth most important cause of death and afflicts about 16 million persons. About 1% of COPD in the USA is associated with α1-antitrypsin (α1-AT) deficiency and is conveniently referred to as α1-AT-COPD. This form of the disease occurs in younger persons, progresses more rapidly, is associated with a higher frequency of panlobular emphysema (PLE) than usual COPD, and may be treated by augmentation therapy with concentrated human α1-AT. However, there is limited evidence that α1-AT replacement modifies the rate of progression of α1-AT-COPD.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.Which end-points …" @default.
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• W2108641738 date "2001-06-01" @default.
• W2108641738 modified "2023-10-18" @default.
• W2108641738 title "Chest computed tomography: is it ready for major studies of chronic obstructive pulmonary disease?" @default.
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• W2108641738 doi "https://doi.org/10.1183/09031936.01.00225201" @default.
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