Convergence of the epidemiology and pathology of COPD
- 1Department of Cardiology and Respiratory Medicine, Hvidovre University Hospital, Hvidovre, Denmark; and North West Lung Centre, South Manchester University Hospital Trust, Manchester, UK
- 2James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, University of British Columbia and St Paul’s Hospital, Vancouver, Canada
- Correspondence to:
Professor J Vestbo
Department of Cardiology and Respiratory Medicine, Hvidovre University Hospital, Kettegaard Alle 30, DK-2650 Hvidovre, Denmark;
- Received 4 May 2005
- Accepted 21 September 2005
- Published Online First 14 October 2005
The epidemiology of chronic obstructive pulmonary disease (COPD) has been dominated by one hypothesis stating that cigarette smoking and chronic bronchitis were the key to pathogenesis and another that asthma, chronic bronchitis, and even emphysema are related to different expressions of a primary airway abnormality. The first hypothesis was rejected in the late 1960s based on a longitudinal study of working men where only a fraction of smokers developed COPD and where development of COPD was independent of the absence or presence of chronic bronchitis. Chronic bronchitis in more advanced COPD was subsequently associated with a more rapid decline in lung function and more frequent exacerbations. The second hypothesis is more difficult to test but longitudinal studies have shown that the presence of bronchial hyperresponsiveness may predict the subjects who go on to develop COPD. This brief review attempts to reconcile these findings with the pathology found in the lung.
Competing interests: none.