Vestbo J, Hogg J C
Department of Cardiology and Respiratory Medicine, Hvidovre University Hospital, Kettegaard Alle 30, DK-2650 Hvidovre, Denmark.
Thorax. 2006 Jan;61(1):86-8. doi: 10.1136/thx.2005.046227. Epub 2005 Oct 14.
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.
慢性阻塞性肺疾病(COPD)的流行病学主要受两种假说主导。一种假说认为,吸烟和慢性支气管炎是发病机制的关键;另一种假说则认为,哮喘、慢性支气管炎,甚至肺气肿与原发性气道异常的不同表现有关。基于对在职男性的纵向研究,第一种假说在20世纪60年代末被否定,该研究发现只有一小部分吸烟者患上了COPD,且COPD的发展与慢性支气管炎的有无无关。在更严重的COPD中,慢性支气管炎随后与肺功能更快速下降以及更频繁的病情加重相关。第二种假说更难验证,但纵向研究表明,支气管高反应性的存在可能预示着哪些受试者会发展为COPD。这篇简短的综述试图将这些发现与肺部的病理学发现相协调。