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本文引用的文献

1
Emphysema: an autoimmune vascular disease?肺气肿:一种自身免疫性血管疾病?
Proc Am Thorac Soc. 2005;2(1):23-5. doi: 10.1513/pats.200405-033MS.
2
Burden and clinical features of chronic obstructive pulmonary disease (COPD).慢性阻塞性肺疾病(COPD)的负担及临床特征
Lancet. 2004;364(9434):613-20. doi: 10.1016/S0140-6736(04)16855-4.
3
Rationale for the Dutch hypothesis. Allergy and airway hyperresponsiveness as genetic factors and their interaction with environment in the development of asthma and COPD.荷兰假说的理论依据。过敏和气道高反应性作为遗传因素及其在哮喘和慢性阻塞性肺疾病发生发展中与环境的相互作用。
Chest. 2004 Aug;126(2 Suppl):96S-104S; discussion 159S-161S. doi: 10.1378/chest.126.2_suppl_1.96S.
4
Standards for the diagnosis and treatment of patients with COPD: a summary of the ATS/ERS position paper.慢性阻塞性肺疾病患者的诊断和治疗标准:美国胸科学会/欧洲呼吸学会立场文件摘要
Eur Respir J. 2004 Jun;23(6):932-46. doi: 10.1183/09031936.04.00014304.
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The nature of small-airway obstruction in chronic obstructive pulmonary disease.慢性阻塞性肺疾病中小气道阻塞的本质。
N Engl J Med. 2004 Jun 24;350(26):2645-53. doi: 10.1056/NEJMoa032158.
6
Impact of sputum bacteria on airway inflammation and health status in clinical stable COPD.临床稳定期慢性阻塞性肺疾病患者痰液细菌对气道炎症及健康状况的影响
Eur Respir J. 2004 May;23(5):685-91. doi: 10.1183/09031936.04.00056804.
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An international survey of chronic obstructive pulmonary disease in young adults according to GOLD stages.一项根据慢性阻塞性肺疾病全球倡议(GOLD)阶段对年轻成年人慢性阻塞性肺疾病进行的国际调查。
Thorax. 2004 Feb;59(2):120-5. doi: 10.1136/thorax.2003.011163.
8
Longitudinal changes in the nature, severity and frequency of COPD exacerbations.慢性阻塞性肺疾病(COPD)急性加重的性质、严重程度和频率的纵向变化。
Eur Respir J. 2003 Dec;22(6):931-6. doi: 10.1183/09031936.03.00038303.
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Hypothesis: does COPD have an autoimmune component?假设:慢性阻塞性肺疾病是否存在自身免疫成分?
Thorax. 2003 Oct;58(10):832-4. doi: 10.1136/thorax.58.10.832.
10
The relationship between emphysema and chronic bronchitis as assessed morphologically.从形态学角度评估肺气肿与慢性支气管炎之间的关系。
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慢性阻塞性肺疾病的流行病学与病理学的融合

Convergence of the epidemiology and pathology of COPD.

作者信息

Vestbo J, Hogg J C

机构信息

Department of Cardiology and Respiratory Medicine, Hvidovre University Hospital, Kettegaard Alle 30, DK-2650 Hvidovre, Denmark.

出版信息

Thorax. 2006 Jan;61(1):86-8. doi: 10.1136/thx.2005.046227. Epub 2005 Oct 14.

DOI:10.1136/thx.2005.046227
PMID:16227325
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2080699/
Abstract

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.

摘要

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。