Sethi Sanjay
Division of Pulmonary, Critical Care and Sleep Medicine, University at Buffalo, State University of New York and the VA Western New York Healthcare System, Buffalo, New York 14215, USA.
Curr Opin Infect Dis. 2004 Apr;17(2):113-9. doi: 10.1097/00001432-200404000-00008.
Acute exacerbations of chronic obstructive pulmonary disease were a poorly defined and understood entity. The application of better study designs and new research methodologies has shed considerable light on the pathogenesis of this common clinical syndrome.
Inflammation is an important component of the pathogenesis of chronic obstructive pulmonary disease, and exacerbations probably represent acute increases in airway inflammation brought about by one or more etiological agents. Environmental particulate and gaseous pollutants have been linked in epidemiological studies with increased respiratory symptoms and mortality in chronic obstructive pulmonary disease. Bacterial, viral and atypical pathogens, either alone or in concert, induce the majority of acute exacerbations.
A bacterial cause of a substantial proportion of exacerbations is now firmly established by the results of bronchoscopy, molecular epidemiology, immunology and airway inflammation studies. Future research should focus on pathogenic mechanisms and host defence against the microbial pathogens associated with acute exacerbations of chronic obstructive pulmonary disease, in order to develop better treatment and prevention strategies.
慢性阻塞性肺疾病急性加重曾是一个定义不清且了解甚少的实体。更好的研究设计和新研究方法的应用已使人们对这一常见临床综合征的发病机制有了相当多的了解。
炎症是慢性阻塞性肺疾病发病机制的一个重要组成部分,急性加重可能代表由一种或多种病因导致的气道炎症急性增加。在流行病学研究中,环境颗粒物和气态污染物与慢性阻塞性肺疾病患者呼吸道症状增加及死亡率上升有关。细菌、病毒和非典型病原体单独或共同作用引发了大多数急性加重。
支气管镜检查、分子流行病学、免疫学和气道炎症研究结果现已明确证实,相当一部分急性加重由细菌引起。未来研究应聚焦于与慢性阻塞性肺疾病急性加重相关的微生物病原体的致病机制及宿主防御,以制定更好的治疗和预防策略。