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当前与吸烟相关的间质性肺疾病的发病机制、诊断和治疗的概念。

Current Concepts in Pathogenesis, Diagnosis, and Management of Smoking-Related Interstitial Lung Diseases.

机构信息

Division of Pulmonary and Critical Care Medicine, Spectrum Health-Michigan State University College of Human Medicine, Grand Rapids, MI.

Division of Pulmonary, Critical Care and Sleep Medicine, University of Texas Health Science Center at Houston-McGovern Medical School, Houston, TX.

出版信息

Chest. 2018 Aug;154(2):394-408. doi: 10.1016/j.chest.2017.11.023. Epub 2017 Dec 5.

Abstract

Tobacco exposure results in various changes to the airways and lung parenchyma. Although emphysema represents the more common injury pattern, in some individuals, cigarette smoke injures alveolar epithelial cells and other lung cells, resulting in diffuse infiltrates and parenchymal fibrosis. Smoking can trigger interstitial injury patterns mediated via recruitment and inappropriate persistence of myeloid and other immune cells, including eosinophils. As our understanding of the role of cigarette smoke constituents in triggering lung injury continues to evolve, so does our recognition of the spectrum of smoking-related interstitial lung changes. Although respiratory bronchiolitis-interstitial lung disease, desquamative interstitial pneumonia, pulmonary Langerhans cell histiocytosis, and acute eosinophilic pneumonia have a well-established association with tobacco use, its role and impact on idiopathic pulmonary fibrosis, combined pulmonary fibrosis and emphysema, and connective tissue disease-related interstitial lung diseases is still ambiguous. Smoking-related interstitial fibrosis is a relatively newly appreciated entity with distinct histopathologic features but with unclear clinical ramifications. Increased implementation of lung cancer screening programs and utilization of CT scans in thoracic imaging have also resulted in increased identification of "incidental" or "subclinical" interstitial lung changes in smokers, the ensuing impact of which remains to be studied.

摘要

烟草暴露会导致气道和肺实质发生各种变化。虽然肺气肿代表了更常见的损伤模式,但在某些个体中,香烟烟雾会损伤肺泡上皮细胞和其他肺细胞,导致弥漫性浸润和实质纤维化。吸烟可通过髓样细胞和其他免疫细胞(包括嗜酸性粒细胞)的募集和不当持续存在来触发间质损伤模式。随着我们对香烟烟雾成分触发肺损伤作用的认识不断发展,我们对与吸烟相关的间质性肺改变的谱也有了更深入的认识。虽然呼吸性细支气管炎-间质性肺病、脱屑性间质性肺炎、肺朗格汉斯细胞组织细胞增生症和急性嗜酸性粒细胞肺炎与烟草使用有明确的关联,但吸烟在特发性肺纤维化、合并性肺纤维化和肺气肿以及结缔组织病相关间质性肺病中的作用和影响仍不明确。与吸烟相关的间质纤维化是一种新近认识到的实体,具有独特的组织病理学特征,但临床意义尚不清楚。肺癌筛查计划的实施增加以及胸部成像中 CT 扫描的应用,也导致吸烟者“偶然”或“亚临床”间质性肺改变的识别增加,其后续影响仍有待研究。

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