The relation of airways responsiveness and atopy to the development of chronic obstructive lung disease.
The relation of airways responsiveness and atopy to the development of chronic obstructive lung disease.
复制标题
气道反应性和特应性与慢性阻塞性肺病发展的关系。
DOI：
10.1093/oxfordjournals.epirev.a036027
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发表时间：
1988
影响因子：
5.5
通讯作者：
Weiss,ST
中科院分区：
文献类型：
--
作者：
Sparrow,D;O'Connor,G;Weiss,ST
背景流行病学数据已确定吸烟是慢性阻塞性肺病的主要病因（1-4）;然而，这种疾病的发病机制仍不确定。目前尚不清楚是什么导致了约15%的吸烟者患慢性阻塞性肺病的易感性，或者为什么85%的吸烟者逃避了慢性气道阻塞的发展（1，5）。本综述将研究流行病学数据，提供线索的发病机制，慢性阻塞性肺疾病和明显的易感性，吸烟者对这种疾病的一个亚组。早期的研究者提出了两种关于慢性阻塞性肺病起源的理论。“英国假说”（1）提出吸烟导致炎症和痰的产生。据推测，这种粘液分泌过多导致气道清除异常，为复发性感染奠定基础。认为复发性感染是由于以下原因所致：缩略语：FEVi，1秒用力呼气量; IG，免疫球蛋白; PC，激发浓度; PD，激发剂量。1规范老化研究，退伍军人管理局门诊诊所，波士顿，MA。2马萨诸塞州波士顿哈佛医学院贝斯以色列医院布莱根妇女医院肺科Charming实验室。转载请求斯科特·T博士。韦斯，钱宁实验室，哈佛医学院，180 Longwood Avenue，Boston，MA 02115。这项工作得到了退伍军人管理局医学研究服务和美国国立卫生研究院国家心肺血液研究所肺部疾病部门的Grant HL-34645的支持。奥康纳博士是国家心脏、肺和血液研究所颁发的个人国家研究服务奖HL-07246的获得者。破坏肺组织并导致肺功能更快下降和气流阻塞。尽管这一假设似乎合乎逻辑，但一些研究人员无法找到粘液分泌过多与慢性阻塞性肺病发展之间的关系，尽管两者都与吸烟有关（1，6，7）。此外，研究未能证明成人呼吸道感染或其治疗与肺功能恶化的关系（1，5，8，9）。荷兰人首次提出的一个假设（10）表明，宿主的内在特征，特别是气道反应性和特应性，是决定个体对随后暴露的反应的重要决定因素。有些人可能会因为吸烟而出现间歇性可逆性气流阻塞，而另一些人则会出现固定性气道阻塞和肺功能更快的下降，还有一些人没有明显的不良反应。根据这一假说，特应性和气道反应性升高与慢性阻塞性肺疾病发展的易感性有关。本文将描述现有的数据，承担荷兰假说，然后将审查概念的发展，这种疾病。
BACKGROUND Epidemiologic data have established that cigarette smoking is the major etiologic factor responsible for chronic obstructive lung disease (1-4); however, the pathogenesis of this disease remains uncertain. It is not known what leads to the susceptibility of the approximately 15 per cent of smokers who develop chronic obstructive lung disease or why 85 per cent of smokers escape the development of chronic airways obstruction (1, 5). This review will examine epidemiologic data that provide clues to the pathogenesis of chronic obstructive lung disease and the apparent susceptibility of a subgroup of smokers to this disease. Early investigators formulated two theories about the origins of chronic obstructive lung disease. The" British hypothesis"(1) proposed that cigarette smoking leads to inflammation and phlegm production. It was postulated that this mucus hypersecretion leads to abnormalities in airway clearance, setting the stage for recurrent infections. Recurrent infections were believed toAbbreviations: FEVi, forced expiratory volume in one second; Ig, immunoglobulin; PC, provocation concentration; PD, provocation dose. 1 Normative Aging Study, Veterans Administration Outpatient Clinic, Boston, MA. 2 Charming Laboratory, Brigham and Women's Hospital, Pulmonary Division, Beth Israel Hospital, Harvard Medical School, Boston, MA. Reprint requests to Dr. Scott T. Weiss, The Channing Laboratory, Harvard Medical School, 180 Longwood Avenue, Boston, MA 02115. This work was supported by the Medical Research Service of the Veterans Administration and by Grant HL-34645 from the Division of Lung Diseases, National Heart, Lung, and Blood Institute, National Institutes of Health. Dr. O'Connor is the recipient of Individual National Research Service Award HL-07246 from the National Heart, Lung, and Blood Institute. destroy lung tissue and to lead to a more rapid decline in lung function and to airflow obstruction. Despite the seeming logic of the hypothesis, several investigators have been unable to find a relation between mucus hypersecretion and the development of chronic obstructive lung disease, although both are related to cigarette smoking (1, 6, 7). In addition, studies have failed to demonstrate a relation of respiratory infections in adult life, or their treatment, to deterioration in lung function (1, 5, 8, 9). A hypothesis first proposed by the Dutch (10) suggested that intrinsic host characteristics, specifically airways responsiveness and atopy, are important determinants of how persons will respond to subsequent exposure. Some persons may experience episodic reversible airflow obstruction as a result of smoking, while others develop fixed airways obstruction and a more rapid decline in lung function, and still others experience no apparent adverse effects. According to this hypothesis, atopy and heightened airways responsiveness are associated with a predisposition to the development of chronic obstructive lung disease. This paper will describe existing data that bear on the Dutch hypothesis and then will review concepts about the development of this disease.