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哮喘的发病机制

Author
Mark Liu, MD
Section Editor
Bruce S Bochner, MD
Deputy Editor
Helen Hollingsworth, MD
Translators
赵丽敏, 主任医师

引言

哮喘的“典型”体征和症状是间歇性呼吸困难、咳嗽和喘鸣。该病已得到充分认识，其特征是程度不同的气流受限和气道高反应性，亦即气道对多种刺激产生的过度收缩反应的表现。

特应症，即针对环境中常见的变应原产生特异性IgE抗体的遗传易感性，是发生哮喘的最强烈的可识别危险因素[1]。尽管哮喘和特应症的关联已无可争议，但尚未明确特应症表现为临床哮喘的具体途径，也未明确在没有特应症时哮喘的发生机制[1]。气道平滑肌(airway smooth muscle, ASM)功能本身的异常、为了应对损伤或炎症的气道重构，以及上皮细胞和间质细胞之间的相互作用似乎改变和增加了气道炎症在产生哮喘的临床表现中的作用。临床上可以定义的哮喘具有不同表型，由此强调的概念认为，哮喘确实是一种有多种潜在机制的综合征[2]。

本文将总结对哮喘的发病机制有贡献的炎症、生理和结构性因素，并着重介绍有助于了解哮喘的临床表现及其治疗方面的内容。

关于哮喘的遗传学、临床危险因素(如，特应症、变应原暴露、病毒性疾病、性别和吸烟)、诊断和处理的讨论参见其他专题。 (参见“哮喘遗传学”和“哮喘的危险因素”和“青少年及成人哮喘的诊断”和“12岁以下儿童的哮喘：初始评估和诊断”)

气道炎症

通过支气管镜检查获得的气道活检组织已经证明，哮喘中的炎症通常涉及的细胞与在鼻腔和皮肤变态反应性应答中起显著作用的细胞类型相同，无论该个体是否存在特应性。这支持了一个观点，即由多种细胞、细胞因子和其他介质介导的肥大细胞激活的后果是发生临床哮喘的关键。 (参见“变态反应性鼻炎(鼻-鼻窦炎)的发病机制”)

                      

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Literature review current through: 2017-07 . | This topic last updated: 2016-05-31.
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