PDF(Pubmed)
Abstract：
BACKGROUND: Chronic cough can be triggered by respiratory and non-respiratory tract illnesses originating mainly from the upper and lower airways, and the GI tract (ie, reflux). Recent findings suggest it can also be a prominent feature in obstructive sleep apnea (OSA), laryngeal hyperresponsiveness, and COVID-19. The classification of chronic cough is constantly updated but lacks clear definition. Epidemiological data on the prevalence of chronic cough are informative but highly variable. The underlying mechanism of chronic cough is a neurogenic inflammation of the cough reflex which becomes hypersensitive, thus the term hypersensitive cough reflex (HCR). A current challenge is to decipher how various infectious and inflammatory airway diseases and esophageal reflux, among others, modulate HCR.
OBJECTIVE: The World Allergy Organization/Allergic Rhinitis and its Impact on Asthma (WAO/ARIA) Joint Committee on Chronic Cough reviewed the current literature on classification, epidemiology, presenting features, and mechanistic pathways of chronic cough in airway- and reflux-related cough phenotypes, OSA, and COVID-19. The interplay of cough reflex sensitivity with other pathogenic mechanisms inherent to airway and reflux-related inflammatory conditions was also analyzed.
RESULTS: Currently, it is difficult to clearly ascertain true prevalence rates in epidemiological studies of chronic cough phenotypes. This is likely due to lack of standardized objective measures needed for cough classification and frequent coexistence of multi-organ cough origins. Notwithstanding, we emphasize the important role of HCR as a mechanistic trigger in airway- and reflux-related cough phenotypes. Other concomitant mechanisms can also modulate HCR, including type2/Th1/Th2 inflammation, presence or absence of deep inspiration-bronchoprotective reflex (lower airways), tissue remodeling, and likely cough plasticity, among others.
OBJECTIVE: The World Allergy Organization/Allergic Rhinitis and its Impact on Asthma (WAO/ARIA) Joint Committee on Chronic Cough reviewed the current literature on classification, epidemiology, presenting features, and mechanistic pathways of chronic cough in airway- and reflux-related cough phenotypes, OSA, and COVID-19. The interplay of cough reflex sensitivity with other pathogenic mechanisms inherent to airway and reflux-related inflammatory conditions was also analyzed.
RESULTS: Currently, it is difficult to clearly ascertain true prevalence rates in epidemiological studies of chronic cough phenotypes. This is likely due to lack of standardized objective measures needed for cough classification and frequent coexistence of multi-organ cough origins. Notwithstanding, we emphasize the important role of HCR as a mechanistic trigger in airway- and reflux-related cough phenotypes. Other concomitant mechanisms can also modulate HCR, including type2/Th1/Th2 inflammation, presence or absence of deep inspiration-bronchoprotective reflex (lower airways), tissue remodeling, and likely cough plasticity, among others.
摘要：
背景：慢性咳嗽可由主要源自上呼吸道和下呼吸道的呼吸道和非呼吸道疾病引发，和胃肠道(即，回流）。最近的研究结果表明，它也可能是阻塞性睡眠呼吸暂停（OSA）的一个突出特征，喉高反应性,和COVID-19。慢性咳嗽的分类不断更新，但缺乏明确的定义。关于慢性咳嗽患病率的流行病学数据提供了信息，但变化很大。慢性咳嗽的潜在机制是咳嗽反射的神经源性炎症，因此术语过敏性咳嗽反射（HCR）。当前的挑战是如何破译各种感染性和炎症性气道疾病和食管反流，其中,HCR调制。
目的：世界过敏组织/过敏性鼻炎及其对哮喘的影响（WAO/ARIA）慢性咳嗽联合委员会回顾了目前的分类文献，流行病学,呈现特征，以及气道和反流相关咳嗽表型中慢性咳嗽的机制途径，OSA,和COVID-19。还分析了咳嗽反射敏感性与气道固有的其他致病机制和反流相关炎症的相互作用。
结果：目前，在慢性咳嗽表型的流行病学研究中,很难明确真实的患病率.这可能是由于缺乏咳嗽分类所需的标准化客观措施以及多器官咳嗽起源的频繁共存。尽管如此,我们强调HCR在气道和反流相关咳嗽表型中作为机制触发因子的重要作用.其他伴随机制也可以调节HCR，包括Type2/Th1/Th2炎症，是否存在深吸气-支气管保护性反射（下气道），组织重塑,和可能的咳嗽可塑性，在其他人中。
目的：世界过敏组织/过敏性鼻炎及其对哮喘的影响（WAO/ARIA）慢性咳嗽联合委员会回顾了目前的分类文献，流行病学,呈现特征，以及气道和反流相关咳嗽表型中慢性咳嗽的机制途径，OSA,和COVID-19。还分析了咳嗽反射敏感性与气道固有的其他致病机制和反流相关炎症的相互作用。
结果：目前，在慢性咳嗽表型的流行病学研究中,很难明确真实的患病率.这可能是由于缺乏咳嗽分类所需的标准化客观措施以及多器官咳嗽起源的频繁共存。尽管如此,我们强调HCR在气道和反流相关咳嗽表型中作为机制触发因子的重要作用.其他伴随机制也可以调节HCR，包括Type2/Th1/Th2炎症，是否存在深吸气-支气管保护性反射（下气道），组织重塑,和可能的咳嗽可塑性，在其他人中。
