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气道重塑:上皮下纤维化和气道平滑肌肥大/增生对哮喘气道狭窄的潜在影响。

Airway remodeling: potential contributions of subepithelial fibrosis and airway smooth muscle hypertrophy/hyperplasia to airway narrowing in asthma.

作者信息

Bento A M, Hershenson M B

机构信息

Department of Pediatrics, University of Chicago, Illinois, USA.

出版信息

Allergy Asthma Proc. 1998 Nov-Dec;19(6):353-8. doi: 10.2500/108854198778612672.

DOI:10.2500/108854198778612672
PMID:9876774
Abstract

Recently, much attention has been focused on the airway structural changes accompanying chronic, severe asthma, and the potential ramifications of these changes for airway function and medical management. Airway remodeling may exaggerate airway narrowing by: (i) thickening of the airway wall internal to the smooth muscle, thereby increasing the luminal obstruction generated by a given degree of smooth muscle shortening; (ii) increasing the amount of smooth muscle, thereby increasing shortening; and/or (iii) reducing the load on the smooth muscle, either by increasing the compliance of the airway wall or by reducing airway-parenchymal interdependence. The possibility also exists that airway remodeling represents a protective mechanism against excessive airway narrowing. The major airway structural changes occurring in asthma are subepithelial protein deposition and increased airway smooth muscle mass (hypertrophy, hyperplasia, or both). Several investigators have found correlations between the magnitudes of subepithelial thickening and smooth muscle hypertrophy/hyperplasia and the severity of airways disease, though interpretation has been made difficult by study differences in patient population, treatment, indices of disease severity, and morphometric technique. Taken together, these data suggest that increases in airway remodeling may contribute significantly to the airflow obstruction observed in patients with asthma. However, data proving a causal relationship between airway remodeling and asthma severity remain elusive.

摘要

近来,人们的诸多关注聚焦于伴随慢性重度哮喘出现的气道结构改变,以及这些改变对气道功能和药物治疗可能产生的影响。气道重塑可能通过以下方式加剧气道狭窄:(i)平滑肌内侧气道壁增厚,从而增加一定程度平滑肌缩短所产生的管腔阻塞;(ii)增加平滑肌数量,进而增加缩短程度;和/或(iii)通过增加气道壁顺应性或减少气道与实质组织的相互依存关系来减轻平滑肌负荷。气道重塑也有可能是一种防止气道过度狭窄的保护机制。哮喘中发生的主要气道结构改变是上皮下蛋白沉积和气道平滑肌质量增加(肥大、增生或两者皆有)。尽管由于患者群体、治疗、疾病严重程度指标和形态测量技术等研究差异使得解读变得困难,但一些研究人员已发现上皮下增厚程度与平滑肌肥大/增生程度和气道疾病严重程度之间存在关联。综合来看,这些数据表明气道重塑增加可能在很大程度上导致了哮喘患者出现气流阻塞。然而,证明气道重塑与哮喘严重程度之间存在因果关系的数据仍然难以获得。

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