哮喘病理。

A Laitinen, L A Laitinen
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引用次数: 14

摘要

由于使用致命哮喘患者的尸检标本作为代表性标本的来源,对呼吸道上皮发生的早期损伤的认识受到了限制。使用支气管镜从哮喘病程早期的患者身上获取标本,使人们对哮喘中发生的病理变化的演变有了新的认识。新诊断的轻度哮喘患者除了呼吸上皮肥大细胞和嗜酸性粒细胞数量增加外,还表现为支气管杯状细胞增生,固有层内嗜酸性粒细胞颗粒蛋白沉积增加。哮喘气道毛细血管后小静脉的内皮间隙更大,提示血浆转运增加可能有助于哮喘发作的已知上皮细胞脱落特征。哮喘性炎症,甚至在病程早期,包括血管通透性改变,炎症细胞浸润,上皮细胞脱落,杯状细胞增生,取代正常纤毛上皮。目前的研究评估了哮喘炎症对上皮细胞相互粘附和由粘附糖蛋白调节的细胞外基质分子的影响,这可能会进一步加深对哮喘气道内发生的病理变化的理解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pathology of asthma.

Appreciation of the early damage that occurs to the respiratory epithelium has been limited by the use of autopsy specimens from fatally stricken asthmatics as a source of representative specimens. The use of bronchoscopy to obtain specimens from patients early in the course of their asthma has allowed a new understanding of the evolution of pathological changes that occur in asthma. Newly diagnosed, mild asthmatics have been shown to have bronchial goblet cell hyperplasia in addition to increased numbers of mast cells and eosinophils in the respiratory epithelium, and increased eosinophil granule protein deposition within the lamina propria. Endothelial gaps in postcapillary venules are greater in asthmatic airways, suggesting that increased plasma transudation may contribute to the known epithelial cell shedding characteristic of asthma attacks. Asthmatic inflammation, even early in the course of the disease, includes vascular permeability changes, inflammatory cell infiltration, epithelial cell shedding, and goblet cell hyperplasia, replacing the normal ciliated epithelium. Current investigation evaluating the effects of asthmatic inflammation on epithelial cell attachment to each other and to the extracellular matrix molecules regulated by adhesion glycoproteins will likely enhance further the understanding of the pathological changes that occur within the asthmatic airway.

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