慢性阻塞性肺疾病与阻塞性睡眠呼吸暂停综合征

慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)与阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea-hypopnea syndrome,OSAHS)往往都表现为气流阻塞,前者气流阻塞于细支气管和支气管,后者于睡眠时反复发生上气道气流阻塞,两者分别存在细支气管、支气管和上气道局部的炎症,同时又由不同机制导致全身系统性炎症.两者在病理生理发展变化上是否可以相互影响目前尚未完全明确.本文主要就OSAHS和COPD与炎症反应的关系、两者的相互关系及预后等方面作相应综述.     

Th17、IL-17与支气管哮喘-慢性阻塞性肺疾病重叠关系的研究

正支气管哮喘(哮喘)和慢性阻塞性肺疾病(慢阻肺)是具有不同病理生理学和炎症表型的异质性疾病。哮喘以慢性气道炎症、气道高反应、多变可逆的气流受限以及随病程延长而出现的气道重构为主要特征,慢阻肺则以持续的呼吸道症状和气流受限为     

糖皮质激素治疗慢性阻塞性肺疾病的现状与展望

COPD的主要特征为不完全可逆的气流受限且进行性加重,气道慢性炎症反应是其主要发病机制之一.COPD和支气管哮喘(简称哮喘)同样属于慢性气道炎症反应疾病,糖皮质激素(简称激素)在哮喘的防治方面已经取得了显著疗效,但其对COPD的治疗作用却一直存在争议.     

类胰蛋白酶与支气管哮喘

支气管哮喘（bronchial asthma，简称哮喘）是由嗜酸性粒细胞、肥大细胞、T细胞、中性粒细胞等多种细胞和细胞组分参与的慢性气道炎症性疾病。这种慢性炎症导致气道反应性增高，出现广泛多变的可逆性气流受限。目前，关于哮喘的发病机制仍未完全阐明，变态反应、气道炎症、气道高反应性及神经等因素及其相互作用被认为与哮喘的发病关系密切。哮喘免疫学机制方面近来研究较多，其中类胰蛋白酶是近年来倍受注意的肥大细胞分泌性介质，它高度选择表达于肥大细胞，在其分泌颗粒中以全酶活性形式大量储存，一旦被释放，类胰蛋白酶表现出持续活性，通过多种途径参与哮喘发病，是哮喘研究领域的又一热点。本文就类胰蛋白酶生物学特点及其与哮喘的关系作一综述。     

低剂量CT空气潴留指标用于支气管哮喘患者病情分析

支气管哮喘(bronchial asthma)是一种常见的以气道慢性炎症为主要特征的慢性气道疾病,常在夜间及凌晨发作或加重,中重度支气管哮喘可严重影响患者生活质量,威胁患者生命安全[1] .在支气管哮喘的治疗过程中根据不同哮喘分级予以不同治疗方案以达到良好控制症状、改善气流受限及降低患者支气管哮喘加重的风险[2] .准...     

支气管哮喘表型分型的研究进展

<正>全球哮喘防治创议(GINA)将支气管哮喘定义为一种慢性呼吸道炎症疾病,以多变且反复发作的临床症状、气流受限、气道高反应性及潜在的气道炎症反应为特征。哮喘发病机制复杂多样,临床表现各不相同,治疗效果及预后因人而异,表现出明显的异质性。学界对于支气管哮喘是有多种临床表现的一种疾病,还是以气流阻塞为共同特征的多种疾病一直存在争议[1,2]。2009年的哮喘防治指南(GINA)第一次提出"表型"这一概念,并提出基于表型     

转化生长因子β在支气管哮喘气道平滑肌重塑中的作用

支气管哮喘（简称哮喘）是一种气道慢性炎症,持续的气道炎症导致气道重塑、不完全可逆的气流受限和进行性的肺功能受损。平滑肌细胞的增殖（包括增生和肥大）是哮喘气道重塑的特征性改变,是哮喘气道反应性和严重程度相关的重要因素之一。转化生长因子β（TGF-β）能够诱导分化、炎症、增生以及凋亡等多种细胞反应,促进平滑肌细胞的增生、肥大和迁移,在气道重塑中发挥重要作用。减少TGF-β的产生以及控制TGF-β的效应有利于对慢性哮喘气道重塑的干预治疗。     

支气管哮喘动物模型的研究状况

支气管哮喘是由嗜酸细胞 (ＥＯＳ)、肥大细胞和Ｔ淋巴细胞等多种炎性细胞参与的慢性气道炎症 ,并由此导致患者的气道高反应性 (ＡＨＲ) ,从而引起气道阻塞 ,气流受限。支气管哮喘发病机制复杂 ,鉴于直接进行人体试验的局限性 ,有关病因的确定、发病机制的探索、新治疗方法的评价、新药的研究与开发在相当程度上均需通过动物实验进行 ,有必要全面了解动物实验性哮喘的制作及其检测方法。一、过敏性哮喘动物模型支气管哮喘为变态反应性气道炎症 ,变应原在支气管哮喘的发生与发展中占有重要地位 ,而导致哮喘的变应原多数为吸入性 ,所以支气管哮…     

转化生长因子β在支气管哮喘气道平滑肌重塑中的作用

支气管哮喘(简称哮喘)是一种气道慢性炎症,持续的气道炎症导致气道重塑、不完全可逆的气流受限和进行性的肺功能受损.平滑肌细胞的增殖(包括增生和肥大)是哮喘气道重塑的特征性改变,是哮喘气道反应性和严重程度相关的重要因素之一.转化生长因子β(TGF-β)能够诱导分化、炎症、增生以及凋亡等多种细胞反应,促进平滑肌细胞的增生、肥大和迁移,在气道重塑中发挥重要作用.减少TGF-β的产生以及控制TGF-β的效应有利于对慢性哮喘气道重塑的干预治疗.     

哮喘与慢性阻塞性肺疾病重叠综合征的研究进展

支气管哮喘(bronchial asthma,简称哮喘)和慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)是两种常见的气道慢性炎症性疾病。哮喘是一种以广泛多变的可逆性气流受限为特征的气道慢性炎症性疾病,这种慢性炎症与气道高反应性相关。而COPD是一组以不完全可逆性气流受限为特征的,病情呈进行性发展的气道慢性炎症性疾病。以前认为哮喘和COPD是两种不同的疾病,具有不同的     

Immunomodulatory effects of melatonin in asthma

We studied the changes in lung and upper airway mechanics in adult human subjects with obstructive sleep apnea/hypopnea syndrome (OSAHS) during wakefulness, sleep, and at arousal from sleep. We used two numerical methods that we have previously developed specifically for dealing with inspiratory flow limitation during sleep: the modified Mead-Whittenberger method, and information-weighted histograms obtained using recursive least squares. Full polysomnography including esophageal pressure and airflow measurements was performed in seven men with OSAHS (respiratory disturbance index: 55.8 +/- 23.2 events/h). Pharyngeal pressure was recorded in four of the subjects to partition lung mechanics into its upper airway and lower lung components. Both techniques showed that total lung resistance and elastance increased significantly (p < 0.05) during obstructed breathing and that this increase was reversed at the end of the obstruction. The partitioning of mechanics showed that upper airway collapse was primarily responsible for the increase in lung resistance. Our results suggest that OSAHS may lead to transient abnormalities in the recruitment of lung units and the gas exchanging capacity of the lungs.     

Eosinophilic bronchitis: clinical features, management and pathogenesis

Eosinophilic bronchitis is a common and treatable cause of chronic cough. The major pathological feature is eosinophilic airway inflammation, similar to that seen in asthma. However, the associated airway dysfunction is quite different, with evidence of heightened cough reflex sensitivity, but no variable airflow obstruction or airway hyperresponsiveness. Recent evidence suggests that the differences in functional association are related to differences in localization of mast cells in airway wall, with airway smooth muscle infiltration occurring in asthma and epithelial infiltration in eosinophilic bronchitis. Diagnosis is usually made with induced sputum analysis after exclusion of other causes for chronic cough on clinical, radiological and lung function assessment. The cough responds well to inhaled corticosteroids but dose and duration of treatment remain unclear. Little is known about the natural history of this condition. However, some patients with COPD without a history of previous asthma have sputum eosinophilia, so one possibility is that some cases of eosinophilic bronchitis may develop fixed airflow obstruction. Further study of this interesting condition will increase our understanding of airway inflammation and airway responsiveness, leading to novel targets for therapeutics for both eosinophilic bronchitis and asthma.     

Eosinophilic Bronchitis

Eosinophilic bronchitis is a common and treatable cause of chronic cough. The major pathological feature is eosinophilic airway inflammation, similar to that seen in asthma. However, the associated airway dysfunction is quite different, with evidence of heightened cough reflex sensitivity, but no variable airflow obstruction or airway hyperresponsiveness. Recent evidence suggests that the differences in functional association are related to differences in localization of mast cells in airway wall, with airway smooth muscle infiltration occurring in asthma and epithelial infiltration in eosinophilic bronchitis.Diagnosis is usually made with induced sputum analysis after exclusion of other causes for chronic cough on clinical, radiological and lung function assessment. The cough responds well to inhaled corticosteroids but dose and duration of treatment remain unclear. Little is known about the natural history of this condition. However, some patients with COPD without a history of previous asthma have sputum eosinophilia, so one possibility is that some cases of eosinophilic bronchitis may develop fixed airflow obstruction. Further study of this interesting condition will increase our understanding of airway inflammation and airway responsiveness, leading to novel targets for therapeutics for both eosinophilic bronchitis and asthma.     

Lung elastic recoil in acute and chronic asthma.

This review emphasizes the mechanisms responsible for maximum expiratory airflow limitation in acute and chronic persistent asthma. The phenomenon of acute but reversible loss of lung elastic recoil during acute asthma is reviewed, although no plausible physiologic explanations are offered. The authors have recently studied adult chronic, stable asthmatics with persistent forced expiratory volume in 1 second less than 80% predicted, despite optimal polytherapy. The asthmatics had unsuspected marked loss of lung elastic recoil in the absence of emphysema that was responsible for a 32 to 35% reduction in maximum expiratory airflow at 80% total lung capacity and a 28 to 60% reduction in maximum expiratory airflow at 70% total lung capacity. Work in progress indicates that persistent reduced maximum expiratory airflow may be present for at least 12 +/- 4 years (mean +/- SD) and suggests possible early loss of lung elastic recoil. These observations provide a challenge to the concept of intrinsic airway narrowing resulting from airway remodeling as the major cause of expiratory maximum expiratory airflow limitation in chronic, moderate asthma and severe, persistent asthma. No morphologic or physiologic abnormalities readily explain the chronic, persistent loss of lung recoil.     

Bronchite à éosinophiles : (Rev Fr Allergol Immunol Clin 2008;48(3):196-200)

Eosinophilic airway inflammation may be encountered in asthma and in non asthmatic eosinophilic bronchitis, which is a recently identified and common cause of chronic cough. Non asthmatic eosinophilic bronchitis may be differentiated from asthma by the absence of airflow limitation and of bronchial hyperreactiveness (potentially reflecting the different localization of mast cells within the airway wall). Diagnosis is based on the confirmation of eosinophilic airway inflammation, usually by induced sputum, in the absence of other causes of chronic cough or of radiological and lung function abnormality. The cough is generally improved by inhaled corticosteroids. The long-term outcome is still not known; non asthmatic eosinophilic bronchitis may lead to the onset of fixed airflow obstruction or asthma.     

Mechanisms of airway remodeling in asthma.

Asthma is a chronic inflammatory disease characterized by reversible airflow limitation and airway hyperresponsiveness. Persistent inflammation in airway tissues may lead to structural changes known as airway remodeling and consequently airway obstruction that is not fully reversible and progressive loss of lung function over time. It is generally accepted that airway remodeling is closely related to progression of airway hyperresponsiveness, and the severity of asthma. The structural changes observed in chronic persistent asthma, which includes airway smooth muscle hypertrophy and hyperplasia, collagen deposition to sub-epithelial basement membrane, hyperplasia of goblet cells, thickening of airway mucosa and an increase in vascularity, are derived from airway inflammation. For instance, the thickened airway mucosa might be produced by cytokines and growth factors released from inflammatory cells and airway epithelial cells, and associated with bronchial hyperreactivity and asthma severity. To date, many studies have identified candidate mechanisms and mediators for these observed structural changes, which are thus potential targets in the treatment of asthma. In this review, we describe the recent knowledge of the mechanisms and clinical implications of airway remodeling in asthma.     

Physiologic similarities and differences between asthma and chronic obstructive pulmonary disease

PURPOSE OF REVIEW: This review examines the physiologic mechanisms responsible for persistent maximum expiratory airflow limitation in nonsmoking patients with acute and chronic moderate to severe persistent asthma in comparison to chronic obstructive pulmonary disease. RECENT FINDINGS: The phenomenon of acute but reversible loss of lung elastic recoil during acute asthma is reviewed, although no plausible pathophysiologic explanation has been offered. Nonsmoking adults with stable asthma and persistent maximum expiratory airflow limitation, despite optimal polytherapy, were shown to have unsuspected and unexplained marked loss of lung elastic recoil in the absence of lung computed tomography scored emphysema. This condition resulted in up to 50% reduction in maximum expiratory airflow. Furthermore, these patients remain at high risk for adverse clinical events, including near-fatal asthma. In chronic obstructive pulmonary disease, reduction in maximum expiratory airflow is related to variable extent of loss of lung elastic recoil secondary to emphysema and concurrent intrinsic airway obstruction or obliteration of small airways. There is also an unexplained loss of lung elastic recoil in primary intrinsic small airways disease in the absence of emphysema. SUMMARY: Nonsmoking patients with moderate-severe persistent asthma and patients with smoking-related chronic obstructive pulmonary disease share similar physiologic mechanisms of expiratory airflow limitation, but probably caused by different anatomic abnormalities.     

Airway remodelling in COPD: It's not asthma!

COPD is defined as airflow limitation that is not reversed by treatment. In asthma, airflow limitation is not only reversible, but also inducible. This is called ‘airway hyperresponsiveness’ (AHR) and is associated with thickening of the airway wall, predominantly the layer of airway smooth muscle, due to more cells, bigger cells and more extracellular matrix (ECM) in proportion to the increase in smooth muscle. AHR is also observed in COPD if the changes in airflow are expressed as a percent of the baseline lung function. However, the absolute change in baseline lung function that can be induced in COPD is actually less than that seen in normal subjects, suggesting that the airways in COPD are resistant not only to opening, but also to closing. This observation agrees with physiological measures showing increased airway wall stiffness in COPD. Like asthma, airway wall thickness is increased in COPD, including the layer of smooth muscle. Unlike asthma, however, fixed airflow obstruction appears to be characterized by a disproportionate increase in the ECM within the smooth muscle layer. In this review, we summarize the studies of airway matrix deposition in COPD and put forward the proposal that the airway remodelling in COPD is different from that in asthma and call for a systematic analysis of airway matrix deposition in COPD.     

Bronchite à éosinophiles

Eosinophilic airway inflammation may be encountered in asthma and in non asthmatic eosinophilic bronchitis, which is a recently identified and common cause of chronic cough. Non asthmatic eosinophilic bronchitis may be differentiated from asthma by the absence of airflow limitation and of bronchial hyperreactiveness (potentially reflecting the different localization of mast cells within the airway wall). Diagnosis is based on the confirmation of eosinophilic airway inflammation, usually by induced sputum, in the absence of other causes of chronic cough or of radiological and lung function abnormality. The cough is generally improved by inhaled corticosteroids. The long-term outcome is still not known; non asthmatic eosinophilic bronchitis may lead to the onset of fixed airway obstruction or asthma.