呼入性氟替卡松治疗支气管扩张：12个月的临床研究

支气管扩张是一种由多种病因引起的消耗性疾病,表现为慢性咳嗽和反复急性发作。支气管扩张有三个病理特点即气道感染、气道炎症和酶的活动。这三者相互作用,引起气道的慢性损伤。许多支气管扩张患者的气道内可能隐藏着铜绿假单孢菌(PA),其发病率很高。大量有害的中性粒细胞被炎     

阻塞性睡眠呼吸暂停低通气综合征与慢性咳嗽

阻塞性睡眠呼吸暂停低通气综合征是慢性咳嗽的病因之一.胃食管反流、鼻后滴流、气道炎症可能是阻塞性睡眠呼吸暂停低通气综合征诱发慢性咳嗽的机制.持续气道正压通气是有效治疗阻塞性睡眠呼吸暂停低通气综合征所致慢性咳嗽的首选治疗方案.     

慢性咳嗽与声带功能障碍

慢性咳嗽是一种常见的临床症状,但是至少有10%的慢性咳嗽患者对于常规药物治疗无效,其中部分可能与声带功能障碍有关.声带功能障碍系由于声带矛盾运动引起气道功能紊乱所致,临床上表现为一系列的气道阻塞症状,有时亦仅表现为慢性咳嗽.语言病理学疗法可用于治疗声带功能障碍引起的慢性咳嗽.     

慢性咳嗽与声带功能障碍

慢性咳嗽是一种常见的临床症状,但是至少有10%的慢性咳嗽患者对于常规药物治疗无效,其中部分可能与声带功能障碍有关.声带功能障碍系由于声带矛盾运动引起气道功能紊乱所致,临床上表现为一系列的气道阻塞症状,有时亦仅表现为慢性咳嗽.语言病理学疗法可用于治疗声带功能障碍引起的慢性咳嗽.     

复方甲氧那明联合孟鲁司特治疗感染后咳嗽45例

感染后咳嗽属于亚急性咳嗽,常发生在轻微急性上呼吸道感染之后,继而出现持续于咳,可能持续3～8w之久,但无气流受限和气道反应性增高,通常发生在呼吸道病毒、肺炎支原体或肺炎衣原体感染的流行季节[1],在病程上有别于慢性咳嗽.感染后咳嗽的病理生理机制尚不十分明确,目前认为是由感染引起的气道炎症伴或不伴短暂性气道高反应性所致.     

仙璐贝用于小儿上气道咳嗽综合征效果观察

上气道咳嗽综合征（UACS）是由多种上呼吸道炎症引起的综合征,是儿童群体慢性咳嗽的常见因素之一,对于儿童健康造成了较大伤害。2010年1月～2011年9月,我们将仙璐贝用于小儿上气道UACS中,取得满意疗效。现报告如下。     

嗜酸性粒细胞性支气管炎研究进展

嗜酸性粒细胞性支气管炎是慢性咳嗽的常见病因, 其存在与支气管哮喘类似的嗜酸细胞性气道炎症却缺乏气道高反应性与气流阻塞, 机制尚未完全明确, 可能与气道炎症分布的部位、炎症介质、重要代谢通路失衡以及气道重塑等差异有关。嗜酸性粒细胞性支气管炎对吸入性糖皮质激素治疗反应良好, 然而停药后易复发, 较长疗程的吸入性糖皮质激素治疗可降低复发率。现有研究显示, 嗜酸性粒细胞支气管炎是一种独立疾病, 而非支气管哮喘或慢性阻塞性肺疾病的前期状态。     

呼吸道病毒感染与哮喘

呼吸道病毒感染引起哮喘急性发作的机制复杂 ,其中气道炎症的加重是核心机制。病毒引起的TH1型免疫反应可通过协助募集TH2 细胞而加重哮喘气道炎症 ;病毒特异性CD8+ T细胞在某些条件下可发生表型转化 ,生成TH2 型细胞因子 ;哮喘的慢性气道炎症也被认为可能与抗病毒免疫有关 ,因此呼吸道病毒感染除了加重哮喘外 ,还可能是哮喘慢性气道炎症和气道重塑的原因之一。     

气道神经源性炎症与慢性咳嗽的发病机制

通常将持续时间超过 8周 ,无明显肺部疾病证据的咳嗽称为慢性咳嗽。由感觉神经末梢释放的神经肽或神经递质所介导的炎症反应称为神经源性炎症。呼吸道中的P物质、神经肽A和降钙素基因相关肽等神经肽引起的气道神经源性炎症在慢性咳嗽发病中起重要作用     

呼吸道病毒感染与哮喘

呼吸道病毒感染引起哮喘急性发作的机制复杂，其中气道炎症的加重是核心机制。病毒引起的TH1型免疫反应可通过协助募集TH2细胞而加重哮喘气道炎症；病毒特异性CD8^-T细胞在某些条件下可发生表型转化，生成TH2型细胞因子；哮喘的慢性气道炎症也被认为可能与抗病毒免疫有关．因此呼吸道病毒感染除了加重哮喘外，还可能是哮喘慢性气道炎症和气道重塑的原因之一。     

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.     

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.     

嗜酸粒细胞性气道炎症和慢性咳嗽

嗜酸粒细胞性气道炎症是以气管和支气管壁存在明显嗜酸粒细胞浸润为特征的一种病理状态.哮喘、咳嗽变异性哮喘及非哮喘性嗜酸粒细胞性支气管炎是慢性咳嗽的常见病因,嗜酸粒细胞性气道炎症是其共同病理过程,提示嗜酸粒细胞性气道炎症与慢性咳嗽的发生可能有密切联系,并呈现不同的临床表型.     

Cough and asthma

Cough variant asthma and the closely related corticosteroid responsive cough syndromes eosinophilic bronchitis and atopic cough are common causes of chronic cough. The diagnosis is often not overt but detailed investigation of airway responsiveness and airway inflammation can be helpful. Cough variant asthma, eosinophilic bronchitis and atopic cough are all associated with eosinophilic airway inflammation, which is similar to that seen in non-cough predominant asthma. However, evidence of activated mast cells and increased concentrations of mast cell products appears to be confined to the conditions associated with cough, suggesting a role for mast cell degranulation in the superficial airway structures in the pathogenesis of cough. Cough variant asthma is typically corticosteroid responsive; leukotriene antagonists and antihistamines also help. Further study of this interesting asthma variant may increase our understanding of the relationship between airway inflammation and airway dysfunction.     

Interpreting the histopathology of chronic cough: a prospective, controlled, comparative study

HYPOTHESIS: Trauma from chronic coughing produces airway inflammation similar to diseases causing cough. DESIGN: Prospective, cross-sectional, controlled, clinicopathologic correlation study in four groups: group 1, cough from intrapulmonary diseases; group 2, cough from extrapulmonary diseases; group 3, cough that was unexplained; and group 4, nonsmoking, asymptomatic control subjects. METHODS: Patients with chronic cough underwent a standardized workup including endobronchial biopsies before treatment. Causes were determined by a favorable response to therapy. Bronchial biopsy samples from control subjects were obtained from surgical specimens. RESULTS: There were 24 adult subjects (13 women and 11 men) with mean cough duration of 8.6 +/- 7.4 years (+/- SD). Thirteen patients had cough due to a specific disease: intrapulmonary diseases in 5 patients, and extrapulmonary diseases in 8 patients. Eleven patients had unexplained cough. Compared to control subjects, there was minimal-to-moderate chronic inflammation in all coughers (p < or = 0.0004), in group 1 (p < or = 0.039), group 2 (p = 0.061), and group 3 (p < or = 0.025) diseases that were not correlated with cough duration. There was no difference in type of inflammation, cough duration, or smoking history between groups, nor were there histologic differences between subjects with explained causes of cough compared with unexplained cough. CONCLUSIONS: Our findings suggest that airway inflammation associated with chronic cough, assessed on morphologic appearance and inflammatory cell counting in hematoxylin-eosin-prepared samples, may be due to the trauma of coughing, and the inflammation may be similar to that seen with diseases putatively thought to cause chronic cough. Investigators must be cautious when attributing pathogenic importance to observed inflammatory changes in airways of coughing subjects.     

Cough threshold to inhaled tartaric acid and bronchial responsiveness to methacholine in patients with asthma and sino-bronchial syndrome.

To evaluate the effect of chronic airway inflammation on cough sensitivity and bronchial responsiveness, we measured the cough threshold to tartaric acid and bronchial responsiveness to methacholine (PC20-FEV1) in 13 asthmatic, 13 bronchitic (sino-bronchial syndrome) and 49 healthy non-atopic subjects. All subjects were non-smokers. The geometric mean value of the cough threshold was 9.55, 5.62 and 12.3% in asthmatic, bronchitic and normal subjects, respectively. The value in bronchitic subjects was significantly (p less than 0.02) lower than that in normal subjects. The geometric mean value of PC20-FEV1 in asthmatic subjects (0.63 mg/ml) was significantly lower than those in bronchitic (8.7 mg/ml) (p less than 0.01) and normal subjects (21.4 mg/ml) (p less than 0.01). There was no correlation between cough threshold and PC20-FEV1 values [correlation coefficient (r) = 0.06, p greater than 0.1]. These results indicate that cough sensitivity is potentiated by chronic airway inflammation in bronchitis but not in asthma and suggest that cough sensitivity and bronchial responsiveness may be independently potentiated by different mechanisms resulting from chronic airway inflammation.     

Airway cough sensitivity to inhaled capsaicin and bronchial responsiveness to methacholine in asthmatic and bronchitic subjects

The objective of this study was to evaluate the effect of chronic airway inflammation on airway cough sensitivity and non-specific bronchial responsiveness, and the relationship between them. The capsaicin cough threshold, defined as the lowest concentration of capsaicin causing five or more coughs, and non-specific bronchial responsiveness, defined as the methacholine concentration causing a 20% fall in forced expiratory volume in 1 s (FEV1) (PC20-FEV1), were measured in 18 asthmatic, 13 bronchitic (sinobronchial syndrome) and 28 healthy non-atopic subjects. All subjects were non-smoking men. The geometric mean values (mumol) of the cough threshold were 18.9 (GSEM 1.29), 8.69 (GSEM 1.29) and 27.6 (GSEM 1.31) in asthmatic, bronchitic and normal subjects, respectively. The value in bronchitic subjects was significantly lower (P < 0.02) than that in normal subjects. The geometric mean value of PC20-FEV1 in asthmatic subjects (0.48 mg/ml (GSEM 1.38)) was significantly lower than that in bronchitic subjects (18.5 mg/ml (GSEM 1.75)) (P < 0.001). There was no correlation between cough threshold and PC20-FEV1 values (correlation coefficient (r) = 0.155). These results indicate that cough sensitivity is potentiated by chronic airway inflammation in bronchitis but not in asthma, and suggest that cough sensitivity and bronchial responsiveness may be independently potentiated by different mechanisms resulting from chronic airway inflammation.     

Eosinophils, bronchitis and asthma: pathogenesis of cough and airflow obstruction

Eosinophilic airway inflammation is commonly observed in chronic cough in patients with asthma and non-asthmatic eosinophilic bronchitis. Indeed asthma and non-asthmatic eosinophilic bronchitis are amongst the commonest causes of chronic cough accounting for about 25 and 10% of cases respectively. In most cases the trigger that causes the cough is uncertain; however removal of potential triggers is important to consider in particular with respect to occupational exposure to known sensitizers. In both conditions the cough improves subjectively and objectively following treatment with corticosteroids. This improvement is associated with the presence of an airway eosinophilia, but whether eosinophilic inflammation is the cause of cough or an epiphenomenon is uncertain. The success of anti-IL5 to reduce eosinophilic inflammation and asthma exacerbations contrasts with the lack of efficacy to modify cough in asthma and therefore challenges a causal association. Both asthma and non-asthmatic eosinophilic bronchitis can lead onto airway remodeling and result in persistent airflow obstruction. However, response to corticosteroid therapy in both conditions is generally very good and the limited long term data available suggests that both usually have a benign course. Interestingly, improvement in airway remodeling in response to anti-IL5 observed using CT imaging and analysis of sub-epithelial matrix deposition does suggest that the eosinophil may play a causal role in airway remodeling.     

Sputum eosinophilia and bronchial responsiveness in patients with chronic non-productive cough responsive to anti-asthma therapy

OBJECTIVE: We aimed to examine airway inflammation and bronchial responsiveness in patients with chronic non-productive cough responsive to anti-asthma therapy. METHODOLOGY: Bronchial responsiveness to methacholine as well as the number of inflammatory cells and concentration of eosinophil cationic protein (ECP) in induced sputum were measured in 42 patients with chronic non-productive cough of unknown origin. Their response to bronchodilator, antiallergic and inhaled or oral glucocorticoid therapy was subsequently assessed. RESULTS: Complete remission of coughing was attained with anti-asthma therapies in 34 patients (responder group), while eight patients did not respond (non-responder group). Twenty patients in the responder group and three in the non-responder group showed bronchial hyperresponsiveness (BHR). The number of eosinophils and ECP levels in the sputum from responders with BHR were significantly increased when compared with those from non-responders and healthy subjects. These sputum measures were also significantly increased in responders without BHR when compared with healthy subjects. However, there were no significant differences in these inflammatory markers between the responders with and without BHR. The neutrophil numbers in the sputum from non-responders and responders both with and without BHR were also significantly higher than in control subjects, but there were no significant differences. CONCLUSIONS: These findings suggest that patients with chronic non-productive cough responsive to anti-asthma therapy characteristically have eosinophilic airway inflammation, which may play an important role in the development of chronic cough. Furthermore, the evaluation of not only bronchial responsiveness but also airway inflammation by examination of induced sputum may be useful for diagnosis and deciding on therapeutic strategies.     

Cigarette smoke-induced airway inflammation as sampled by the expired breath condensate

Airways exposed to smoke respond with inflammatory processes. The airway inflammation generally present in smokers causes persistent cough and phlegm production, reactive airway disease, and tissue infiltration by inflammatory cells. Although the short-term response may be protective, long-term pathological consequences include swelling of the airway epithelium, mucus hypersecretion, and increased airway reactivity characteristic of chronic bronchitis and chronic obstructive lung disease and the tissue destruction characteristic of emphysema. The natural history of these diseases is poorly understood, because human airway tissue is available for study only at autopsy, from surgical specimens, or from procedures such as bronchoscopy or thoracotomy. A noninvasive method of monitoring the inflammation is by analyzing expired breath condensate, which contains a diluted sample of airway surface liquid. The study of expired breath condensate may offer a more practical approach to sampling airway chemistry and make it possible to study the detailed inflammatory response to airborne particulates.