阻塞性睡眠呼吸暂停低通气综合征和慢性阻塞性肺疾病重叠综合征的研究进展

阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea-hypopnea syndrome,OSAHS)和慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)是常见的肺部疾病,Flenley首次将两者共存命名为重叠综合征(overlap syndrome,OS)。既往研究认为,COPD与OSAHS并存于同一     

阻塞性睡眠呼吸暂停低通气综合征与哮喘

最近研究表明阻塞性睡眠呼吸暂停低通气综合征(OSAHS)是支气管哮喘急性加重的独立危险因素。OSAHS常涉及睡眠时上气道吸气气流受限及气道塌陷,常与日间症状如嗜睡、抑郁、精力难以集中等相关。支气管哮喘常表现为气道慢性炎症、气道高反应、可逆性气道气流受限等。现已有大量学者对其相关性作出研究,但未达成统一共识。目前认为神经反射因素、胃食管反流、气道及全身炎症反应、睡眠结构紊乱、肥胖、心血管疾病、激素治疗及鼻部疾病等可能是OSAHS与哮喘相互影响及作用的机制。本文就OSAHS与哮喘的相关性及其机制作一综述。     

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     

气道重叠综合征研究新进展

慢性阻塞性肺疾病(chronic obstructive pulmonary diseases,COPD)、支气管哮喘、阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea hypopnea syndrome,OSAHS)三者虽然是不同的疾病,有着各自的定义、病因病机、临床特征与治疗指南,但它们同属气道阻塞性疾病,尽管三者气道阻塞的部位不同.临床研究显示它们在流行病学、气道炎症与重塑、临床表现、治疗等方面出现两两或三者重叠现象,它们不是简单的叠加,而是成为一种疾病状态,这使临床医师在诊断、治疗上出现困惑.因此,我们参考了国内外最新研究文献,对此作一综述,并提出"气道重叠综合征"的概念,以供临床参考.     

阻塞性睡眠呼吸暂停-慢性阻塞性肺疾病重叠综合征的研究进展

阻塞性睡眠呼吸暂停低通气综合征(OSAHS)是呼吸科常见的一种疾病,以睡眠时上气道反复塌陷引起的间歇性缺氧并伴有睡眠片段化为特征。当OSAHS合并慢性阻塞性肺疾病(COPD)时称为重叠综合征,两种疾病在发生、发展上存在复杂的交互作用,严重影响患者的生活质量和预后,现对OSAHS与COPD之间相互影响及可能的机制作一综述...     

吸烟导致的氧化应激在慢性阻塞性肺疾病发病机制中的作用

慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)是一种可以预防、可以治疗的疾病,以不完全可逆的气流受限为特征;气流受限呈进行性加重,与肺部对有害气体或颗粒的异常炎症反应有关.COPD的发病机制有多种,其中吸烟是影响COPD的一个主要的危险因素.吸烟引起氧化应激可直接损伤气道上皮,加重气道的炎症反应、炎前基因的表达,并导致蛋白酶/抗蛋白酶失衡最终导致气流受限.     

睡眠呼吸障碍与慢性阻塞性肺疾病

睡眠呼吸障碍涉及多学科，与传统的呼吸系统疾病有着密切联系。慢性阻塞性肺疾病（chronic obstructive pulmonary disease，COPD）是呼吸系统的常见病和多发病，患病率和死亡率均居高不下，且夜间死亡率明显高于日间。阻塞性睡眠呼吸暂停低通气综合征（OSAHS）也是一种常见的临床病症，主要表现为睡眠中反复出现上气道阻塞，导致反复的呼吸停止（睡眠窒息）和低通气，造成夜间二氧化碳（CO2）潴留、酸中毒和低氧血症等病理生理改变，从而引发重要器官出现功能和器质性改变，严重危害人类健康。COPD与OSAHS并存称为重叠综合征。     

中性粒细胞在慢性阻塞性肺疾病中的作用

慢性阻塞性肺疾病(chronic obstructive pneumonia discase,COPD)是以不完全可逆的气流受限为特征的慢性炎症性疾病.中性粒细胞可能在COPD的发展过程中发挥主要作用.活化的中性粒细胞释放蛋白酶、活性氧和细胞因子,引起肺组织损伤,最终导致气道黏液高分泌,气流受限和肺气肿.     

肺气肿影像学研究进展及临床应用

肺气肿是指肺终末细支气管远端气腔的异常永久性扩张，伴随着气道壁破坏，没有明显的纤维化。若肺气肿患者具有气流阻塞时，则存在慢性阻塞性肺病（chronic obstructive pulmonary disease，COPD）。没有气流阻塞的肺气肿不属于COPD。目前诊断COPD的金标准是肺功能检查。影像学检查可以早期发现肺气肿，并提示COPD。     

慢性阻塞性肺疾病营养不良的因素分析及治疗进展

慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)患者常合并营养不良,影响患者的肺功能和免疫功能.COPD营养不良是独立于气流阻塞严重程度之外影响COPD患者预后的原因之一,是COPD预后不良的独立危险因素.     

The nature, severity and distribution of obstructive airway lesions in COPD studied by morphometry and computer-assisted 3-D reconstruction

The severity of obstructive bronchial lesions and their distribution in the airway tree were studied in autopsy lungs from ten patients with various types of chronic obstructive pulmonary disease (COPD), where the changes of bronchial dimension were studied by morphometry and the 3-D distribution of obstructive lesions by computer-assisted 3-D reconstruction. A case of paraquat intoxication was added in order to study the airway changes in lungs with early fibrotic changes. In each case, morphometry was performed on microscopic lung sections where the initial diameter of bronchi was estimated from that of the accompanying pulmonary arteries. The varyingly constricted airways and arteries were standardized into a circular state by measuring the perimeter length L of the epithelial basement membrane (BM) and the internal elastic membrane (IEM) with a digital image analyzer; D(br), the anatomical diameter of an airway, and D(pa), that of an artery, were calculated at this state of completely stretched BM or IEM. Rs, the ratio of luminal stenosis by thickened epithelia, was also determined from the area of epithelium simultaneously measured. Three-D reconstruction of airway was performed in cases typically representing different types of obstruction; from microscopic, sometimes macroscopic serial sections, where the 2-D images were inputted into a computer which integrated in its display a 3-D picture. It was shown that in lungs with chronic bronchitis, the bronchial dimension did not significantly differ from that of ordinary lungs. Overt shrinkage of bronchial dimension was demonstrated in chronic obstructive bronchiolitis; in both diffuse panbronchiolitis (DPB) and broncho-bronchiolitis obliterans (BBO), narrowing of the peripheral airways combined with ectasis of the proximal bronchi proved to be a common feature. However, reconstruction disclosed an essential difference between these in the distribution of occlusive lesions, which mainly involved the respiratory bronchioles in DPB, while in BBO, the site of obstruction was from the terminal to slightly upper bronchioles. Also in pulmonary emphysema, the pattern of bronchial dimension was a narrowing in the periphery, both in the centrilobular and panlobular types. Especially worth of attention was that the study disclosed the presence of a type of COPD hitherto poorly defined. In a patient who had a 25-year history of COPD and died of respiratory failure, the lungs, only mildly emphysematous, were shown to have uniformly narrowed bronchioles; also mucus hypersecretion and elevated Rs appeared to have contributed to the obstruction.(ABSTRACT TRUNCATED AT 400 WORDS)     

Increased in vitro histamine responses in human small airways smooth muscle from patients with chronic obstructive pulmonary disease

We tested the hypothesis that abnormal responses of airway smooth muscle contribute to the pathogenesis of airway obstruction in chronic obstructive pulmonary disease (COPD). For this purpose, lung tissue from 10 patients with and 10 patients without COPD was obtained during thoracotomies. Lung function was measured preoperatively. The in vitro responses of isolated bronchioles were measured using histamine, leukotriene (LT)C4, and methacholine as contracting agents, and the results of the in vitro measurements were compared between patients with and without COPD. Histamine efficacy (maximal isometric force, Tmax) in vitro of bronchioles from patients with COPD was significantly greater than the histamine Tmax of the bronchioles from patients without COPD (p less than 0.01). This difference was probably not due to histamine tachyphylaxis or the production of relaxing prostaglandins by airways without COPD, as neither mechanism could be detected in separate experiments on airways without COPD. No differences were found between in vitro bronchiolar responses to LTC4 and methacholine in patients with and patients without COPD. Increased histamine responses of small airways may be one of the determinants of airway obstruction in COPD.     

Structural abnormalities and inflammation in COPD: a focus on small airways

Chronic obstructive pulmonary disease (COPD) is characterized by poorly reversible airflow limitation associated with airway remodelling and inflammation of both large and small airways. The site of airflow obstruction in COPD is located in the small airways, justifying a focus on this compartment. The structural abnormalities that are found in bronchioles with a diameter less than 2mm are characterized by increased airway wall thickness with peribronchial fibrosis, and by luminal obstruction by mucous exudates. Destruction of alveolar walls, the hallmark of emphysema, may be related to protease-antiprotease imbalance, and to mechanisms involving apoptosis, senescence, and autoimmunity. Cigarette smoke inhalation triggers the recruitment of innate immune cells (neutrophils and macrophages) and putatively adaptive immunity mediated via T and B lymphocytes and lymphoid follicles in the small airways. These data suggest a potential role for therapies that can target remodelling and inflammation in the small airways of patients with COPD.     

慢性阻塞性肺疾病呼出气冷凝液中的生物标记物及其意义

呼出气冷凝液(exhaled breath condensate,EBC)是一种无创研究气道内衬液成分的方法,也为评估肺部炎症提供可能.目前普遍认为,慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)是以气道、肺实质和肺血管的慢性炎症为特征的疾病.通过对COPD患者EBC的收集和检测,可实现对气道炎症的实时、无创、简单、重复的监测.     

慢性阻塞性肺疾病呼出气冷凝液中的生物标记物及其意义

呼出气冷凝液(exhaled breath condensate,EBC)是一种无创研究气道内衬液成分的方法,也为评估肺部炎症提供可能.目前普遍认为,慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)是以气道、肺实质和肺血管的慢性炎症为特征的疾病.通过对COPD患者EBC的收集和检测,可实现对气道炎症的实时、无创、简单、重复的监测.     

Systemic and upper and lower airway inflammation at exacerbation of chronic obstructive pulmonary disease

RATIONALE: In addition to pulmonary involvement, stable chronic obstructive pulmonary disease (COPD) is associated with nasal and systemic inflammation. Although exacerbations of COPD are associated with increased pulmonary and systemic inflammation, determinants of the systemic response remain obscure, and nor is it known whether there is nasal involvement. OBJECTIVES: To investigate upper airway, lower airway, and systemic inflammation at exacerbation of COPD. METHODS: We sampled sputum, nasal wash, and serum from 41 exacerbations (East London cohort) for analysis of pathogenic microorganisms and inflammatory indices (sputum/nasal wash leukocytes, interleukin [IL]-6, IL-8, and myeloperoxidase; serum IL-6 and C-reactive protein). Values were compared with stable COPD. MEASUREMENTS AND MAIN RESULTS: Exacerbation of COPD is associated with greater nasal, sputum, and serum inflammation than the stable state. At exacerbation, inflammatory markers were highly correlated within nasal wash and serum (all r >/= 0.62, p < 0.001), but not sputum. The degree of upper airway inflammation correlated with the degree of lower airway inflammation (e.g., nasal wash/sputum myeloperoxidase; r = 0.50, p = 0.001). The degree of systemic inflammation correlated with the degree of lower airway inflammation (e.g., serum IL-6/sputum IL-8; r = 0.35, p = 0.026), and was greater in the presence of a sputum bacterial pathogen (29.0 g/dl C-reactive protein difference, p = 0.002). We did not find relationships between the upper airway and systemic compartments. CONCLUSIONS: Exacerbation of COPD is associated with pan-airway inflammation; the systemic inflammatory response is proportional to that occurring in the lower airway and greater in the presence of a bacterial pathogen.     

慢性阻塞性肺疾病气道黏液高分泌研究进展

慢性阻塞性肺疾病(COPD)是由慢性气道和肺实质炎症引起的进行性气流受限的阻塞性疾病,气流受限不完全可逆.COPD是全球范围内慢性病发病和死亡的重要原因,而气道黏液高分泌是COPD发病和死亡的重要因素.黏液高分泌导致黏液纤毛清除受损、细菌定植、气道黏液栓形成以及气体交换功能障碍.为了阻止这个恶性循环,必须控制气道慢性炎...     

Exhaled nitric oxide--is it really a good marker of airway inflammation in bronchial asthma?

BACKGROUND: The concentration of exhaled nitric oxide ([NO]) has been reported to reflect the inflammatory process of airways in patients with bronchial asthma, particularly when they are steroid naive. However, it is not fully understood whether it equally reflects the degree of airway inflammation in patients receiving inhaled corticosteroids, but whose symptoms are not necessarily well controlled. OBJECTIVE: To examine whether the exhaled [NO] really reflects airway inflammation in patients with bronchial asthma, regardless of treatment with inhaled steroids. METHODS: Exhaled [NO] was measured in patients with bronchial asthma (43 steroid treated and 32 steroid naive), chronic obstructive pulmonary disease (COPD) (n = 36), bronchiectasis (n = 10) and in control subjects (n = 26). We examined in each asthmatic group whether the exhaled [NO] correlated with parameters reflecting airway inflammation. RESULTS: Exhaled [NO] was significantly correlated with symptom score, clinical severity, circulating eosinophil count, and the percentage of eosinophils in induced sputum in the steroid-naive asthmatics, but not in the steroid-treated asthmatics, although airway inflammation in this group was not well controlled, as evidenced by clinical symptoms and the higher percentage of eosinophils in induced sputum. Exhaled [NO] from the patients with COPD (6.2 +/- 0. 7 ppb) or bronchiectasis (5.4 +/- 1.3 ppb) was not significantly increased compared with the controls (6.0 +/- 1.0 ppb), and was significantly lower than in the asthmatic patients as a whole (19.0 +/- 2.0 ppb). CONCLUSIONS: Although exhaled [NO] is a useful marker of airway inflammation for differential diagnosis and evaluation of severity in steroid-naive patients with bronchial asthma, it may not be as useful in steroid-treated patients.