慢性阻塞性肺疾病系统性炎症的治疗进展

慢性阻塞性肺疾病机制复杂,不仅表现为肺部的局部炎症,而且存在系统性炎症反应,后者导致一些肺外器官受损.目前,正在研究针对于控制系统性炎症的新的治疗方法.综述了治疗COPD患者系统性炎症的新方法.     

024 体外循环术后肺损伤及其防治

体外循环术后肺功能障碍一直是心脏外科最常见的临床并发症之一.体外循环引起的系统性炎症反应被认为是导致体外循环术后肺损伤的首要因素,各种旨在降低系统性炎症反应的肺保护措施也层出不穷.本文就近年来有关体外循环术后肺损伤发生的分子生物机制和防治方面的研究作一综述.     

慢性阻塞性肺疾病与慢性炎症

慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)患病率高、病程长、病死率高,已成为严重的社会负担.小气道炎症是COPD的主要病变及导致肺功能进行性损害的主要原因,同时大量研究证明COPD患者存在系统性炎症,但目前对于COPD气道炎症与系统性炎症的关系尚不十分明确.     

稳定期慢性阻塞性肺疾病气道炎症与系统性炎症关系的研究

目的 初步探讨稳定期慢性阻塞性肺疾病(COPD)气道炎症与系统性炎症的关系.方法 入选符合中华医学会呼吸病学分会2007年COPD指南的稳定期COPD患者35例.检测肺功能、痰定量细菌培养及痰细胞计数与分类、测定血浆纤维蛋白原、血清C反应蛋白(C-reactive protein,CRP)水平,分析气道炎症与系统性炎症...     

慢性阻塞性肺疾病骨骼肌功能障碍分子机制研究进展

骨骼肌功能障碍是慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)患者的重要并发症.它的发生与氧化应激,骨骼肌纤维类型的转换,全身系统性的炎症,骨骼肌的线粒体功能障碍有关.本文就其可能分子机制及治疗前景作一综述.     

慢性阻塞性肺疾病骨骼肌功能障碍分子机制研究进展

骨骼肌功能障碍是慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)患者的重要并发症.它的发生与氧化应激,骨骼肌纤维类型的转换,全身系统性的炎症,骨骼肌的线粒体功能障碍有关.本文就其可能分子机制及治疗前景作一综述.     

体外循环术后肺损伤及其防治

体外循环术后肺功能障碍一直是心脏外科最常见的临床并发症之一。体外循环引起的系统性炎症反应被认为是导致体外循环术后肺损伤的首要因素,各种旨在降低系统性炎症反应的肺保护措施也层出不穷。本文就近年来有关体外循环术后肺损伤发生的分子生物机制和防治方面的研究作一综述。     

体外循环术后肺损伤及其防治

体外循环术后肺功能障碍一直是心脏外科最常见的临床并发症之一，体外循环引起的系统性炎症反应认为是导致体外不术后肺损伤的首要因素，各种旨在降低系统性炎症反应的肺保护措施也层出不穷，本文就近来有关体外循环术后肺损伤发生的分子生物制和防治方面的研究作一综述。     

炎症及NLRP3炎性小体在肺动脉高压中的作用研究进展

肺动脉高压是以肺动脉压力进行性升高为主要特征的肺血管疾病,可导致右心衰竭甚至死亡,目前尚无特效药。近年医学界发现炎症参与了肺动脉高压的发生、发展,其中NLRP3炎性小体作为启动固有免疫应答的关键炎症信号平台有望成为人们系统性认识肺动脉高压炎症性质的蛋白复合物,也可能是治疗的潜在靶点。本文就炎症及NLRP3炎性小体在肺动脉高压中的作用进行综述。     

显微镜下多血管炎相关肺纤维化3例及文献复习

显微镜下多血管炎（microscopic polyangiitis,MPA）是一种主要累及小血管的系统性坏死性血管炎,多见于中老年患者,肾脏及肺为其最常受累及的器官。肺受累表现为肺泡出血、坏死性气道炎症、间质炎症及纤维化,其影像表现不具有特征性。     

Local and systemic inflammation in chronic obstructive pulmonary disease

There is growing evidence for systemic inflammation in chronic obstructive pulmonary disease (COPD). Increased circulating levels of inflammatory cytokines and acute phase proteins occur in stable disease, and COPD exacerbations are notably associated with pulmonary and systemic inflammation. Although the course of inflammation is determined by the balance between pro- and antiinflammatory mediators, in COPD most attention has focused on the former. During exacerbation, however, upregulation of antiinflammatory markers occurs. The main causes of systemic inflammation in COPD remain to be elucidated, although systemic hypoxia is a candidate factor. Although a relationship between lung and systemic inflammation has been suggested, experimental evidence indicates no direct correlations in the regulation of inflammation in the pulmonary and systemic compartments. Longitudinal studies are needed to unravel the role of systemic inflammation in the course of COPD, to analyze the role of acute exacerbations on the chronicity of inflammation, and to evaluate the response of systemic inflammation to different interventions. Emphasis should be placed on the identification of signaling pathways induced and/or altered in skeletal muscle by inflammation, as muscle wasting is a prominent feature of chronic inflammatory disease conditions and contributes significantly to impaired physical functioning and health status in COPD.     

Effects of corticosteroids on systemic inflammation in chronic obstructive pulmonary disease

Patients with chronic obstructive pulmonary disease (COPD) are predisposed to atherosclerosis and coronary artery disease, but the underlying mechanisms are unclear. Although there is wide acceptance that atherosclerosis is related to systemic inflammation, the cause(s) and mechanism(s) of pulmonary inflammation in stable COPD remain unknown. Infectious (bacterial and viral) as well as noninfectious agents can cause acute exacerbations in COPD, and they intensify local and systemic inflammation. Although it is not known how systemic inflammation develops in stable COPD, there is good evidence to suggest that it occurs and that the intensity of systemic inflammation is linked to the severity of airflow obstruction. We postulate that systemic inflammation provides the linkage between COPD and atherosclerosis. Inhaled corticosteroids have been shown to improve health outcomes in COPD, but the mechanism by which this occurs is a pivotal and challenging question that has yet to be answered. To prove the concept that inhaled corticosteroids could suppress systemic inflammation (as exemplified by serum C-reactive protein [CRP] levels), a double-blind, placebo-controlled clinical trial was conducted in a group of patients with mild to moderate COPD. We found that withdrawal of inhaled corticosteroids increased serum CRP levels, and that reintroduction of inhaled fluticasone could suppress CRP levels.     

Local and systemic inflammation in patients with chronic obstructive pulmonary disease: soluble tumor necrosis factor receptors are increased in sputum

Chronic obstructive pulmonary disease (COPD) is characterized by significant chronic inflammation in the pulmonary compartment as well as in the circulation. This study aimed to elucidate the relationship between local and systemic inflammation in smoking-induced COPD by assessing levels of soluble (s) tumor necrosis factor (TNF) receptors, TNF-alpha, and interleukin-8 (IL-8) in induced sputum and in plasma. Sputum induction was performed in 18 subjects with COPD (FEV(1) 56% predicted) and 17 healthy smokers (FEV(1) 99% predicted). Patients with COPD showed significantly higher percentages of neutrophils and levels of sTNF-R55 and IL-8 in sputum as compared with control subjects, whereas sputum sTNF-R75 levels tended to be higher in COPD. Sputum TNF-alpha levels were similar in both groups. When comparing sTNF receptors in sputum and plasma, no direct correlations were found despite elevation of circulating sTNF-R75 levels in patients with COPD. In addition, sputum sTNF receptors were inversely related to the FEV(1) in patients with COPD, whereas circulating sTNF receptors were not, suggesting different regulation of inflammation in the pulmonary and systemic compartment. When subjects were divided according to their current smoking status, levels of sTNF-R55, sTNF-R75, and IL-8 in sputum were significantly elevated in ex-smoking versus currently smoking patients with COPD, suggesting ongoing inflammation in airways and circulation of patients with COPD after smoking cessation.     

慢性阻塞性肺疾病合并症研究进展

慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)表现为慢性肺部及全身炎症反应,以进行性不完全可逆性气流受限为特征.COPD患者往往合并一种或多种肺外症状(COPD合并症),这可能是COPD慢性炎症反应的伞身表现,也可能与共同的危险因素(如吸烟、年龄等)有关.这些合...     

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.     

COPD骨骼肌功能障碍机制研究进展

COPD 是一种以不完全可逆的气流受限为特征的慢性衰竭性疾病。除肺部的病变外, COPD 患者还伴随着其他系统性疾病,其中之一就是骨骼肌功能障碍(skeletal muscle dysfunction, SMD)。SMD 的发生机制是多重因素的,系统性和局部性因素都有参与。系统性因素包括系统性炎症,氧化和氮化应激,营养不良,类固醇激素,肌肉的失用和急性加重等;局部性因素包括肌肉炎症,氧化和氮化应激,局部解剖性和代谢性因素。本文简要地总结了这些因素对于 COPD 患者 SMD 的影响的机制。     

Systemic inflammation and comorbidities in chronic obstructive pulmonary disease

The relationship between systemic inflammation and comorbidities in patients with chronic obstructive pulmonary disease (COPD) is unclear. This article discusses (1) the prevalence and clinical impact of comorbidities in COPD; (2) the current knowledge on definition, prevalence, consequences, and treatment of systemic inflammation in COPD; and (3) the relationship of systemic inflammation and lung cancer in COPD.     

Aspects on pathophysiological mechanisms in COPD

Chronic obstructive pulmonary disease (COPD) is a condition which is characterized by irreversible airway obstruction due to narrowing of small airways, bronchiolitis, and destruction of the lung parenchyma, emphysema. It is the fourth most common cause of mortality in the world and is expected to be the third most common cause of death by 2020. The main cause of COPD is smoking but other exposures may be of importance. Exposure leads to airway inflammation in which a variety of cells are involved. Besides neutrophil granulocytes, macrophages and lymphocytes, airway epithelial cells are also of particular importance in the inflammatory process and in the development of emphysema. Cell trafficking orchestrated by chemokines and other chamoattractants, the proteinase-antiproteinase system, oxidative stress and airway remodelling are central processes associated with the development of COPD. Recently systemic effects of COPD have attracted attention and the importance of systemic inflammation has been recognized. This seems to have direct therapeutic implications as treatment with inhaled glucocorticosteroids has been shown to influence mortality. The increasing body of knowledge regarding the inflammatory mechanism in COPD will most likely have implications for future therapy and new drugs, specifically aimed at interaction with the inflammatory processes, are currently being developed.