慢性阻塞性肺疾病的全身效应

 慢性阻塞性肺疾病（Chronic Obstructive Pulmonary Disease,COPD）是一种常见病、多发病,其典型表现为气流受限和气道重塑,导致肺的结构与功能的改变。由于COPD的患者多种炎症介质的激活使患者处于系统性炎症状态,使得COPD不仅仅是呼吸系统的疾病,同时还包含许多肺外表现,即全身效应。常见的全身性表现包括：骨骼肌萎缩、恶液质、骨质疏松;而慢性炎症使COPD的患者缺血性心脏病、肺动脉高压、糖尿病等疾病的患病率大大增加。     

慢性阻塞性肺疾病药物治疗研究

慢性阻塞性肺疾病（COPD）是一种最常见的慢性气道疾病,其起病较为缓慢、病程较长、病情迁延难愈,在早期没有自觉症状。伴随着病情的不断发展,可出现终身不愈的慢性咳嗽,并在气道、肺血管、肺实质内出现炎症应激反应,也会并发慢性呼吸衰竭、自发性气胸、慢性肺源性心脏病等疾病,严重影响患者正常工作与生活质量。目前,临床针对COPD的治疗仍以药物为主,药物治疗的目标在于改善临床症状、提高生活质量,延缓或减弱肺功能减退,预防和治疗并发症,提高存活率,避免或减少用药副作用。因此,寻求合适的药物治疗方案来满足COPD患者的临床治疗需求对于改善患者预后具有十分重要意义。本文通过对COPD致病机制、药物治疗方案作一综述,旨在为临床治疗该疾病提供参考依据。     

应用BIPAP通气治疗慢性阻塞性肺疾病呼吸衰竭的体会

目的　探讨基层医院开展双气道正压通气 (BIPAP)疗法在慢性阻塞性肺疾病 (COPD)呼吸衰竭患者治疗的应用价值 .方法　分析了 2 0例COPDⅡ型呼衰患者应用BIPAP通气 ,观察通气过程中症状体征变化 ,监测血气变化 .结果　除 2例须中途停机转院治疗外 ,其余 18例均取得较满意的疗效 ,气促减轻 ,呼吸频率减慢 ,辅助呼吸肌活动均减轻或消失 .PaO2 明显上升 (p <0 .0 1) ,PaCO2 降低 (p <0 .0 1) .18例平均住院天数缩短 .结论　BIPAP通气可改善缺氧 ,纠正二氧化碳潴留及呼吸性酸中毒 ,缩短住院时间 ,增加抢救成功率     

嗜酸性粒细胞在慢性阻塞性肺疾病中的研究现状

慢性阻塞性肺疾病（COPD）是一种复杂的异质性疾病,其气道炎症以中性粒细胞、巨噬细胞为主。近年研究发现某些COPD患者存在气道嗜酸性粒细胞（EOS）炎症,且具有某些明显特征,这提示了EOS参与了部分COPD患者的发病环节。鉴于EOS在COPD气道炎症中发病的重要性,本文就EOS与COPD的关系进行综述,以期为COPD的临床诊疗提供帮助。     

慢性阻塞性肺疾病患者的康复治疗

慢性阻塞性肺疾病（COPD）是呼吸系统常见病和多发病,因肺功能进行性减退,严重影响患者的劳动力和生活质量,随着人口老龄化,其患病率有逐年上升之势,对社会经济和人民健康都造成巨大的负担。近年来随着COPD研究的日益完善,在药物治疗的基础上进行康复锻炼及营养支持已成为治疗COPD的重要组成部分,合理的康复治疗可以减轻COPD患者的症状,提高生活质量。     

150例慢性阻塞性肺疾病患者的临床治疗研究

目的：研究慢性阻塞性肺疾病患者的临床治疗方法和效果。方法搜集2013年4月~2014年4月我院接收的慢性阻塞性肺疾病150例患者,按照就诊日期单双号分为对照组、实验组。对实验组77例应用多索茶碱,对对照组73例应用氨茶碱。观察对照组、实验组的治疗效果,并对比。结果与对照组相比,实验组PaO2、FEV1/FVC、PaCO2改善情况较好,治疗有效率较高,差异显著,有统计学意义(P<0.05)。结论对慢性阻塞性肺疾病患者应用多索茶碱,疗效较好,值得推广。     

慢性阻塞性肺疾病的分子遗传学研究进展

本文综述了慢性阻塞性肺疾病的主要发病因素和分子遗传学改变。应用现代分子生物学技术研究分子遗传学改变,将有助于及早确定慢性阻塞性肺疾病的发病原因和将来更好的用于疾病的预防和治疗。     

慢性阻塞性肺疾病合并肺动脉高压的药物治疗进展

慢性阻塞性肺疾病（COPD）作为一种慢性肺部疾病被人们熟知。近年来,随着对其认识的加深,COPD的各种并发症,尤其是肺动脉高压（PH）得到越来越多的关注。COPD合并PH患者的病死率升高且预后较差,严重影响了患者的生活质量,且对该疾病的治疗尚缺乏疗效确切的药物。为了充分了解该疾病的治疗现状,就COPD合并PH的药物治疗...     

慢性阻塞性肺疾病与免疫

1 慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)是一种呼吸系统常见的慢性疾病,现居当前疾病死亡原因的第4位.据预测,到2020年,COPD将成为全球范围主要死因的第3位.COPD以不完全可逆的气流受限为特征,而气流受限与小气道、肺泡对有害颗粒、气体产生的异常炎症反应有关.2004年Hogg等~([1])研究发现:COPD的病程与气道壁的厚度、小气道管腔内炎性渗出物量强相关.     

Effects of training at mild exercise intensities on quadriceps muscle energy metabolism in patients with chronic obstructive pulmonary disease

Aim: To study the effects of physical training at mild intensities on skeletal muscle energy metabolism in eight patients with chronic obstructive pulmonary disease (COPD) and eight paired healthy sedentary subjects. Methods: Energy metabolism of patients and controls vastus lateralis muscle was studied before and after 3 months of cycling training at mild exercises intensities. Results: The total amount of work accomplished was about 4059 ± 336 kJ in patients with COPD and 7531 ± 1693 kJ in control subjects. This work corresponds to a mechanical power set at 65.2 ± 7.5% of the maximum power for patients with COPD and 52 ± 3.3% of the maximum power in control group. Despite this low level of exercise intensities, we observed an improvement in mitochondrial oxidative phosphorylation through the creatine kinase system revealed by the increased apparent K_m for ADP (from 105.5 ± 16.1 to 176.9 ± 26.5 μm , P < 0.05 in the COPD group and from 126.9 ± 16.8 to 177.7 ± 17.0, P > 0.05 in the control group). Meanwhile, maximal mechanical and metabolic power increased significantly from 83.1 ± 7.1 to 91.3 ± 7.4 Watts (P < 0.05) and from 16 ± 0.8 to 18.7 ± 0.98 mL O₂ kg^?1 min^?1 (P < 0.05) only in the COPD group. Conclusion: This study shows that physical training at mild intensity is able to induce comparable changes in skeletal muscles oxidative energy metabolism in patients with COPD and sedentary healthy subjects, but different changes of maximal mechanical and metabolic power.     

Invasive pulmonary aspergillosis in chronic obstructive pulmonary disease: an emerging fungal pathogen

Acute invasive pulmonary aspergillosis occurs predominantly in immunocompromised hosts, with increasing numbers of cases of invasive aspergillosis among patients with chronic obstructive pulmonary disease (COPD) being reported. Among 13 cases of invasive aspergillosis diagnosed in COPD patients admitted to the intensive care unit with acute respiratory distress, the only risk factor for invasive fungal infection was corticosteroid treatment. Invasive aspergillosis should be suspected in COPD patients receiving steroid treatment who have extensive pulmonary infiltrates. Survival depends on rapid diagnosis and early appropriate treatment. A decrease or interruption of steroid treatment should be considered as part of the overall therapeutic strategy.     

慢性阻塞性肺疾病动物模型研究概况

慢性阻塞性肺病(chronic obstructive pulmonary disease,COPD)由基因-环境交互作用而致病,目前COPD拟临床研究大多是采用诱发性动物模型。动物选择根据实际需要以鼠、猪和灵长类动物为主。造模方法主要是将可诱发COPD的危险因素,强加于动物以诱导COPD的发生。造模时间的长短则与诱因的性质和暴露量密切相关。模型建成后主要从肺功能、肺部病理改变等方面,并采用血清炎症因子、细胞因子检测等手段对模型进行评价,但在实际操作中尚有待进一步的评估。     

慢性阻塞性肺病患者心理状况及影响因素

调查慢性阻塞性肺疾病（COPD）患者心理状况和影响因素,对60例患者和60例健康者对照,应用焦虑和抑郁情绪表（HAO）对两组进行问卷调查,结果显示,患者评分显著差于健康者,年龄、病程和通气功能与患者抑郁症状和总分呈显著性相关,提示患者伴有心理障碍,重视和兼顾心理症状诊治颇有必要。     

Immune response in chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a major public health problem because of its high prevalence, rising incidence and associated socio-economic cost. The inhalation of toxic particles and gases, mostly tobacco smoke, is the main risk factor for COPD. Yet, not all smokers are equally susceptible to these toxic effects and only a percentage of them develop the disease (so-called ‘susceptible smokers’). This, in combination with the observation that COPD shows familial aggregation, suggests that the genetic background of the smoker is a key element in the pathogenesis of the disease. On the other hand, it is well established that ‘susceptible’ smokers exhibit an enhanced inflammatory response of the lung parenchyma as compared with ‘resistant’ smokers (i.e., those who manage to maintain lung function within the normal age range despite their habit). Importantly, in COPD patients this inflammatory response does not resolve after quitting smoking, again at variance with resistant smokers. All in all, these observations suggest that the pathogenesis of COPD may involve, in some patients, an autoimmune component which contributes to the enhanced and persistent inflammatory response that characterizes the disease. Here we: i) review briefly the pathobiology of COPD; ii) present the available scientific evidence supporting a potential role for autoimmunity in COPD; iii) propose a three-step pathogenic hypothesis in the transition from smoking to COPD; and iv) discuss potential implications for the diagnosis and treatment of this frequent, growing, devastating and costly disease.     

Neutrophils and emerging targets for treatment in chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is characterized by a decreased airflow due to airway narrowing that, once it occurs, is not fully reversible. The disease usually is progressive and associated with an enhanced inflammatory response in the lungs after exposure to noxious particles or gases. After removal of the noxious particles, the inflammation can continue in a self-sustaining manner. It has been established that improper activation of neutrophils lies at the core of the pathology. This paper provides an overview of the mechanisms by which neutrophils can induce the pulmonary damage of COPD. As the pathogenesis of COPD is slowly being unraveled, new points of intervention are discovered, some of which with promising results.     

Severe chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) exacts a heavy toll on society, yet its prevention, diagnosis and treatment receives inadequate attention from both the medical community and from society at large. Guidelines released in 2001 from the Global Initiative for Chronic Obstructive Lung Disease (GOLD) are aimed at redressing this inequity. In this review, we integrate information from the GOLD guidelines with recent updates on the prevention, treatment and management as related specifically to the most severe form of this disease. In order to help distinguish COPD from other disorders that may mimic or confound its treatment, we place particular emphasis on the definition, underlying pathophysiology and diagnosis of COPD. In addition, we discuss future directions in pharmacotherapy.     

Leukotriene pathway inhibitors in asthma and chronic obstructive pulmonary disease

Leukotrienes can be generated from a wide variety of cells including mast cells and eosinophils. The biological properties of these products include bronchial smooth muscle contraction, stimulation of mucous production, enhancement of vascular permeability, and recruitment of eosinophils. These properties can contribute significantly to the pathobiology of asthma. Recently, zafirlukast and montelukast, and zileuton, leukotriene D₄ receptor antagonists and 5-lipoxygenase inhibitors, respectively, have been developed and are available for treating asthma. Studies have found these compounds modify bronchospasm with exercise, the pulmonary reaction to aspirin in sensitive subjects, and the airway response to inhaled antigen. Furthermore, in patients with chronic asthma, leukotriene modifiers improve airflow obstruction, decrease the need for rescue medication, and diminish symptoms. Moreover, these drugs can prevent asthma exacerbations. However, there is little evidence that these medications have potent anti-inflammatory activity. Nonetheless, leukotriene modifiers represent new, and effective, therapeutics in the treatment of asthma; at present, the positioning of these products in relationship to inhaled corticosteroids, for example, in the treatment of asthma has not been fully defined but will emerge with further study and use in the clinic setting.