Chronic obstructive pulmonary disease

Morbidity and mortality associated with chronic airway disease are expected to continue to rise over the coming years. Accordingly, increased attention will need to be directed toward the diagnosis and treatment of COPD in the elderly population. Cessation of cigarette smoking should be pursued in all patients regardless of age. The goals of bronchodilator therapy are to reduce respiratory symptoms and to improve functional capacity without causing adverse effects. In addition, supplemental oxygen, phlebotomy for polycythemia, general exercise training, and specific respiratory muscle training may further augment exercise tolerance. Complications of COPD, such as upper respiratory infections and right heart failure, should be recognized early and treated appropriately. Implementation of a pulmonary rehabilitation program, as discussed in the next article, should complement medical therapy in the treatment of elderly patients with COPD.     

Chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a major cause of death and disability worldwide. Recognition that the burden of this disorder will continue to increase over the next 20 years despite medical intervention has stimulated new research into the underlying mechanisms, leading to a rational basis for evaluation of existing therapies, and has suggested novel treatment approaches. Tobacco exposure remains the main but not exclusive cause of COPD. Whether the lung is injured by changes in the balance of proteases and antiproteases, tissue damage by oxidative stress, or a combination of the two is still not known. The genetic basis of susceptibility to COPD is now being studied as is the role of computed tomography in the identification of structural damage in individuals with less symptomatic disease. Clinical diagnosis still relies heavily on an appropriate history confirmed by abnormal spirometry. Smoking cessation is possible in a substantial proportion of individuals with symptoms but is most effective if withdrawal is supported by pharmacological treatment. Treatment with long-acting inhaled bronchodilators and, in more severe disease, inhaled corticosteroids reduces symptoms and exacerbation frequency and improves health status. Rehabilitation can be even more effective, at least for a year after the treatment. Recent guidelines have made practical suggestions about how to optimise these treatments and when to consider addition of oxygen, surgery, and non-invasive ventilation. Regular review of this guidance is important if future management advances are to be implemented effectively.     

Chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is characterised by progressive airflow obstruction that is only partly reversible, inflammation in the airways, and systemic effects or comorbities. The main cause is smoking tobacco, but other factors have been identified. Several pathobiological processes interact on a complex background of genetic determinants, lung growth, and environmental stimuli. The disease is further aggravated by exacerbations, particularly in patients with severe disease, up to 78% of which are due to bacterial infections, viral infections, or both. Comorbidities include ischaemic heart disease, diabetes, and lung cancer. Bronchodilators constitute the mainstay of treatment: β(2) agonists and long-acting anticholinergic agents are frequently used (the former often with inhaled corticosteroids). Besides improving symptoms, these treatments are also thought to lead to some degree of disease modification. Future research should be directed towards the development of agents that notably affect the course of disease.     

New concepts in the pathobiology of chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is characterized by an abnormal persistent inflammatory response to cigarette smoke. This noxious insult leads to emphysema and airway remodeling, manifested by squamous and mucous metaplasia of the epithelium, smooth muscle hypertrophy, and airway wall fibrosis. These pathologic abnormalities interact synergistically to cause progressive airflow obstruction. Although it has been accepted that the spectrum of COPD is vast, the reasons for the development of different phenotypes from the same exposure to cigarette smoke have not been determined. Furthermore, it is becoming increasingly clear that airways disease and emphysema often coexist in many patients, even with a clear clinical phenotype of either emphysema or chronic bronchitis. Recent studies have focused on the nature of the inflammatory response to cigarette smoke, the inflammatory cell lines responsible for COPD pathogenesis, and new biomarkers for disease activity and progression. New cytokines are being discovered, and the complex interactions among them are being unraveled. The inflammatory biomarker that has received the most attention is C-reactive protein, but new ones that have caught our attention are interleukin (IL)-6, tumor necrosis factor-alpha, IL-8, and IL-10. Further research should focus on how these new concepts in lung inflammation interact to cause the various aspects of COPD pathology.     

慢性阻塞性肺疾病:思考与展望

慢性阻塞性肺疾病(慢阻肺)是一种常见慢性病。相比以前我们对慢阻肺的有限认识,目前研究结果表明慢阻肺的临床与生物学特征具有明显的复杂性和异质性。本文重点结合目前国际上几个大型临床队列研究结果,对慢阻肺高危人群的识别、诊断、评估及治疗方面的进展进行了阐述与展望。     

Chronic obstructive pulmonary disease: brief review

The aim of this short review is to draw attention to chronic obstructive pulmonary disease (COPD), a clinical syndrome associated with emphysema and/or chronic bronchitis, in the light of the current scientific knowledge. The reason is that COPD has high socio-economic costs and the most recent projections place it among the first causes of mortality and morbidity due to chronic disease. The nosography, the clinical picture, including the systemic manifestations, the pathogenesis and the pathophysiological mechanisms, with special emphasis on expiratory flow limitation and pulmonary hyperinflation, leading to the most relevant symptoms and signs of the disease, have been reviewed. Finally a brief analysis of the costs due to the disease is also provided.     

慢性阻塞性肺疾病表型的研究进展

目前COPD的诊断、评估和治疗面临着困境.一方面,COPD定义为不完全可逆的气流受限疾病,根据气流受限严重程度指导治疗[1];而另一方面,COPD又是具有肺和多种肺外效应的多系统疾病,因此,患者在临床表现、生理学、影像学、对治疗的反应、肺功能下降速度和死亡等方面存在明显的异质性.目前普遍认为,FEV1本身不能全面反映疾病的复杂性,也不能单独用FEV1作为疾病诊断、评估和治疗的手段[2-3],但目前尚无其他替代标准.解决这种问题的有效方法是对COPD综合征的重要组成部分进行识别及分组,形成亚组(即表型,phenotype),这种亚组能反映疾病的预后,并指导对患者的治疗[4-5].     

慢性阻塞性肺疾病与自身免疫

慢性阻塞性肺疾病是一种与肺部对香烟烟雾等有害气体或有害颗粒的异常炎症反应有关的慢性疾病.近来研究显示慢性阻塞性肺疾病存在自身免疫成分.抗内皮细胞抗体、抗弹性蛋白抗体可导致肺气肿;吸烟和微生物感染可通过多种途径介导自身免疫性肺组织损伤;CD4+CD25+调节性T细胞上调不足可促进自身免疫反应性淋巴细胞介导的肺部炎症持续进展.探讨自身免疫在慢性阻塞性肺疾病中的作用,为其发病机制、诊断和治疗提供新思路.     

慢性阻塞性肺病和骨质疏松

慢性阻塞性肺病(COPD)不仅是肺部疾病,而且是一种全身性疾病.骨质疏松是COPD患者的肺外表现之一.随着COPD患者病情加重,骨质疏松的发病率亦有所增加.但COPD患者发生骨质疏松的机制至今尚未完全明确.探讨COPD患者骨质疏松症的发生情况及影响因素,有助于提高对COPD发生骨质疏松的早期认识,预防骨质疏松的发生、发展,对改进COPD患者的生活质量和延长生命具有重要意义.     

慢性阻塞性肺疾病与肺构形重建

目的　观察慢性阻塞性肺疾病（ Ｃ Ｏ Ｐ Ｄ） 合并肺心病尸检２０ 例的肺部病变特征及其与肺构形重建的关系。方法　常规或低压（１８４ ～３３４ ｍ ｍ Ｈｇ） 福尔马林灌注固定肺组织。用点计数法检测大肺片的肺气肿百分值。常规切片、 Ｚｅｉｓｓ 显微测微器定量测量细支气管的病变特征和肺间质纤维化所占百分值。天狼猩红苦味酸染色,偏振光镜观察,真彩色图像分析Ⅰ、Ⅲ两型胶原分布比值。结果　 Ｃ Ｏ Ｐ Ｄ 病例中以不规则型和囊泡型肺气肿最多见（１７／２０） ,１３ 例有中度和重度肺气肿,心重＞ ４００ｇ 者６ 例。肺纤维化组织占肺总切面积平均为（２７１ ±２９） ％ ,对照组为（１２０ ±１８） ％ ;Ⅰ型与Ⅲ型胶原面积比为５６∶１ ,对照组为１３∶１ ; Ｃ Ｏ Ｐ Ｄ 组１ ５０４ 支细支气管均有慢性细支气管炎,其中合并急性炎症者占３８ ％ ;管腔狭窄和纤维性闭锁者占５３ ％ 。结论　急、慢性细支气管炎和细支气管周围炎是 Ｃ Ｏ Ｐ Ｄ 的重要肺部病变,也是导致肺组织和血管构形重建的重要环节。     

慢性阻塞性肺病与胃食管反流病

目的：了解慢性阻塞性肺病(COPD)患者中胃食管反流病(GERD)的发生率及探讨GERD与COPD的关系。方法：从医院门诊收集89例COPD患者[第1秒用力呼气量(FEV_1)=1．37±0．53],同时选取88例非COPD患者为对照组,所有病例完成反流性疾病诊断问卷、慢性黏液高分泌症(CMH)问卷和肺功能检查。结果：COPD组中GERD发生率为18%,对照组为16%。气道阻塞严重(根据肺功能判断)的COPD患者没有更高的GERD发生率,各不同严重程度的COPD患者的GERD发生率分别为11%(轻度)、24%(中度)、11%(重度)和19%(极重度)。气促程度严重的COPD患者中GERD发生率较气促程度轻者升高(29%比15%,P=0．19)。有CMH的患者中27%表现GERD,而无CMH患者中仅8%表现GERD(P＜0．05)。结论：本研究发现COPD患者中GERD的发生率没有明显增高,但气促症状严重的患者表现较高的GERD发病率。CMH与GERD有显著的相关性,提示CMH的潜在作用及在治疗有CMH的COPD患者时需考虑GERD影响。     

慢性阻塞性肺疾病与凝血-纤溶功能异常

慢性阻塞性肺疾病（COPD）是以气道、肺实质和肺血管的慢性炎症为特征。因肺内通气血流比例失调致慢性缺氧，可继发红细胞增多和血黏滞度增高，引起血流高黏、高聚、高凝及微血栓形成。COPD急性加重期凝血-纤溶功能异常进一步恶化，对病情进展的影响已经为临床高度关注。研究同时发现COPD与静脉血栓栓塞症（VTE）关系密切，其合并深静脉血栓（DVT）甚至肺血栓栓塞症（PTE）已成为重要的医疗保健问题。