Tuberculosis and its incidence, special nature, and relationship with chronic obstructive pulmonary disease

Tuberculosis (TB) and chronic obstructive pulmonary disease (COPD) carry a significant burden in terms of morbidity and mortality worldwide. This review article focuses on different aspects of Tuberculosis in terms of the relationship with COPD such as in the development of chronic airflow obstruction as a sequel to active TB and reviewing the key role of cigarette smoking in the pathogenesis of both conditions. Patients diagnosed with TB may often have extensive co-morbidity such as COPD and the effect of an underlying diagnosis of COPD on outcomes in TB is also reviewed.     

Limited functional performance in chronic obstructive pulmonary disease: nature, causes and measurement

Patients with chronic obstructive pulmonary disease (COPD) frequently describe limitations in functional performance. These limitations predict mortality, adversely affect health-care burden and impair health-related quality of life. The optimal method for quantifying the functional performance in COPD subjects has not been established. This paper discusses the (i) nature of limited functional performance reported by individuals with COPD, (ii) mechanisms that contribute to these limitations, (iii) assessment techniques available to provide markers of functional performance and (iv) areas for further research in measuring functional performance of COPD subjects.     

New therapies for chronic obstructive pulmonary disease,lung regeneration

Chronic obstructive pulmonary disease (COPD) is characterized by the presence of airflow limitations that are not fully reversible and is a major cause of chronic morbidity and mortality worldwide. Although there has been extensive research examining the molecular mechanisms underlying the development of COPD, there is no proven clinically effective treatment for promoting recovery from established COPD. At present, regeneration is the only hope for a cure in patients with COPD. In this article, we review current treatments for COPD, focusing particularly on recent advances in lung regeneration based on two major approaches: regeneration-promoting agents and cell therapy. Retinoic acids are the major focus among regeneration-promoting agents, while mesenchymal stem cells are the main topic in the field of cell-based therapy. This article aims to provide valuable information for developing new therapies for COPD.     

Anemia in chronic obstructive pulmonary disease: A systematic review

IntroductionChronic obstructive pulmonary disease (COPD) is a type of obstructive lung disease that is characterized by poor airflow and airway inflammation. It is estimated that the global prevalence of COPD is about 13.1%. Anemia is associated with increased morbidity and hospitalization duration. In this systematic review, we investigate the association between all types of anemia and COPD progression.MethodsWe systematically searched electronic databases, including Scopus, Medline/PubMed, EMBASE, Web of Sciences (WOS), and Cochrane Library, using the following mesh-standardized keywords: (((anemia1 OR anaemia1) OR “chronic anemia disease” [Mesh] OR “CAD” OR “iron deficiency anemia” OR” IDA” OR) AND (“COPD” [Mesh] OR “chronic obstructive pulmonary disease”)) until February 2022.ResultsOverall of 11,158 studies were included. Ultimately, 59 studies were included in the analysis. The most apparent findings from the analysis were that exacerbation of COPD, increased hospitalization, and increased long-term mortality were associated with anemia. Further analysis showed that iron deficiency (ID) is a common finding in COPD and is accompanied by an increase in the systolic pulmonary artery pressure.ConclusionDespite the comfortable control of anemia, the absence of treatment can be life-threatening in patients with COPD. Our systematic results showed significant homogeneity between studies on the increased mortality rate in anemic COPD, increased hospitalization, and decreased quality of life.     

Angiotensin-converting-enzyme gene polymorphisms, smoking and chronic obstructive pulmonary disease

While tobacco smoking is the main risk factor for chronic obstructive pulmonary disease (COPD) only a fraction of smokers go on to develop the disease. We investigated the relationship between the insertion (I) – deletion (D) polymorphisms in the Angiotensin converting enzyme (ACE) gene and the risk of developing COPD in smokers by determining the distribution of the ACE genotypes (DD, ID and II) in 151 life-long male smokers. 74 of the smokers had developed COPD (62 ± 2 years; FEV₁ 44 ± 6 % reference) whereas the rest retained normal lung function (56 ± 2 yrs; FEV₁ 95 ± 3 % reference). In addition, we genotyped 159 males recruited randomly from the general population. The prevalence of the DD genotype was highest (p = 0.01) in the smokers that developed COPD and its presence was associated with a 2-fold increase in the risk for COPD (OR 2.2; IC95% 1.1 to 5.5). Surprisingly, the 151 individuals in the smoking population did not demonstrate Hardy-Weinberg equilibrium unlike the 159 recruited from the general population. Our results suggest that ACE polymorphisms are associated with both the smoking history of an individual and their risk of developing COPD.     

Pulmonary epithelium, cigarette smoke, and chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a complex chronic inflammatory disease involving a wide variety of cells and inflammatory mediators. The most important etiological factor in the development of this disease is cigarette smoking. Much of the research into the mechanisms of COPD has been concerned with the induction of inflammation and the role of neutrophils and macrophages in the pathophysiology of the disease. The possible contribution of the epithelium to the development of COPD has only recently become apparent and remains unclear. In this article we review research into the effect of cigarette smoke on the pulmonary epithelium with particular emphasis on oxidative stress, proteolytic load, pro-inflammatory cytokine and chemokine profile and epithelial secretions. In addition, we have also reviewed how cigarette smoke may affect epithelial damage and repair processes.     

血管内皮生长因子与慢性阻塞性肺疾病

慢性阻塞性肺疾病是一个发病率和死亡率都很高的慢性疾病，其发病机制涉及肺内细胞的凋亡，肺实质细胞的减少，炎性细胞的浸润和气道、血管的重构。血管内皮生长因子作为一个可特异作用于内皮细胞，调节血管内皮细胞生长、分化、修复及发挥功能的重要因子，与慢性阻塞性肺疾病的发生有着密切的联系。     

慢性阻塞性肺疾病发病机制的研究进展

目前,COPD的高发病率和病死率是在世界范围内导致巨大经济和社会负担的主要原因。COPD发病机制复杂,炎症反应、氧化应激、蛋白酶／抗蛋白酶失衡、细胞凋亡是COPD发病机制的关键环节,感染是造成COPD急性加重和病情进展的主要因素,自身免疫可能是导致COPD患者戒烟后肺内炎症持续存在的主要原因。香烟烟雾引起的肺损伤最终形成自我放大的持续过程,导致临床症状及病理改变。     

Mechanisms of atherothrombosis in chronic obstructive pulmonary disease

Patients affected by chronic obstructive pulmonary disease (COPD) have an increased risk of atherothrombotic acute events, independent of smoking and other cardiovascular risk factors. As a consequence, myocardial ischemia is a relevant cause of death in these patients. We reviewed studies concerning the potential mechanisms of atherothrombosis in COPD. Bronchial inflammation spreads to the systemic circulation and is known to play a key role in plaque formation and rupture. In fact, C-reactive protein blood levels increase in COPD and provide independent prognostic information. Systemic inflammation is the first cause of the hypercoagulable state commonly observed in COPD. Furthermore, hypoxia is supposed to activate platelets, thus accounting for the increased urinary excretion of platelet-derived thromboxane in COPD. The potential metabolic risk in COPD is still debated, in that recent studies do not support an association between COPD and diabetes mellitus. Finally, oxidative stress contributes to the pathogenesis of COPD and may promote oxidation of low-density-lipoproteins with foam cells formation. Retrospective observations suggest that inhaled corticosteroids may reduce atherothrombotic mortality by attenuating systemic inflammation, but this benefit needs confirmation in ongoing randomized controlled trials. Physicians approaching COPD patients should always be aware of the systemic vascular implications of this disease.     

Exacerbations of chronic obstructive pulmonary disease--a patients' perspective.

BACKGROUND: Exacerbations are now an important clinical variable for research into, and management of, chronic obstructive pulmonary disease (COPD). Emphasis is usually on reductions in the incidence of exacerbations and their impact on quality of life. For such research to be useful and comparable there needs to be a clearly defined understanding of what is meant by the term 'exacerbation'. The aim of this study was to explore the notion of COPD exacerbations from the viewpoint of patients who had recently suffered an exacerbation. METHODS: Using principles from grounded theory we conducted semi-structured, in-depth interviews with 23 volunteers from Denmark, the Netherlands and the UK who were identified as having had a COPD exacerbation. Interviews were recorded locally and translated into English for analysis. Notable themes were identified for each informant and their occurrences compared. RESULTS: Patients' reasons for consulting fell into four categories: 'frightening change'; 'change in sputum colour'; 'gradual deterioration'; and 'opportunistic diagnosis'. Most patients consulted frequently about their COPD, but did not afford their exacerbations the same degree of prominence as healthcare professionals (HCPs). CONCLUSIONS: These data provide a new way of thinking about COPD exacerbations, offering a greater understanding and classification of the reasons underlying the decision of COPD patients to consult with HCPs. They suggest that the patient perspective of exacerbations is more complex than previously thought. These findings could be applied to clinical practice and research, facilitating focussed decisions on COPD management.     

The role of anticholinergic bronchodilators in adult asthma and chronic obstructive pulmonary disease

Our renewed interest in anticholinergic bronchodilator therapy has been sparked by the development of safe yet effective quaternary anticholinergic compounds including ipratropium bromide, oxitropium and atropine methonitrate. These agents offer gradual and sustained bronchodilatation to patients with asthma and to patients with COPD. However, their role in the maintenance treatment of these two diseases differs significantly. In asthma, the anticholinergic drugs have useful additive properties when used with adrenergic drugs or theophylline. They may be a particularly useful component of combination regimens in patients with disease of more than mild severity and in older patients. The combination of inhaled adrenergic and anticholinergic drugs is also useful in the acute setting for acute exacerbations of asthma. In chronic obstructive lung disease, the anticholinergic compounds offer greater bronchodilatation than adrenergic drugs for the majority of patients. Thus, the inhaled anticholinergic drugs may be considered as useful initial choices in the chronic maintenance therapy of COPD.     

联合吸入福莫特罗和布地奈德干粉剂对稳定期COPD的疗效观察

目的观察中重度COPD稳定期患者联合吸入福莫特罗和布地奈德干粉剂的临床疗效。方法48例中重度COPD稳定期患者随机分为2组,治疗组（n=24）联合吸入长效B2受体激动剂福莫特罗和糖皮质激素布地奈德。对照组（n=24）为空白对照组,不吸入福莫特罗和布地奈德。观察2组用药12周后肺功能的变化,StGeorge’s呼吸问卷（SGRQ）等情况,通过六分钟步行试验（6MWT）观察运动耐力的变化以及随访3—6个月急性加重的人次、住院人次。结果用药12周后治疗组FEV1、FVC、最大肺活量（FVC）、FEV1／FVC及FEV1占预计值（％）比对照组明显改善,2组比较差异有显著性（P〈0．05）,治疗组运动耐力（6MWT）增加,随访3～6个月治疗组急性加重人次明显减少,与对照组比较差异有显著性（P〈0．05）。结论联合吸入长效β2受体激动剂福莫特罗和糖皮质激素布地奈德可以改善稳定期中重度COPD患者肺功能与运动耐力,减少急性加重的发作,副反应少,值得临床进一步推广。     

肺康复治疗对稳定期COPD患者肺功能及血气分析的影响

目的探讨肺康复治疗对稳定期慢性阻塞性肺疾病（COPD）患者肺功能及血气分析的影响。方法将80例稳定期COPD患者随机分为肺康复组（n=40）与对照组（n=40）,肺康复组给予体能锻炼、呼吸肌锻炼、氧疗、心理与行为干预等肺康复治疗措施,治疗6～8周,治疗前后测定肺功能及血气分析,比较两组患者肺功能及血气分析的变化。结果观察组治疗后肺功能、血气分析较治疗前及对照组治疗后均显著改善（P〈0．01）。结论肺康复治疗可提高稳定期COPD患者肺功能及血气分析,从而提高患者的生存质量。     

慢性阻塞性肺疾病的鼠模型与临床研究的关系

慢性阻塞性肺疾病（COPD）是临床状况复杂,具有多种特征的疾病,是在“气流受限,不完全可逆”,这一共同病理生理特征下统一起来。与肺部对有害气体或有害颗粒的异常炎症反应有关。鼠是最有代表性的动物种类,与人基因极为相似,是提供于实验操控基因表达的最有利的动物。用不同的实验方法可制备多样的COPD鼠模型：①用气管内滴注组织降解酶导致肺损害发展为肺气肿,进一步证明蛋白酶／抗蛋白酶失衡理论;②鼠吸入烟草烟雾和有毒刺激物导致COPD样损伤,暴露因素与品系基因易感有关;③在没有外界刺激下,一些自然基因突变的品系,可自发成肺气肿。无论是单一因素还是多因素共同干预制备鼠模型,都将为研究COPD的基因一环境交互作用,以及COPD的发病机制提供有价值的实验数据及理论。     

奥扎格雷钠对慢性阻塞性肺疾病合并慢性肺源性心脏病的临床治疗研究

目的观察奥扎格雷钠注射液对慢性肺源性心脏病患者血小板功能和心肺功能的影响。方法将80例COPD三级合并慢性肺源性心脏病急性发作的患者,随机分为对照组和干预组各40例,对照组给予吸氧、平喘、祛痰、利尿等支持治疗,纠正水电解质失衡,并根据病原学选择有效的抗生素。干预组在上述治疗的基础上给予奥扎格雷钠注射液160mg,1次／天,15天为1疗程。观察两组患者心功能、血小板功能指标、纤溶指标、肺功能、血气分析变化情况。结果干预组治疗后心功能、血小板各项参数改善情况明显好于对照组。FEV1／FVC升高幅度显著大于对照组,血氧分压和血氧饱和度的升高幅度及二氧化碳分压下降幅度显著大于对照组。结论奥扎格雷钠能有效改善肺心病患者血液高凝和低氧状态,降低肺循环阻力。     

Periodic limb movement during sleep and chronic obstructive pulmonary disease

The aim of this work was to study whether chronic obstructive pulmonary disease (COPD) subjects exhibited periodic limb movement (PLMs) during sleep. A retrospective case control study was conducted in the referral sleep disorders laboratory in the University of Patras in southwest Greece. A sample of 23 COPD subjects was compared with 14 severe obstructive sleep apnea (OSA) subjects and 18 periodic limb movement disorder (PLMD) subjects. The PLM Index (PLMI) and PLMs Arousal Index (PLMAI) in COPD subjects differ (p<0.05) from severe OSA patients. The PLMAI differ (p < 0.05) between COPD and PLMD subjects. Spearman’s correlation showed a positive statistical significant correlation between PLMI and PLMAI in the entire population and in COPD subjects. There was no statistical significant correlation between sleep-related symptoms and the occurrence of PLMs disorder in COPD patients. In our study, PLMs with associated arousals are often seen in COPD subjects. Further prospective studies will be necessary to clarify the mechanisms whereby the reduction in PLMs in COPD patients improved their sleep and quality of life.     

慢性阻塞性肺病痰培养分析及健康指导

目的了解慢性阻塞性肺病急性加重期（AECOPD）患者痰培养的细菌种类。方法对95例AECOPD患者有痰培养结果的病例进行分析。结果经细菌学鉴定为革兰氏阳性球菌18例（占18．94％）,革兰氏阴性杆菌74例（77．89％）,真菌3例（占3．16％）。结论①革兰氏阴性杆菌为AECOPD患者的主要致病菌,部分患者并有真菌感染;②根据痰培养结果可提供恰当的健康指导。