慢性阻塞性肺气肿的治疗进展

慢性阻塞性肺气肿是一种以不完全可逆的气流受限为特征的疾病,在我国北方地区发病率、病死率均较高^[1]。严格地说,肺气肿不是一种独立的疾病,而是一个解剖,结构术语,是慢性支气管炎或其他慢性肺部疾患发展的结果,主要是肺组织终末支气管远端部分包括呼吸性细支气管、肺泡管、肺泡囊和肺泡的膨胀和过度充气,导致肺组织弹力减退,容积增大。     

中性粒细胞迁移与肺部疾病的研究进展

中性粒细胞迁移(neutrophil migration)是中性粒细胞重要的生物学功能之一，是中性粒细胞由骨髓或外周血趋化到病变部位活化并履行功能的必经步骤，近年来研究表明中性粒细胞迁移对肺部疾病的发生发展有着重要的作用，尤其在支气管哮喘、慢性阻塞性肺疾病、肺癌、急性呼吸窘迫综合征等疾病中起关键作用，这或许为肺部疾病的诊治提供新的方向。本文对中性粒细胞的产生、释放、黏附、迁移及与肺部疾病的关系进行综述。     

1-磷酸鞘氨醇与肺部疾病的研究进展

1-磷酸鞘氨醇(sphingosine-1-phosphate,S1P)是一种具有生物活性的细胞膜的重组成部分以及鞘脂类代谢产物之一.S1P也是调节细胞内外多种生物学功能的重信号分子,通过与5种G蛋白偶联受体亚型结合(即S1PR1-S1PR5)产生不同的生物学功能,包括调节细胞增殖、存活、凋亡、炎症诱导及血管再生等.近年来研究表明S1P及其S1PR/SPHK对肺部疾病的发生发展起着重的作用,尤其对支气管哮喘、肺纤维化、肺炎、支气管扩张、慢性阻塞性肺病(chronicobstructivepulmonarydisease,COPD)以及肺癌的发生发展起着关键的作用,这或许为肺部疾病的治疗提供一个新途径.     

慢性阻塞性肺疾病血栓前状态研究进展

慢性阻塞性肺疾病可以阻碍肺部正常通气,影响人们正常的生活工作,不仅如此,我国15岁以上的人3%患有该病,且呈不断上升的趋势。如果在患有慢性阻塞性肺疾病的基础上并发血栓,不仅给慢性阻塞性肺疾病的治疗带来影响,还可能加重病情,因此我们不得不在治疗慢性阻塞性肺疾病的基础上预防血栓的形成,这就要求我们必须详细掌握慢性阻塞性肺疾病血栓前状态。近几年来随着人们对预防血栓的重视度增加,对慢性阻塞性肺疾病血栓前状态的研究不断深入,取得了较好的研究进展。本文对慢性阻塞性肺疾病血栓前状态的研究进展作一综述,为预防慢性阻塞性肺疾病相关血栓性疾病提供科学依据。     

血清suPAR、PAI-1对慢性阻塞性肺疾病合并支气管扩张的诊断价值

目的 研究血清可溶性尿激酶型纤溶酶原激活物受体(suPAR)、纤溶酶原激活物抑制剂-1(PAI-1)对慢性阻塞性肺疾病(COPD)合并支气管扩张的诊断价值。方法 在2019年10月至2021年4月,共纳入265例稳定期中重度COPD患者作为研究对象,根据支气管扩张程度将他们分为无支扩组(n=135)和COPD合并支扩组(n=130)。另外纳入100例无肺部疾病或无法控制的慢性疾病志愿者作为对照组。酶联免疫吸附检测血清suPAR、PAI-1和血清炎症因子水平,使用肺功能仪检测肺通气和弥散功能。结果 COPD患者血清suPAR、PAI-1水平均高于对照组(P<0.05),且COPD合并支扩组血清suPAR、PAI-1水平较无支扩组升高更明显(P<0.05)。血清suPAR与第1秒用力呼气容积占预计值百分比(FEV1%pre)、第1秒用力呼气容积/用力肺活量(FEV1/FVC)、一氧化碳弥散量占预计值百分比(DLCO%pre)呈负相关性(P<0.05),与残气量/肺总量、高分辨率计算机断层扫描(HRCT)评分、血清白细胞介素(IL)-6水平呈正相关(P<0.05)。血...     

慢性阻塞性肺疾病骨骼肌萎缩的治疗现状

慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)不仅是一种局限于呼吸道和肺部的疾病,还是一种可以累及肺外各器官的全身疾病,其肺外效应包括心血管疾病、焦虑和抑郁及骨骼肌萎缩等疾病,其中骨骼肌萎缩严重影响患者的生活质量及预后,造成巨大的社会和经济负担.然而,肌肉组织固有的适应性为骨骼肌萎缩提供了治疗机会.适当的干预措施可逆转或延迟骨骼肌萎缩的发展进程.     

早期慢性阻塞性肺疾病诊断与防治研究

慢性阻塞性肺疾病（COPD）是以持续气流受阻进行性发展为特征的一种可预防和治疗的疾病。COPD发病率、致残率较高,严重威胁人类健康安全。目前,早发现、早诊断、早治疗是我国COPD防治的重要手段。我国早期COPD病例数量大,不同患者症状存在明显差异性。研究早期COPD诊治情况,有望探索对患者进行个体化治疗的方法,进一步促进临床治疗策略的制定,提高慢性阻塞性肺疾的临床诊治研究水平。本文现就COPD早期的诊治研究进行综述,以期为临床诊治慢性阻塞性肺疾提供理论参考依据。     

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。     

嗜酸性粒细胞胞外诱捕网在慢性气道疾病发病机制中的作用

嗜酸性粒细胞胞外诱捕网(eosinophil extracellular traps,EETs)由DNA纤维、组蛋白及嗜酸性粒细胞游离颗粒组成,是嗜酸性粒细胞发挥作用的重要途径。最近研究显示EETs在多种呼吸系统疾病例如哮喘、变应性支气管肺曲霉病及慢性阻塞性肺疾病的发生发展过程中都发挥重要作用,EETs可通过直接破坏气...     

高氧致早产鼠BALF及肺组织中MDA、SOD的变化

目的观察丙二醛(MDA)、超氧化物歧化酶(SOD)在高氧致(CLD)早产鼠支气管肺泡灌洗液(BALF)及肺组织中的变化.方法用高浓度氧致早产鼠CLD为研究对象,应用生化方法同步检测肺组织和BALF中MDA含量及SOD的活性.结果实验组肺组织中SOD的活性呈升高趋势,但与对照组比较,肺组织和BALF中SOD的活性均无差异(P>0.05、P>0.05),实验组肺组织和BALF中MDA的水平呈同相变化,自吸入高氧的第3d开始升高,(P<0.05),7d达高峰并持续至14d(P<0.01),21d时虽有下降,但仍高于对照组(P<0.05).结论 SOD、MDA的动态变化,可间接反应肺部疾病的变化,对慢性肺疾病的诊断、鉴别诊断、活动性判断及预后均有一定的价值.同时也证实机体的氧化与抗氧化失衡是高氧所致早产儿慢性肺疾病的发病原因之一.     

食管癌患者放射性肺损伤预测因素分析及其与 COPD的相关性研究

目的 分析食管癌患者放射性肺损伤（RILI）预测因素,以及其与慢性阻塞性肺疾病（COPD）的相关性。方法 选取2014年1月~2017年12月我院收治的食管癌患者265例为研究对象,均行立体定向放射治疗（SBRT）治疗,治疗前均行肺功能检查,治疗后均行HRCT检查随访RILI的发生情况,回顾性分析RILI的预测因素及其与COPD是否存在相关性。结果 0、1、2、3、4、5级RP发生率分别为38.49%、38.11%、17.74%、5.28%、0.38%、0,其中12例患有间质性肺疾病的患者,9例（75.00%）发生例3级以上的RILI;发生RILI≥1级的相关因素有年龄、总剂量、V20、GOLD分级;重度及极重度COPD组患者的0级RILI的发生率为54.17%,高于轻中度COPD组（42.31%）及无COPD组（30.22%）。结论 年龄、总剂量、V20、GOLD分级与1级以上（有影像学变化）的RILI有相关性,重度COPD的RILI较正常或轻度COPD患者相对较轻,患有间质性肺疾病的患者多发生3级以上的RILI。     

戒烟与肺康复对慢阻肺患者发病机制及疗效的研究

慢性阻塞性肺疾病是目前最常见的高发病率,高伤残率,高死亡的一种疾病,发病机制比较复杂,同时吸烟在慢阻肺的危险因素中是最重要的一项,可以通过破坏支气管,加重气道炎症和气道重塑,通过气道壁和肺实质产生炎症作用,从而导致结构和功能的改变。戒烟可以有效预防慢阻肺患者早期死亡,是需要长期坚持预防的措施。肺康复治疗能明显改善患者的肺功能,在慢阻肺预防控制中起到非常重要的作用。本文主要通过介绍戒烟,早期肺康复的干预,肺康复的传统以及现代模式等方面对肺康复的效果进行综述。     

基于“互联网+”的移动医疗技术在慢性阻塞性肺病稳定期管理的应用及问题研究

随着互联网的发展,移动医疗技术也越来越成熟,在慢性阻塞性肺病稳定期管理的应用方面取得较大进展。通过该技术对于稳定期慢阻肺患者线上复诊、调整治疗等提供了方便,从而使患者提高对于自身疾病认识,持续监测自身健康,提高治疗疾病的依从性。本文综述了移动医疗技术在稳定期慢阻肺的应用现状,并对互联网移动医疗技术应用的局限性及发展方向进行探讨。     

Ageing mechanisms that contribute to tissue remodeling in lung disease

Age is a major risk factor for chronic respiratory diseases such as idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD) and certain phenotypes of asthma. The recent COVID-19 pandemic also highlights the increased susceptibility of the elderly to acute respiratory distress syndrome (ARDS), a diffuse inflammatory lung injury with often long-term effects (ie parenchymal fibrosis). Collectively, these lung conditions are characterized by a pathogenic reparative process that, rather than restoring organ function, contributes to structural and functional tissue decline. In the ageing lung, the homeostatic control of wound healing following challenge or injury has an increased likelihood of being perturbed, increasing susceptibility to disease. This loss of fidelity is a consequence of a diverse range of underlying ageing mechanisms including senescence, mitochondrial dysfunction, proteostatic stress and diminished autophagy that occur within the lung, as well as in other tissues, organs and systems of the body. These ageing pathways are highly interconnected, involving localized and systemic increases in inflammatory mediators and damage associated molecular patterns (DAMPs); along with corresponding changes in immune cell function, metabolism and composition of the pulmonary and gut microbiomes. Here we comprehensively review the roles of ageing mechanisms in the tissue remodeling of lung disease.     

Hypertensive Pulmonalarterienveränderungen bei chronisch-entzündlichen Lungenerkrankungen

Summary 150 cases of chronic inflammatory lung diseases of unknown aetiology and assumed hyperergic (immuno-reactive) pathogenesis were examined for hypertensive pulmonary arterial lesions and for chronic cor pulmonale. Hypertensive lesions of the small pulmonary arteries were found in more than half of the cases with chronic disorders of long duration, but were inconspicuous in diseases of acute progressive character. Hypertensive lesions were found regularly in chronic interstitial pneumonia, frequently in scleroderma and rheumatoid arthritis and occasionally in dermatomyositis and disseminated lupus erythematosus. Chronic Cor pulmonale occurred in 16% of the cases with hypertensive arterial lesions of grade I (hypertrophy of media) and in 50% of grade II/III (hypertrophy of media and intimai fibrosis). Interstitial lung fibrosis plays an important role in the pathogenesis of cor pulmonale: two thirds of the cases with interstitial lung fibrosis had developed cor pulmonale and all the cases with cor pulmonale also had interstitial lung fibrosis.Hypertensive arterial lesions of grade IV–VI according to Heath and Edwards (angiitis, plexogenic and angiomatoid lesions) have been described in severe cases of pulmonary hypertension (congenital cardiac shunts, primary pulmonary hypertension). In secondary forms of pulmonary hypertension, as represented by our material, these changes are of little importance.

     

Chronic inflammation and lung fibrosis: pleotropic syndromes but limited distinct phenotypes

Experimental models of lung fibrosis have been disappointing in predicting therapeutic responses to a wide variety of interventions in clinical fibrosing lung diseases. There are multiple potential reasons, but this fundamentally calls into question the validity of the models and their fidelity to clinical syndromes. We propose that the clinical diseases associated with pulmonary fibrosis, although manifesting a broad array of widely different clinical presentations and features, result in essentially two distinct phenotypes of fibrosis that we will describe. The most common and problematic of these are not effectively modeled experimentally. In this review, we present several clinical entities as examples of the phenotypic distinctions. The first two represent the extremes: postinflammatory fibrosis observed in hypersensitivity pneumonitis (HP) and dysregulated matrix deposition as observed in idiopathic pulmonary fibrosis (IPF). We also present a third clinical entity, that of lung disease associated with rheumatoid arthritis (rheumatoid lung), representing a condition that can manifest as either phenotype, and offering a potential opportunity to explore the mechanisms underlying the pathogenesis of the two distinct fibrotic phenotypes.     

Overview of novel therapeutic targets for asthma and chronic obstructive pulmonary disease

Obstructive lung diseases, in particular asthma and chronic obstructive pulmonary disease, are a worldwide health problem that is increasing in incidence. While significant progress has been made in the control of symptoms, further advances must be made in modifying the clinical situation in terms of disease progression. Numerous pathogenetic studies have demonstrated that inflammatory responses play a crucial role in the development of chronic lung obstruction, while current molecular findings have provided a myriad of new and promising therapeutic targets. The aim of this article is to provide an overview of clinically and pharmacologically relevant targets for asthma and chronic obstructive pulmonary diseases, considering currently investigated therapeutic approaches.     

Obstructive lung diseases and risk of rheumatoid arthritis

ABSTRACT

Introduction: Smoking is an established risk factor for both lung diseases and rheumatoid arthritis (RA). Chronic mucosal airway inflammation may result in immune tolerance loss, neoantigen formation, and production of RA-related autoantibodies that increase the subsequent risk of RA. In this review, we aimed to summarize the current evidence supporting the role of obstructive lung diseases and subsequent risk of RA.

Areas covered: We identified scientific articles discussing the biologic mechanisms linking mucosal airway inflammation and RA risk. We also identified studies investigating asthma, chronic obstructive pulmonary disease, bronchiectasis, cystic fibrosis, chronic tuberculous and nontuberculous mycobacterial infections, and interstitial lung disease with subsequent risk for RA.

Expert opinion: The current evidence supports the hypothesis that mucosal airway inflammation may increase the risk of developing RA. However, most studies investigating this relationship have been retrospective and may not have adequately addressed the role of smoking. Larger prospective studies may provide stronger evidence for obstructive lung disease and RA risk. Determining the role of obstructive lung disease in RA pathogenesis may provide opportunity for RA prevention and screening strategies, while identifying novel biologic mechanisms that could offer targets to improve treatment and outcomes.     

Natural killer cells in infection and inflammation of the lung

The lungs are a major site of entry of pathogens into the body and thus require rapid and effective innate responses to prevent pathogens establishing infection and to limit their spread. Additionally, the immune response in the lung must be tightly regulated such that pathogens are cleared, but immunopathology and chronic inflammation are prevented. In this review, I consider the role of natural killer (NK) cells in pulmonary infection and inflammation, specifically their contributions to influenza, tuberculosis, asthma and chronic obstructive pulmonary disease (COPD), which are major causes of morbidity and mortality world‐wide. Despite evidence of the importance of NK cells in these diseases, there are still major gaps in our understanding of how their function is regulated in this unique tissue environment. Understanding how different beneficial and detrimental effector functions of NK cells are triggered will be crucial if NK cells are to be exploited therapeutically in respiratory disease.