治疗哮喘慢性阻塞性肺疾病双功能药物的研究现状

慢性阻塞性肺疾病(COPD)与支气管哮喘均是以气流受限为特征的慢性呼吸道系统疾病，其病因来源多、发病机制复杂，严重影响患者生活质量。目前治疗这两种慢性呼吸系统疾病的一线药物为M受体拮抗药、β受体激动药和吸入糖皮质激素。然而，单一疗法对加重的COPD或哮喘的疗效有限。长效M受体拮抗药/长效β受体激动药、长效β受体激动药/糖皮质激素等联合疗法的疗效优势已在长期的COPD和哮喘临床治疗实践中得到证实。若能把多个药物的功能整合在一个药物分子上，将能显著提高药效、降低制剂的开发难度并提高患者的用药顺应性。本文将系统介绍目前COPD和支气管哮喘的治疗靶点以及目前双功能药物的临床前和临床研究现状，以期指导后续药物的研发方向。     

临床药师对哮喘和慢性阻塞性肺疾病患者的药学监护实践

目的 探讨临床药师对哮喘和慢性阻塞性肺疾病(COPD)患者的药学监护模式.方法 以临床资料为例,结合哮喘和COPD治疗指南,为住院患者制定个体化的药学监护计划并实施全程药学监护,介绍哮喘和COPD患者药学监护的主要内容.结果 对哮喘和COPD患者实施药学监护,可及时发现患者的药物治疗问题,避免严重后果的出现,促进临床合理用药.结论 本监护模式具有可行性和实用性.     

慢性阻塞性肺病的临床药物治疗和预防

慢性阻塞性肺病﹙COPD﹚是老年人常见疾病,是一种以气流受限为特征的进行性发展的疾病,COPD患者常常由慢性支气管炎或哮喘发展而来。由哮喘发展而来的COPD患者常伴有喘息症状。死亡率居所有死因的第4位。药物治疗中多加支气管扩张剂或糖皮质激素,以维持重要器官的功能,缩短其急性加重期,改善肺功能,扩张支气管和减少肺内的过度充气为主。由哮喘而引起的COPD和COPD合并哮喘的老年患者,其病情相对复杂,并发症多,预后较差。吸烟和室内污染是其发展的危险因素。因此预防为主极为重要。COPD患者的合理膳食,适当的体育锻炼,长期的家庭氧疗,积极治疗共患疾病,对老年COPD患者应给予较多的社会支持和关爱,以延缓患者疾病进展及生命质量下降的速度,从而提高COPD患者的生命质量。文章就近年来治疗慢性阻塞性肺病取得地一定临床疗效做一综述。     

加强联合吸入治疗在慢性气道阻塞性疾病中的认识

慢性阻塞性肺疾病(COPD)和哮喘是最常见的慢性气道阻塞性疾病,尽管两者发病机制、诊治措施不尽相同,但气道炎症和气道阻塞是它们的相似点.随着近年临床研究的广泛开展,越来越多的证据支持联合治疗是治疗COPD和哮喘的重要方法.本文综述联合吸入治疗在COPD和哮喘中的应用及临床遇到的一些问题.     

对慢性阻塞性肺疾病并发支气管哮喘患者的药学监护

目的:探讨临床药师在慢性阻塞性肺疾病(COPD)并发支气管哮喘(哮喘)患者治疗中发挥药学服务的途径和方式方法,保障患者用药的安全有效,改善患者的依从性。方法:采用查阅文献结合病例分析,依据COPD并发哮喘患者的药物治疗特点,对患者进行药学监护,有针对性提出用药建议。结果:通过药学监护,明显提高了COPD并发哮喘患者用药的安全性和有效性,避免了不良反应事件的发生。结论:临床药师积极开展药学服务,协同临床医师优化给药方案,有利于患者的用药安全有效。     

慢性阻塞性肺疾病临床药物治疗现状

慢性阻塞性肺疾病(COPD)是一种常见的呼吸系统慢性疾病，COPD不但严重影响人们的健康，而且还带来沉重的社会和经济负担，已成为一个重要的社会公共卫生问题。当前临床缺乏长期有效的治疗药物，而临床上用于治疗COPD的药物主要有岛受体激动剂、抗胆碱能药物、黄嘌呤类及茶碱类等药物，目前临床上常用于治疗COPD的药物有各自的特点，现将COPD的临床药物治疗现状分述如下。     

慢性阻塞性肺疾病患者730例治疗现状分析

<正>慢性阻塞性肺疾病(COPD)是临床常见的慢性气道疾病,稳定期规范化药物治疗可减少COPD患者的急性加重,提高生活质量,减少患者经济负担[1]。本研究通过对COPD稳定期患者的临床症状、急性加重病史、肺功能和药物治疗情况进行调查及综合评估,分析A、B、C、D四类临床特征患者的治疗现状与2011版慢性阻塞性肺疾病全球防治创议(GOLD)推荐药物治疗的差距。     

无创通气技术（NIPPV）治疗难治性哮喘急性发作

无创通气技术（NIPPV）临床应用日益广泛,其应用适应证也在不断扩大,但NIPPV在治疗哮喘中的经验远不及治疗慢性阻塞性肺疾病（COPD）及呼吸衰竭,由于重症哮喘患者在治疗过程中病情可迅速恶化，NIPPV治疗有贻误插管的危险，应用者应严格掌握适应证。临床上有一部分患者经常规药物治疗后，症状难以控制称为难治性哮喘（RA）。难治性哮喘急性发作是临床医生面临的一个难题。     

慢性阻塞性肺疾病治疗药物研究进展

慢性阻塞性肺疾病（COPD）是一种气流受限且不完全可逆,同时病情进行性加重的慢性呼吸系统疾病。COPD病理机制复杂,病症主要包括肺功能降低、气道及肺组织慢性炎症、咳嗽、消瘦、活动量减少等。以往临床上一般采用支气管扩张剂和抗炎药物对COPD进行治疗,随着对该疾病病理机制的深入研究,抗氧化治疗也已逐渐应用于临床。笔者现对包括支气管扩张剂、抗炎药物及抗氧化治疗药物在内的COPD治疗药物的研究进展进行综述。     

解整合素-金属蛋白酶33基因位点多态性与哮喘-慢性阻塞性肺疾病重叠综合征的相关性研究

<正>气道高反应是支气管哮喘的高危因素或是支气管哮喘的前期表现,如果支气管哮喘得不到控制,则会出现气道重塑、肺功能下降,进一步发展出现慢性阻塞性肺疾病的病理改变及临床特点,后期即成为哮喘-慢性阻塞性肺疾病重叠综合征(ACOS)。哮喘和气道高反应性被认为是慢性阻塞性肺疾病(COPD)的危险因素,在我国2013年COPD诊治指南中已明确提出。哮喘与COPD是两种临床常见病,但其发病原因     

Interleukin-9 as a possible therapeutic target in both asthma and chronic obstructive airways disease

Asthma and chronic obstructive pulmonary disease (COPD) are important causes of morbidity and mortality worldwide. Both asthma and COPD are characterized by airflow limitation but distinct differences occur in the pulmonary inflammatory responses in the two conditions. Treatment options for asthma and COPD are limited (especially so for COPD), and both are in need of novel therapeutic interventions. Interleukin-9 (IL-9) is a potential target for such a therapy. This Th2-type cytokine, is secreted by a number of different cell types, and has multiple effects on a wide range of cells within the lung. In this review we will summarize current knowledge about the immunobiology of IL-9 and discuss the role played by IL-9 in inflammation in both asthma and COPD, and its potential as a therapeutic target.     

Exacerbations of asthma and chronic obstructive pulmonary disease (COPD): focus on virus induced exacerbations

Asthma and chronic obstructive pulmonary disease (COPD) are the 2 most prevalent chronic airway diseases. Much of the morbidity, mortality and health care costs of the diseases are associated with acute exacerbations, which are episodes of increased symptoms and airflow obstruction. Over the last decade evidence has emerged implicating virus respiratory tract infections as a major cause of exacerbations of both asthma and COPD. Current therapies are not very effective in the prevention or treatment of virus-induced exacerbations and exacerbations are therefore a major unmet medical need. The development of new and novel treatments requires a better understanding of the molecular and cellular mechanisms linking virus infection with exacerbations of asthma and COPD. This article provides an overview of current knowledge regarding the mechanisms of virus-induced exacerbations in both asthma and COPD. It will also review existing treatments and future treatments that are in advanced stages of development.     

Novel therapies for the treatment of inflammatory airway disease

Asthma and chronic obstructive pulmonary disease (COPD) are diseases of the airways with an underlying inflammatory component. The prevalence and healthcare burden of asthma and COPD is still rising and is predicted to continue to rise in the current century. The β-agonists and corticosteroids form the basis of the treatments available to alleviate the symptoms of asthma, whereas the treatments available for COPD have been shown to have a limited effect on slowing the progression of the disease. Asthma and COPD are both in need of novel, safe treatments to tackle the underlying inflammation that characterises their pathology. The inflammatory processes inherent in asthma and COPD provide the opportunity for innovative drug research. This review will outline the new approaches and targets being investigated, which may provide opportunities for novel therapeutic interventions in these debilitating diseases.     

Novel therapies for the treatment of inflammatory airway disease

Asthma and chronic obstructive pulmonary disease (COPD) are diseases of the airways with an underlying inflammatory component. The prevalence and healthcare burden of asthma and COPD is still rising and is predicted to continue to rise in the current century. The beta-agonists and corticosteroids form the basis of the treatments available to alleviate the symptoms of asthma, whereas the treatments available for COPD have been shown to have a limited effect on slowing the progression of the disease. Asthma and COPD are both in need of novel, safe treatments to tackle the underlying inflammation that characterises their pathology. The inflammatory processes inherent in asthma and COPD provide the opportunity for innovative drug research. This review will outline the new approaches and targets being investigated, which may provide opportunities for novel therapeutic interventions in these debilitating diseases.     

Small molecule inhibitors of cell signaling: novel future therapeutics for asthma and chronic obstructive pulmonary diseases

The respiratory diseases asthma and chronic obstructive pulmonary disease (COPD) exhibit common, key pathological features, including the development of airflow limitations such as thickening of the airway wall, and the presence of an inflammatory process. However, that is where their similarities end. A large number of medications for asthma are available to decrease inflammation and prevent or reverse airway constriction, while very few therapeutics, if any, exist for the effective management of COPD. Nonetheless, despite the availability of medications for asthma, the epidemic is continuing to increase and existing therapies offer little or no relief for chronic asthmatics. It is obvious that a high, unmet medical need remains for both asthma and COPD, and innovative therapeutic agents are urgently required. New therapies need to be developed to target not only the inflammatory component of asthma and COPD, but also the remodeling aspects of these diseases. This review summarizes the emerging treatments for chronic asthma and COPD, from early discovery to late clinical stages, and discusses the therapeutic rationale behind these treatments. We believe that there is still much to be learned about the mechanisms involved in the development and treatment of these debilitating respiratory diseases, however, much promise lies in the future of these new therapeutics.     

Oxidants in asthma and in chronic obstructive pulmonary disease (COPD)

Experimental and clinical evidences suggest that oxidants play a role in the pathogenesis of respiratory disorders characterised by chronic airway inflammation such as asthma and chronic obstructive pulmonary disease (COPD). The respiratory system is chronically exposed to environmental pollutants, including oxidants. Exogenous sources of oxidants are particularly relevant to the pathogenesis of COPD, being cigarette smoke an extremely rich source of oxidants. In addition, the inflammatory cells recruited to the airways of patients with asthma and COPD, have an exceptional capacity to produce oxidants. Many decades of research have produced a significant amount of data indicating pro-oxidative molecular mechanisms putatively relevant in the pathogenesis of the oxidative stress which characterises these diseases, both locally and systemically. As a consequence, a drug therapy able to restore the redox imbalance in asthma and COPD would probably exert clinical and functional benefits. Indeed, currently available therapies for asthma and COPD can exert an inhibitory effect on oxidant production in the airways. However, it is unknown whether the efficacy of the treatment is somehow linked to the pharmacological modulation of the oxidant/antioxidant balance. So far, it appears that the potential role of antioxidant compounds in the treatment of asthma and COPD has not been fully explored.     

Economic burden in direct costs of concomitant chronic obstructive pulmonary disease and asthma in a Medicare Advantage population

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a highly prevalent disease whose sufferers consume a large amount of resources. Among community-dwelling Medicare beneficiaries, 12% reported that they had COPD in 2002. For clinicians, differentiating COPD from asthma may be difficult, but among patients with COPD and asthma, approximately 20% have both conditions. The economic impact of concomitant asthma and COPD is potentially large but has not been studied. OBJECTIVE: To assess the cost burden of asthma in patients with COPD in a Medicare Advantage population. METHODS: We reviewed the database of a large health plan that contained information from more than 30 distinct plans covering approximately 25 million members. We identified Medicare beneficiaries aged 40 years or older with medical and pharmacy benefits and medical claims with International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) diagnosis codes for COPD or asthma over a 1-year identification period (calendar year 2004). We assigned patients to 2 cohorts based on diagnoses on medical claims (any diagnosis field) during 2004; the COPD cohort had at least 1 medical claim for COPD, and the COPD + asthma cohort had at least 1 claim for COPD and at least 1 claim for asthma. A patient's index date was the first date during 2004 in which there was a medical claim with a diagnosis code for COPD or asthma. To confirm diagnosis, each patient was required to have at least 1 additional claim for COPD (COPD cohort) or at least 1 claim for COPD and at least 1 claim for asthma (COPD + asthma cohort) during the 24-month period from 12 months before through 12 months after the index date. We excluded patients who (1) were not continuously enrolled during the 12 months before and after the index date and (2) did not have at least 1 pharmacy claim for a drug of any type (to verify pharmacy benefits). Outcome measures included the use of emergency room (ER) and hospital services, and cost (net provider payment after subtraction of member cost share), categorized as all-cause, non-respiratory, and respiratory-related. ER use and inpatient hospital stays were identified using place-of-service codes. A minimum of 2 consecutive dates of service (length of stay [LOS] of at least 1 day) was required to indicate an inpatient hospitalization. An LOS of at least 1 day was required to distinguish inpatient services from other services (e.g., procedures or tests) reported on claims with an inpatient place of service. Multivariate analyses adjusted for age, gender, census region, and Charlson Comorbidity Index (CCI). Ordinary least squares regression was used to predict respiratory-related total health care costs, and logistic regression was used to predict the occurrence of at least 1 acute event, defined as use of either an ER or an inpatient hospital. All 2-way interactions were considered, and only those with significant results were included in the models. All reported P values were 2-sided with a 0.05 significance level. RESULTS: During 2004, 68,532 individuals within the database were enrolled in a Medicare Advantage plan. After application of the other inclusion criteria, we excluded approximately 11% of the patients who did not have 1 pharmacy claim of any type. There were 8,086 patients (11.8%) who had at least 1 medical claim with diagnosis codes for COPD and at least 1 other medical claim for either COPD or asthma and were continuously enrolled for at least 24 months. The COPD + asthma cohort numbered 1,843 patients (22.8%), and the COPD cohort numbered 6,243 patients (77.2%). Compared with COPD patients without asthma, patients with COPD + asthma were slightly younger, and a higher proportion was female. There were differences between the 2 cohorts in geographic distribution, and the COPD + asthma cohort had a higher disease severity with a mean CCI score of 2.6 (standard deviation [SD], 2.1) compared with the COPD cohort (2.3 [2.3], P < 0.001). Respiratory-related pharmacy costs were a relatively small part of total respiratory-related health care costs: approximately 5.7% for the COPD cohort and 8.8% for the COPD + asthma cohort. Respiratory-related costs accounted for 22.0% of total all-cause health care costs for the COPD cohort and 28.7% for the COPD + asthma cohort. Mean ([SD], median) unadjusted respiratory-related health care costs were $7,240 ([$15,057], $1,957) for the COPD + asthma cohort and $5,158 ([$11,881], $808) in the COPD cohort. After adjusting for covariates, patients in the COPD + asthma cohort were more likely to have at least 1 acute event (e.g., ER visits and hospitalizations) than patients in the COPD cohort (adjusted odds ratio, 1.6; 95% CI, 1.4-1.7) and had $1,931 (37.1%) greater adjusted respiratory-related health care costs--$7,135 versus $5,204 for the COPD cohort (P < 0.001). CONCLUSION: Medicare beneficiaries with COPD and asthma incur higher health care costs and use more health care services than those with COPD without asthma.     

哮喘、慢性阻塞性肺病患者血清IL-18和总IgE水平的相关性

目的 探讨IL-18、总IgE、Th1和Th2类细胞因子在哮喘、慢性阻塞性肺病(COPD)发病时血清水平的变化及其相关性.方法 随机收集哮喘急性发作期患者50例(哮喘组),老年COPD急性加重期患者80例(COPD组),健康者50例(对照组)血清,采用双抗体夹心酶联免疫吸附试验检测血清IL-18、总IgE、IL-8、IL-4、IFN-γ水平.结果 CDPD组急性期IL-18、IL-8、IL-4、IFN-γ水平分别高于对照组1.8、25.2、116、150.8倍.哮喘组IL-18、IL-8、IL-4分别高于对照组29.9、3.4、5.2倍.哮喘组血清总IgE水平高于对照组223.2倍,而COPD组血清总IgE水平与对照组相比无显著性差异.COPD血清中IL-18与IL-8、IFN-γ,IL-8与IL-4呈正相关;哮喘组IL-18与IL-8、IL-4、总IgE,IL-4与总IgE呈正相关.结论 高血清IL-18提示细胞闪子参与哮喘及COPD的发病过程.哮喘发作时IL-18与总IgE正相关,而在COPD急性加重期无相关性,表明COPD和哮喘是两类有不同发生机制的气道炎症.