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Pulmonary Arterial Pressure Response During Exercise in COPD: A Correlation with C-Reactive Protein (hsCRP) COPD运动时肺动脉压反应与c反应蛋白(hsCRP)的相关性
Q3 Medicine Pub Date : 2016-01-29 DOI: 10.2174/1874306401610010001
J. Varga, A. Pálinkás, Imre Lajkó, I. Horváth, K. Boda, A. Somfay
Background: The non-invasive assessment of pulmonary haemodynamics during exercise provides complementary data for the evaluation of exercise tolerance in patients with COPD. Methods: Exercise echocardiography in the semi-supine position was performed in 27 patients with COPD (C) with a forced expiratory volume in one second (FEV1) of 36±12% predicted and 13 age and gender-matched non-COPD subjects (NC). COPD patients also underwent cardiopulmonary exercise testing with gas exchange detection (CPET). Furthermore, serum high sensitive C-reactive protein (hsCRP), a marker of systemic inflammation, was also measured. Results: The maximal work rate (WRmax) and aerobic capacity (VO2peak) were significantly reduced (WRmax: 77±33 Watt, VO2peak: 50±14 %pred) in COPD. Pulmonary arterial systolic pressure (PAPs) was higher in COPD versus controls both at rest (39±5 vs. 31±2 mmHg, p<0.001), and at peak exercise (72±12 vs. 52±8 mmHg, p<0.001). In 19 (70%) COPD patients, the increase in PAPs was above 22 mmHg. The change in pressure (dPAPs) correlated with hsCRP (r2=0.53, p<0.0001) and forced vital capacity (FVC) (r2=0.18, p<0.001). Conclusion: PAPs at rest and during exercise were significantly higher in COPD patients and correlated with higher hsCRP. This may indicate a role for systemic inflammation and hyperinflation in the pulmonary vasculature in COPD. The study was registered at ClinicalTrials.gov webpage with NCT00949195 registration number.
背景:运动期间肺血流动力学的无创评估为COPD患者运动耐量的评估提供了补充数据。方法:对27例预测1秒用力呼气量(FEV1)为36±12%的COPD患者(C)和13例年龄和性别匹配的非COPD患者(NC)进行半仰卧位运动超声心动图检查。COPD患者还进行了心肺运动试验,并进行了气体交换检测(CPET)。此外,还测量了血清高敏c反应蛋白(hsCRP),这是全身炎症的标志。结果:COPD患者最大工作速率(WRmax)和有氧能力(VO2peak)显著降低(WRmax: 77±33 Watt, VO2peak: 50±14% pred)。COPD患者的肺动脉收缩压(pap)在静止时(39±5比31±2 mmHg, p<0.001)和运动高峰时(72±12比52±8 mmHg, p<0.001)均高于对照组。在19例(70%)COPD患者中,pap升高高于22 mmHg。血压变化(dpap)与hsCRP (r2=0.53, p<0.0001)和用力肺活量(FVC) (r2=0.18, p<0.001)相关。结论:COPD患者休息和运动时的pap均显著升高,且与hsCRP升高相关。这可能表明慢性阻塞性肺疾病中肺血管系统的系统性炎症和恶性膨胀的作用。该研究已在ClinicalTrials.gov网页注册,注册号为NCT00949195。
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引用次数: 14
Prevalence of Work-Related Asthma in Primary Health Care: Study Rationale and Design 初级卫生保健中与工作相关的哮喘患病率:研究原理和设计
Q3 Medicine Pub Date : 2015-11-13 DOI: 10.2174/1874306401509010127
Ventura Rabell-Santacana, Rafael Panadès-Valls, Rosa Vila-Rigat, Enric HernÁndez-Huet, Joan Sivecas-Maristany, Xavier Blanché-Prat, Gemma Prieto, L. Muñoz, Pere Torán
Background : Occupational Asthma (OA) is the most frequent origin of occupational respiratory diseases in industrialized countries and accounts for between 5% and 25% of asthmatic patients. The correct and early diagnosis of OA is of great preventive and socio-economic importance. However, few studies exist on OA’s prevalence in Catalonia and in Spain and those affected are mainly treated by the public health services and not by the occupational health services, which are private. Objective : To determine the prevalence of OA in patients diagnosed with asthma in the Primary Healthcare system and to evaluate the socio-economic impact of OA in the Primary Healthcare system. Methods/Design : We will carry out an observational, transversal and multi-center study in the Primary Healthcare Service in the Barcelona region (Catalonia, Spain), with 385 asthmatic workers aged between 16 and 64 who are currently working or have been working in the past. We will confirm the asthma diagnosis in each patient, and those meeting the inclusion criteria will be asked to answer a questionnaire that aims to link asthma to the patient’s past employment history. The resulting diagnosis will be of either occupational asthma, work-aggravated asthma or common asthma. We will also collect socio-demographic information about the patients, about their smoking status, their exposure outside of the workplace, their work situation at the onset of the symptoms, their employment history, their symptoms of asthma, their present and past medical asthma treatment, and, in order to estimate the economic impact in the Primary Healthcare system, where they have been attended to and treated. Prevalence will link OA or work-aggravated asthma to the total of patients participating in the study with a asthma diagnosis. Discussion : The results will show the prevalence of OA and work-aggravated asthma, and shall provide valuable information to set out and apply the necessary personal and technical measures, either in the public or in the occupational health services. No studies evaluating the costs generated by the OA in the Primary Healthcare system have been carried out.
背景:职业性哮喘(OA)是工业化国家最常见的职业性呼吸系统疾病,占哮喘患者的5%至25%。正确、早期诊断骨关节炎具有重要的预防和社会经济意义。然而,关于加泰罗尼亚和西班牙OA患病率的研究很少,受影响的人主要由公共卫生服务机构治疗,而不是由私营职业卫生服务机构治疗。目的:确定初级卫生保健系统中诊断为哮喘的OA患者的患病率,并评估OA在初级卫生保健系统中的社会经济影响。方法/设计:我们将在巴塞罗那地区(西班牙加泰罗尼亚)的初级卫生保健服务中开展一项观察性、横向和多中心研究,纳入385名年龄在16至64岁之间、目前正在工作或曾经工作过的哮喘工人。我们将确认每位患者的哮喘诊断,并要求符合纳入标准的患者回答一份问卷,旨在将哮喘与患者过去的工作史联系起来。结果诊断为职业性哮喘、工作加重性哮喘或普通哮喘。我们还将收集有关患者的社会人口统计信息,包括他们的吸烟状况、工作场所以外的暴露情况、症状出现时的工作情况、他们的就业史、哮喘症状、他们目前和过去的哮喘药物治疗情况,以及为了估计对他们就诊和治疗的初级卫生保健系统的经济影响。患病率将OA或工作加重哮喘与参与研究的哮喘诊断患者总数联系起来。讨论:结果将显示OA和工作加重哮喘的患病率,并将提供有价值的信息,以制定和应用必要的个人和技术措施,无论是在公共或职业卫生服务。尚未开展评估初级卫生保健系统中OA产生的成本的研究。
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引用次数: 2
Hot Topic: [How Can We Target Pulmonary Inflammation in Cystic Fibrosis? (Guest Editor: Catherine M. Greene)] 热门话题:如何在囊性纤维化中靶向肺部炎症?(特邀编辑:凯瑟琳·m·格林)]
Q3 Medicine Pub Date : 2010-04-07 DOI: 10.2174/1874306401004010018
C. Greene
With each year our enhanced understanding of the pathogenesis of cystic fibrosis (CF) is challenged by new discoveries related to the increasingly complex nature of this disorder. Originally described as a genetic disorder principally due to defective chloride ion conductance at epithelial surfaces and a predisposition to bacterial colonization have been moved into the category of an inflammatory disorder because of increasing research efforts. As our knowledge of the molecular and cellular events associated with CF has burgeoned, we now have a greater appreciation of its protean inflammatory manifestations. This Mini-Hot Topic on “Mechanisms of Pulmonary Inflammation in Cystic Fibrosis” presents a series of comprehensive review articles in which the authors describe novel mechanisms regulating inflammation in the CF lung and propose and dissect the potential benefits and side-effects of diverse treatments aimed at ameliorating the inflammatory consequences of CF lung disease.
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引用次数: 5
Proline-Glycine-Proline (PGP) and High Mobility Group Box Protein-1 (HMGB1): Potential Mediators of Cystic Fibrosis Airway Inflammation 脯氨酸-甘氨酸-脯氨酸(PGP)和高迁移率群盒蛋白-1 (HMGB1):囊性纤维化气道炎症的潜在介质
Q3 Medicine Pub Date : 2010-03-30 DOI: 10.2174/1874306401004010032
A. Gaggar, S. Rowe, H. Matthew, J. Blalock
Cystic fibrosis (CF) is chronic lung disease characterized by an unrelenting neutrophil-predominant airway inflammatory response. This inflammation leads to extracellular matrix (ECM) remodeling and eventually to the development of bronchiectasis. While many components of the immune response in CF have been well-characterized, recent data suggests that small molecules may play an important and underappreciated role in this inflammation. This review will examine two novel molecules: proline-glycine-proline (PGP) and high mobility group box protein-1 (HMGB1), and their potential impact in CF lung disease. This review will provide a brief overview of CF lung disease and background on both HMGB1 and PGP. It will then focus on these molecules in a murine model of CF-like airway disease and in human biological specimens from CF individuals. Finally, this manuscript will address possible mechanisms for therapeutic targeting of these bioactive mediators.
囊性纤维化(CF)是一种慢性肺部疾病,以持续的中性粒细胞为主的气道炎症反应为特征。这种炎症导致细胞外基质(ECM)重塑,最终发展为支气管扩张。虽然CF免疫反应的许多组成部分已经被很好地表征,但最近的数据表明,小分子可能在这种炎症中发挥重要作用,但未被充分认识。本文将对脯氨酸-甘氨酸-脯氨酸(PGP)和高迁移率群盒蛋白-1 (HMGB1)这两个新分子及其在CF肺部疾病中的潜在影响进行综述。本文将简要介绍CF肺部疾病以及HMGB1和PGP的背景。然后,它将集中在CF样气道疾病的小鼠模型和CF个体的人类生物标本中研究这些分子。最后,本文将讨论这些生物活性介质治疗靶向的可能机制。
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引用次数: 18
The Role of Sphingolipids and Ceramide in Pulmonary Inflammation in Cystic Fibrosis 鞘脂和神经酰胺在囊性纤维化肺部炎症中的作用
Q3 Medicine Pub Date : 2010-03-30 DOI: 10.2174/1874306401004010039
K. A. Becker, J. Riethmüller, Yang Zhang, E. Gulbins
Sphingolipids and in particular ceramide have been shown to be critically involved in the response to many receptor-mediated, but also receptor-independent, mainly stress stimuli. Recent studies demonstrate that ceramide plays an important role in the pathogenesis of cystic fibrosis, a hereditary metabolic disorder caused by mutations of the Cystic Fibrosis Transmembrane Conductance Regulator. Patients with cystic fibrosis suffer from chronic pulmonary inflammation and microbial lung infections, in particular with Pseudomonas aeruginosa. Chronic pulmonary inflammation in these patients seems to be the initial pathophysiological event. Inflammation may finally result in the high infection susceptibility of these patients, fibrosis and loss of lung function. Recent studies demonstrated that ceramide accumulates in lungs of cystic fibrosis mice and causes age-dependent pulmonary inflammation as indicated by accumulation of neutrophils and macrophages in the lung and increased pulmonary concentrations of Interleukins 1 and 8, death of bronchial epithelial cells, deposition of DNA in bronchi and high susceptibility to Pseudomonas aeruginosa infections. Genetic or pharmacological inhibition of the acid sphingomyelinase blocks excessive ceramide production in lungs of cystic fibrosis mice and corrects pathological lung findings. First clinical studies confirm that inhibition of the acid sphingomyelinase with small molecules might be a novel strategy to treat patients with cystic fibrosis.
鞘脂,特别是神经酰胺,已被证明在许多受体介导的反应中起关键作用,但也不依赖于受体,主要是应激刺激。最近的研究表明,神经酰胺在囊性纤维化的发病机制中起重要作用,囊性纤维化是一种由囊性纤维化跨膜传导调节因子突变引起的遗传性代谢疾病。囊性纤维化患者患有慢性肺部炎症和微生物肺部感染,特别是铜绿假单胞菌。慢性肺部炎症似乎是这些患者的初始病理生理事件。炎症最终可能导致这些患者的高感染易感性、纤维化和肺功能丧失。最近的研究表明,神经酰胺在囊性纤维化小鼠的肺部积聚,并引起年龄依赖性肺部炎症,表现为肺中中性粒细胞和巨噬细胞积聚,肺中白细胞介素1和8浓度升高,支气管上皮细胞死亡,支气管DNA沉积,以及对铜绿假单胞菌感染的高易感性。遗传或药理学抑制酸性鞘磷脂酶可阻断囊性纤维化小鼠肺部过度神经酰胺的产生,并纠正病理肺表现。首次临床研究证实,用小分子抑制酸性鞘磷脂酶可能是治疗囊性纤维化患者的一种新策略。
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引用次数: 14
Antiproteases as Therapeutics to Target Inflammation in Cystic Fibrosis 抗蛋白酶作为治疗囊性纤维化靶炎症的药物
Q3 Medicine Pub Date : 2010-03-30 DOI: 10.2174/1874306401004010020
D. Quinn, S. Weldon, C. Taggart
Cystic Fibrosis (CF) is the most common fatal inherited disease of Caucasians, affecting about 1 in 3000 births. Patients with CF have a recessive mutation in the gene encoding the CF transmembrane conductance regulator (CFTR). CFTR is expressed in the epithelium of many organs throughout the exocrine system, however, inflammation and damage of the airways as a result of persistent progressive endobronchial infection is a central feature of CF. The inflammatory response to infection brings about a sustained recruitment of neutrophils to the site of infection. These neutrophils release various pro-inflammatory compounds including proteases, which when expressed at aberrant levels can overcome the endogenous antiprotease defence mechanisms of the lung. Unregulated, these proteases can exacerbate inflammation and result in the degradation of structural proteins and tissue damage leading to bronchiectasis and loss of respiratory function. Other host-derived and bacterial proteases may also contribute to the inflammation and lung destruction observed in the CF lung. Antiprotease strategies to dampen the excessive inflammatory response and concomitant damage to the airways remains an attractive therapeutic option for CF patients.
囊性纤维化(CF)是白种人最常见的致命遗传性疾病,每3000个新生儿中就有1个患病。CF患者在编码CF跨膜传导调节因子(CFTR)的基因中存在隐性突变。CFTR在整个外分泌系统的许多器官的上皮中表达,然而,持续进行性支气管内感染引起的气道炎症和损伤是CF的主要特征。对感染的炎症反应导致中性粒细胞持续募集到感染部位。这些中性粒细胞释放各种促炎化合物,包括蛋白酶,当这些化合物在异常水平表达时,可以克服肺部内源性抗蛋白酶防御机制。不受调节,这些蛋白酶会加剧炎症,导致结构蛋白降解和组织损伤,导致支气管扩张和呼吸功能丧失。其他宿主源性和细菌性蛋白酶也可能导致CF肺的炎症和肺破坏。抗蛋白酶策略抑制过度的炎症反应和伴随的气道损伤仍然是CF患者的一个有吸引力的治疗选择。
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引用次数: 11
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Open Respiratory Medicine Journal
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