Pub Date : 2016-01-29DOI: 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.
{"title":"Pulmonary Arterial Pressure Response During Exercise in COPD: A Correlation with C-Reactive Protein (hsCRP)","authors":"J. Varga, A. Pálinkás, Imre Lajkó, I. Horváth, K. Boda, A. Somfay","doi":"10.2174/1874306401610010001","DOIUrl":"https://doi.org/10.2174/1874306401610010001","url":null,"abstract":"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.","PeriodicalId":39127,"journal":{"name":"Open Respiratory Medicine Journal","volume":"10 1","pages":"1 - 11"},"PeriodicalIF":0.0,"publicationDate":"2016-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68068176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2015-11-13DOI: 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.
{"title":"Prevalence of Work-Related Asthma in Primary Health Care: Study Rationale and Design","authors":"Ventura Rabell-Santacana, Rafael Panadès-Valls, Rosa Vila-Rigat, Enric HernÁndez-Huet, Joan Sivecas-Maristany, Xavier Blanché-Prat, Gemma Prieto, L. Muñoz, Pere Torán","doi":"10.2174/1874306401509010127","DOIUrl":"https://doi.org/10.2174/1874306401509010127","url":null,"abstract":"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.","PeriodicalId":39127,"journal":{"name":"Open Respiratory Medicine Journal","volume":"9 1","pages":"127 - 139"},"PeriodicalIF":0.0,"publicationDate":"2015-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68068105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2010-04-07DOI: 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.
{"title":"Hot Topic: [How Can We Target Pulmonary Inflammation in Cystic Fibrosis? (Guest Editor: Catherine M. Greene)]","authors":"C. Greene","doi":"10.2174/1874306401004010018","DOIUrl":"https://doi.org/10.2174/1874306401004010018","url":null,"abstract":"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.","PeriodicalId":39127,"journal":{"name":"Open Respiratory Medicine Journal","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2010-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68067988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2010-03-30DOI: 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.
{"title":"Proline-Glycine-Proline (PGP) and High Mobility Group Box Protein-1 (HMGB1): Potential Mediators of Cystic Fibrosis Airway Inflammation","authors":"A. Gaggar, S. Rowe, H. Matthew, J. Blalock","doi":"10.2174/1874306401004010032","DOIUrl":"https://doi.org/10.2174/1874306401004010032","url":null,"abstract":"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.","PeriodicalId":39127,"journal":{"name":"Open Respiratory Medicine Journal","volume":"4 1","pages":"32 - 38"},"PeriodicalIF":0.0,"publicationDate":"2010-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68068044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2010-03-30DOI: 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.
{"title":"The Role of Sphingolipids and Ceramide in Pulmonary Inflammation in Cystic Fibrosis","authors":"K. A. Becker, J. Riethmüller, Yang Zhang, E. Gulbins","doi":"10.2174/1874306401004010039","DOIUrl":"https://doi.org/10.2174/1874306401004010039","url":null,"abstract":"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.","PeriodicalId":39127,"journal":{"name":"Open Respiratory Medicine Journal","volume":"44 1","pages":"39 - 47"},"PeriodicalIF":0.0,"publicationDate":"2010-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68068057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2010-03-30DOI: 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.
{"title":"Antiproteases as Therapeutics to Target Inflammation in Cystic Fibrosis","authors":"D. Quinn, S. Weldon, C. Taggart","doi":"10.2174/1874306401004010020","DOIUrl":"https://doi.org/10.2174/1874306401004010020","url":null,"abstract":"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.","PeriodicalId":39127,"journal":{"name":"Open Respiratory Medicine Journal","volume":"4 1","pages":"20 - 31"},"PeriodicalIF":0.0,"publicationDate":"2010-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/1874306401004010020","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68068006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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