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chronic obstructive pulmonary disease - Top 30 Publications

Biomarkers for differentiation of patients with asthma and chronic obstructive pulmonary disease.

Asthma and chronic obstructive pulmonary disease (COPD) are airflow limitation diseases with similar clinical manifestations but different pathophysiologic mechanisms. To implement the appropriate treatment, it is important to distinguish between asthma and COPD which sometimes might result difficult in clinical practice. We evaluated biomarkers to distinguish between asthma and COPD.

Use of a Remote Inhaler Monitoring Device to Measure Change in Inhaler Use with Chronic Obstructive Pulmonary Disease Exacerbations.

Remote inhaler monitoring is an emerging technology that enables the healthcare team to monitor the time and location of a patient's inhaler use. We assessed the feasibility of remote inhaler monitoring for chronic obstructive pulmonary disease (COPD) patients and the pattern of albuterol inhaler use associated with COPD exacerbations.

Symptom-reducing actions: a concept analysis in the context of chronic obstructive pulmonary disease.

Patients with Chronic Obstructive Pulmonary Disease (COPD) have multiple symptoms. Nursing care is based on six core competencies and one of them is person-centred care that includes the aspect of professional symptom relief. The aim was to clarify a meaning of the concept of Symptom-reducing actions in the context of COPD. Databases MEDLINE and CINAHL were searched between 1982 and February 2016 and 26 publications were found. Two dictionaries and three books were investigated. The method of Walker & Avant was followed. The use of the concept of Symptom-reducing actions may be categorized by the sub-concepts of supervision, information, and patient education. Exploration of defining attributes was symptom management, instructions, support, motivation, explanation, advice, teaching, and learning. Antecedent occurrences were related to factors that affect the patient's level of function such as physical performance and cognitive function. Symptom-reducing actions offer a way to support patients with COPD in self-management. Symptom-reducing actions can mediate facts in a purposeful process performed by the nurse to enable the patient to take control over and manage unpleasant symptoms by a person-centred, planned process. The nurse can achieve this via supervision, information, and patient education with an integrated emotional component. Evaluating the outcomes is needed.

3D diffusion-weighted (129) Xe MRI for whole lung morphometry.

To obtain whole lung morphometry measurements from (129) Xe in a single breath-hold with 3D multiple b-value (129) Xe diffusion-weighted MRI (DW-MRI) with an empirically optimized diffusion time and compressed sensing for scan acceleration.

Interferon-λs: Front-Line Guardians of Immunity and Homeostasis in the Respiratory Tract.

Type III interferons (IFNs), also termed lambda IFNs (IFNλs) or interleukins-28/29, constitute a new addition to the IFN family. They are induced upon infection and are particularly abundant at barrier surfaces, such as the respiratory and gastrointestinal tracts. Although they signal through a unique heterodimeric receptor complex comprising IFNLR1 and IL10RB, they activate a downstream signaling pathway remarkably similar to that of type I IFNs and share many functions with them. Yet, they also have important differences which are only now starting to unfold. Here, we review the current literature implicating type III IFNs in the regulation of immunity and homeostasis in the respiratory tract. We survey the common and unique characteristics of type III IFNs in terms of expression patterns, cellular targets, and biological activities and discuss their emerging role in first line defenses against respiratory viral infections. We further explore their immune modulatory functions and their involvement in the regulation of inflammatory responses during chronic respiratory diseases, such as asthma and chronic obstructive pulmonary disease. Type III IFNs are, therefore, arising as front-line guardians of immune defenses in the respiratory tract, fine tuning inflammation, and as potential novel therapeutics for the treatment of diverse respiratory diseases, including influenza virus infection and asthma.

Hydrogen Sulfide Inhibits Cigarette Smoke-Induced Endoplasmic Reticulum Stress and Apoptosis in Bronchial Epithelial Cells.

Background: Apoptosis of lung structural cells contributes to the process of lung damage and remodeling in chronic obstructive pulmonary disease (COPD). Our previous studies demonstrated that exogenous hydrogen sulfide (H2S) can reduce the lung tissue pathology score, anti-inflammation and anti-oxidation effects in COPD, but the effect of H2S in regulating cigarette smoke (CS) induced bronchial epithelial cell apoptosis and the underlying mechanisms are not clear. Objectives: To investigate the effect of H2S on CS induced endoplasmic reticulum stress (ERS) and bronchial epithelial cell apoptosis. Methods: Male Sprague-Dawley rats randomly divided into four groups for treatment: control, CS, NaHS + CS, and propargylglycine (PPG) + CS. The rats in the CS group were exposed to CS generated from 20 commercial unfiltered cigarettes for 4 h/day, 7 days/week for 4 months. Since the beginning of the third month, freshly prepared NaHS (14 μmol/kg) and PPG (37.5 mg/kg) were intraperitoneally administered 30 min before CS-exposure in the NaHS and PPG groups. 16HBE cells were pretreated with Taurine (10 mM), 5 mmol/L 4-phenylbutyric acid (4-PBA) or NaHS (100, 200, and 400 μM) for 30 min, and then cells were exposed to 40 μmol/L nicotine for 72 h. ERS markers (GRP94, GRP78) and ERS-mediated apoptosis markers 4-C/EBP homologous protein (CHOP), caspase-3 and caspase-12 were assessed in rat lung tissues and human bronchial epithelial cells. The apoptotic bronchial epithelial cells were detected by Hoechst staining in vitro and TUNEL staining in vivo. Results: In CS exposed rats, peritoneal injection of NaHS significantly inhibited CS induced overexpression ERS-mediated apoptosis markers and upregulation of apoptotic rate in rat lungs, and inhibiting the endogenous H2S production by peritoneal injection of PPG exacerbated these effects. In the nicotine-exposed bronchial epithelial cells, appropriate concentration of NaHS and ERS inhibitors taurine and 4-PBA inhibited nicotine-induced upregulation of apoptotic rate and overexpression of ERS-mediated apoptosis markers. Conclusion: H2S inhibited lung tissue damage by attenuating CS induced ERS in rat lung and exogenous H2S attenuated nicotine induced ERS-mediated apoptosis in bronchial epithelial cells.

The Salford Lung Study: a pioneering comparative effectiveness approach to COPD and asthma in clinical trials.

The Salford Lung Study (SLS) of patients with asthma and chronic obstructive pulmonary disease (COPD) is a practical, community-based, randomized, open-label pragmatic study on the efficacy and safety of the once-daily dry powder inhaler that combines the inhaled corticosteroid fluticasone furoate (FF) with the long-acting beta2 agonist vilanterol (VI). The asthma component of the SLS is not yet reported but the COPD component, done over a 12-month period, found a statistically significant 8.4% reduction in COPD exacerbations when compared to usual care. No differences in adverse events, including serious adverse events and pneumonia, were noted. The importance of real-world findings, such as those found in the SLS COPD trial with inhaled FF/VI, is discussed in comparison to classical randomized controlled trials (RCTs) with inhaled FF/VI in COPD patients. The real-world, community-based pragmatic RCT like the SLS provides additional generalizable data with direct clinical applicability and potential usefulness in the development of practice guidelines. The results from the SLS, along with those of large and small RCTs, are supportive of the use of once-daily FF/VI in COPD maintenance therapy.

Proactive palliative care for patients with COPD (PROLONG): a pragmatic cluster controlled trial.

Patients with advanced chronic obstructive pulmonary disease (COPD) have poor quality of life. The aim of this study was to assess the effects of proactive palliative care on the well-being of these patients.

Relation of elevated serum uric acid levels to first-degree heart block and other cardiac conduction defects in hospitalized patients with type 2 diabetes.

Several studies have reported that moderately elevated serum uric acid levels are associated with an increased risk of tachyarrhythmias (mainly atrial fibrillation) in patients with and without type 2 diabetes mellitus (T2DM). It is currently unknown whether an association also exists between elevated serum uric acid levels and cardiac conduction defects in patients with T2DM.

Interleukin-22 attenuates double-stranded RNA-induced upregulation of PD-L1 in airway epithelial cells via a STAT3-dependent mechanism.

Double-stranded RNA derived from viruses induces host immune responses. PD-L1, also known as B7-H1, is an immune-checkpoint molecule associated with the escape of viruses from host immune systems, which plays a role in the persistence of viral infection, resulting in exacerbations of underlying diseases such as asthma and chronic obstructive pulmonary disease. Interleukin (IL)-22 is produced from various immune cells and has protective properties on mucosal tissue. The binding of IL-22 to IL-22 receptor induces STAT3 activation. We investigated the effect of IL-22 on the expression in airway epithelial cells in vitro and in mouse lungs in vivo after the stimulation with an analog of viral double-stranded RNA, polyinosinic-polycytidylic acid (poly I:C). Stimulation with poly I:C upregulated PD-L1 expression on BEAS-2B cells. This upregulation of PD-L1 was attenuated by IL-22 administration. STAT3 phosphorylation was induced by IL-22 and poly I:C. Treatment of cells with STAT3 siRNA abolished the effect of IL-22 on the poly I:C-induced upregulation of PD-L1. This upregulation of PD-L1 was also attenuated by IL-11, a cytokine inducing STAT3 phosphorylation, in BEAS-2B cells. In mouse lung cells in vivo, IL-22 suppressed poly I:C-induced upregulation of PD-L1. These results suggest that IL-22 attenuates virus-induced upregulation of PD-L1 in airway epithelial cells via a STAT3-dependent mechanism.

Steroid sparing effects of doxofylline.

Glucocorticosteroids are widely used in the treatment of asthma and chronic obstructive pulmonary disease (COPD). However, there are growing concerns about the side effect profile of this class of drug, particularly an increased risk of pneumonia. Over the last two decades there have been many attempts to find drugs to allow a reduction of glucocorticosteroids, including xanthines such as theophylline. Use of xanthines has been shown to lead to a reduction in the requirement for glucocorticosteroids, although xanthines also have a narrow therapeutic window limiting their wider use. Doxofylline is another xanthine that has been shown to be of clinical benefit in patients with asthma or COPD, but to have a wider therapeutic window than theophylline. In the present study we have demonstrated that doxofylline produces a clear steroid sparing effect in both an allergic and a non-allergic model of lung inflammation. Thus, we have shown that concomitant treatment with a low dose of doxofylline and a low dose of the glucocorticosteroid dexamethasone (that alone had no effect) significantly reduced both allergen-induced eosinophil infiltration into the lungs of allergic mice, and lipopolysaccharide (LPS)-induced neutrophil infiltration into the lung, equivalent to a higher dose of each drug. Our results suggest that doxofylline demonstrates significant anti-inflammatory activity in the lung which can result in significant steroid sparing activity.

IL-1β upregulates Muc5ac expression via NF-κB-induced HIF-1α in asthma.

The manifest and important feature in respiratory diseases, including asthma and COPD (chronic obstructive pulmonary disease), is the increased numbers and hypersecretion of goblet cells and overexpression of mucins, especially Muc5ac. Many proinflammatory cytokines play important roles in goblet cell metaplasia and overproduction of Muc5ac. However, the effect of IL-1β on Muc5ac expression in asthma remains unknown. Here, we detected the correlation between IL-1β and Muc5ac in asthma patients and further explored the mechanism of IL-1β-induced Muc5ac overexpression. Our results showed that Muc5ac and IL-1β were up-regulated in 41 patients with asthma and that Muc5ac overexpression was related with IL-1β in asthma (R(2)=0.668, p≪0.001). Furthermore, the correlation between IL-1β and Muc5ac is higher in severe group than that in moderate group. In vitro experiments with normal human bronchial epithelial cells (NHBECs) showed that IL-1β up-regulated Muc5ac expression in NHBEC in a time- and dosage-dependent manner. Hypoxia-induced HIF-1α was responsible for Muc5ac expression mediated by IL-1β. Knocking down HIF-1α by siRNA decreased Muc5ac expression under hypoxia even in IL-1β-treated NHBEC cells. Luciferase reporter assay showed that HIF-1α enhanced Muc5ac promoter activity in HEK293T cells. HIF-1α could specifically bind to the promoter of Muc5ac by EMSA. The correlation among IL-1β, HIF-1α and Muc5ac was observed in patients with asthma. Mechanically, NF-κB activation was essential to IL-1β-induced HIF-1α upregulation via the canonical pathway of NF-κB. The level of nuclear p65, a subunit of NF-κB, was obviously increased in NHBEC cells under IL-1β treatment. IL-1β did not change either HIF-1α or Muc5ac expression when inhibiting NF-κB signaling with Bay11-7082, an inhibitor of NF-κB. Collectively, we concluded that IL-1β up-regulated Muc5ac expression via NF-κB-induced HIF-1α in asthma and provided a potential therapeutic target for asthma.

Muscle α-adrenergic responsiveness during exercise and ATP-induced vasodilation in chronic obstructive pulmonary disease patients.

Sympathetic vasoconstriction is blunted in exercising muscle (functional sympatholysis) but becomes attenuated with age. We tested the hypothesis that functional sympatholysis is further impaired in chronic obstructive pulmonary disease (COPD) patients. We determined leg blood flow (LBF) and calculated leg vascular conductance (LVC) during 1) femoral-arterial Tyramine infusion (evokes endogenous norepinephrine release; 1 µmol min(-1) kg leg mass(-1)); 2) one-legged knee-extensor exercise with and without Tyramine infusion (10 W and 20% of maximal workload (WLmax)); 3) ATP (0.05 µmol min(-1) kg leg mass(-1)) and Tyramine infusion; and 4) incremental ATP infusions (0.05, 0.3 and 3.0 µmol min(-1)kg leg mass(-1)). We included ten patients with moderate to severe COPD and eight age-matched healthy controls. During exercise, LBF tended to be lower at 10 W (P=0.05) and 20% WLmax (P=0.09) and LVC was lower (P<0.05) at 20% WLmax in the COPD patients. Tyramine reduced LVC in both groups at 10 W exercise (COPD: -3 ±1; controls: -3±1 mL min(-1)mmHg(-1) P<0.05, respectively) and 20% WLmax (COPD: -4±1; controls: -3±1 mL min(-1)mmHg(-1) P<0.05, respectively) with no difference between groups. Incremental ATP infusions induced dose-dependent vasodilation with no difference between groups and also the vasoconstrictor response to Tyramine infused together with ATP was not different between groups (COPD: -0.03±0.01 versus controls: -0.04±0.01 L min(-1) kg leg mass(-1), P>0.05). Compared with age-matched healthy controls, the vasodilatory response to ATP is intact in COPD patients and their ability to blunt sympathetic vasoconstriction (functional sympatholysis) as evaluated by intra-arterial Tyramine during exercise or ATP infusion is maintained.

A qualitative study of COPD-patients' experience of a telemedicine intervention.

Clinically stable patients with chronic obstructive pulmonary disease (COPD) are often followed at regular intervals regardless of the needs. Our aim was to investigate the patient perspective on receiving telemedicine with weekly submission of readings and regular video consultations (Net-COPD) as an alternative to visits in the respiratory outpatient clinic and investigating the role of telemedicine in management of severe COPD.

Risk of exacerbation following pneumonia in adults with heart failure or chronic obstructive pulmonary disease.

Recent evidence demonstrates increased short-term risk of cardiac complications and respiratory failure among patients with heart failure (HF) and chronic obstructive pulmonary disease (COPD), respectively, concurrent with an episode of community-acquired pneumonia (CAP). We evaluated patients with pre-existing HF or COPD, beginning 30 days after CAP diagnosis, to determine if CAP had a prolonged impact on their underlying comorbidity.

The Effect of Music Therapy on Anxiety and Various Physical Findings in Patients With COPD in a Pulmonology Service.

This interventional study was carried out to determine the effect of music therapy on anxiety and the various physical findings in patients with chronic obstructive pulmonary disease in the pulmonary diseases service. Ninety-six patients (28 females, 68 males) of 114 adult patients who were hospitalized between November 10, 2013, and March 10, 2014, were included in the study. Ninety-six patients were separated in 3 groups. The data for the study were collected from a questionnaire form of sociodemographic and clinical characteristics, a patient follow-up form, and the Beck Anxiety Scale. SPPS 11.5 was used for data analysis. The Kolmogorov-Smirnov Test was used to determine whether the data showed normal distribution. The nonparametric Kruskal-Wallis Test was used to determine the differences between mean anxiety scores on day 0, day 5, and day 15, and the differences in physiological findings on day 0, day 5, and day 15. There was a significant decrease in anxiety level average on day 5 (P ≤ .0001) and day 15 (P ≤ .0001) of the study in both the Western classical music and Turkish classical music groups compared with control group. There was also a significant decrease in systolic blood pressure and diastolic blood pressure averages in both music groups compared with control group (P ≤ .005). There was no significant difference in heart rates and respiration rate average between the Western classical music and Turkish classical music groups compared with the control group (P > .05).

The Effect of Progressive Relaxation Exercises on Fatigue and Sleep Quality in Individuals With COPD.

This randomized controlled experimental study was conducted to investigate the effect of progressive muscle relaxation exercises on dyspnea, fatigue, and sleep quality in individuals with chronic obstructive pulmonary disease. A Descriptive Questionnaire and the Chronic Obstructive Pulmonary Disease and Asthma Fatigue Scale, Chronic Obstructive Pulmonary Disease and Asthma Sleep Scale and Medical Research Council Dyspnea Scale were used for data collection. The decrease in the mean dyspnea, fatigue, and sleep scores in the intervention group was statistically significantly more pronounced than the patients in the control group (P < .05). Progressive relaxation exercises can be implemented to decrease the dyspnea, fatigue, and sleep problems seen in patients with moderate and advanced chronic obstructive pulmonary disease by nurses working in the clinic.

Hospital-acquired conditions: predictors and implications for outcomes following spine tumor resection.

OBJECTIVE Hospital-acquired conditions (HACs) significantly compromise patient safety, and have been identified by the Centers for Medicare and Medicaid Services as events that will be associated with penalties for surgeons. The mitigation of HACs must be an important consideration during the postoperative management of patients undergoing spine tumor resection. The purpose of this study was to identify the risk factors for HACs and to characterize the relationship between HACs and other postoperative adverse events following spine tumor resection. METHODS The 2008-2014 American College of Surgeons' National Surgical Quality Improvement Program database was used to identify adult patients undergoing the resection of intramedullary, intradural extramedullary, and extradural spine lesions via current procedural terminology and ICD-9 codes. Demographic, comorbidity, and operative variables were evaluated via bivariate statistics before being incorporated into a multivariable logistic regression model to identify the independent risk factors for HACs. Associations between HACs and other postoperative events, including death, readmission, prolonged length of stay, and various complications were determined through multivariable analysis while controlling for other significant variables. The c-statistic was computed to evaluate the predictive capacity of the regression models. RESULTS Of the 2170 patients included in the study, 195 (9.0%) developed an HAC. Only 2 perioperative variables, functional dependency and high body mass index, were risk factors for developing HACs (area under the curve = 0.654). Hospital-acquired conditions were independent predictors of all examined outcomes and complications, including death (OR 2.26, 95% CI 1.24-4.11, p = 0.007), prolonged length of stay (OR 2.74, 95% CI 1.98-3.80, p < 0.001), and readmission (OR 9.16, 95% CI 6.27-13.37, p < 0.001). The areas under the curve for these models ranged from 0.750 to 0.917. CONCLUSIONS The comorbidities assessed in this study were not strongly predictive of HACs. Other variables, including hospital-associated factors, may play a role in the development of these conditions. The presence of an HAC was found to be an independent risk factor for a variety of adverse events. These findings highlight the need for continued development of evidence-based protocols designed to reduce the incidence and severity of HACs.

Different expression about induced sputum cell sorting in the two main types of chronic obstructive pulmonary disease.

The difference in expression of sputum cells types between the two main types of chronic obstructive pulmonary disease (COPD) is largely unknown. This study aims to investigate the difference and then wants to depend on sputum cells sorting to direct the treatment of COPD.

The importance of symptoms in the longitudinal variability of clusters in COPD patients: A validation study.

Cluster analysis has been utilized to explore phenotypic heterogeneity in chronic obstructive pulmonary disease (COPD). To date, little is known about the longitudinal variability of clusters in COPD patients. We aimed to evaluate the 2-year cluster variability in stable COPD patients.

Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia diagnosed by tranbronchoscopic cryoprobe biopsy technique.

Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) remains a poorly understood clinical entity. It is currently classified as a premalignant condition by the World Health Organization (WHO). Symptoms are similar to those associated with obstructive lung disease, including breathlessness and cough. The presentation is often initially ascribed to other diseases such as asthma or chronic obstructive pulmonary disease. Here, we present what we believe is the first described case of DIPNECH diagnosed by transbronchoscopic cryoprobe biopsy. The patient presented with chronic cough, dyspnoea, pulmonary function tests consistent with obstruction, and a computed tomography (CT) scan of chest with multiple nodules. The patient went on to have transbronchoscopic cryoprobe biopsies of the lung, which confirmed the diagnosis of DIPNECH.

Association of Body Mass Index and Postoperative Acute Kidney Injury in Patients Undergoing Laparoscopic Surgery.

Whether the deleterious effects of carbon dioxide pneumoperitoneum on the kidneys are exacerbated in the obese population remains unknown. We hypothesized that increased body mass index (BMI) is associated with an increased incidence of postoperative acute kidney injury (AKI) in patients undergoing noncardiac laparoscopic surgery.

Systemic effects of chronic obstructive pulmonary disease in young-old adults' life-space mobility.

The objective was to assess whether dyspnea, peripheral muscle strength and the level of physical activity are correlated with life-space mobility of older adults with COPD.

Comparison of the peripheral blood eosinophil count using near-patient testing and standard automated laboratory measurement in healthy, asthmatic and COPD subjects.

Near-patient testing (NPT) allows clinical decisions to be made in a rapid and convenient manner and is often cost effective. In COPD the peripheral blood eosinophil count has been demonstrated to have utility in providing prognostic information and predicting response to treatment during an acute exacerbation. For this potential to be achieved having a reliable NPT of blood eosinophil count would be extremely useful. Therefore, we investigated the use of the HemoCue(®) WBC Diff System and evaluated its sensitivity and specificity in healthy, asthmatic and COPD subjects. This method requires a simple skin prick of blood and was compared to standard venepuncture laboratory analysis. The HemoCue(®) WBC Diff System measured the peripheral blood eosinophil count in healthy, asthma and COPD subjects with very close correlation to the eosinophil count as measured by standard venepuncture. The correlations were unaffected by disease status. This method for the measurement of the peripheral blood eosinophil count has the potential to provide rapid near-patient results and thus influence the speed of management decisions in the treatment of airway diseases.

Impact and associations of eosinophilic inflammation in COPD: analysis of the AERIS cohort.

Eosinophilic inflammation in chronic obstructive pulmonary disease (COPD) predicts response to treatment, especially corticosteroids. We studied the nature of eosinophilic inflammation in COPD prospectively to examine the stability of this phenotype and its dynamics across exacerbations, and its associations with clinical phenotype, exacerbations and infection.127 patients aged 40-85 years with moderate to very severe COPD underwent repeated blood and sputum sampling at stable visits and within 72 h of exacerbation for 1 year.Blood eosinophils ≥2% was prevalent at baseline, and predicted both predominantly raised stable-state eosinophils across the year (area under the curve 0.841, 95% CI 0.755-0.928) and increased risk of eosinophilic inflammation at exacerbation (OR 9.16; p<0.001). Eosinophils ≥2% at exacerbation and eosinophil predominance at stable visits were associated with a lower risk of bacterial presence at exacerbation (OR 0.49; p=0.049 and OR 0.25; p=0.065, respectively). Bacterial infection at exacerbation was highly seasonal (winter versus summer OR 4.74; p=0.011) in predominantly eosinophilic patients.Eosinophilic inflammation is a common and stable phenotype in COPD. Blood eosinophil counts in the stable state can predict the nature of inflammation at future exacerbations, which when combined with an understanding of seasonal variation provides the basis for the development of new treatment paradigms for this important condition.

Effect of erdosteine on the rate and duration of COPD exacerbations: the RESTORE study.

Oxidative stress contributes to chronic obstructive pulmonary disease (COPD) exacerbations and antioxidants can decrease exacerbation rates, although we lack data about the effect of such drugs on exacerbation duration.The RESTORE (Reducing Exacerbations and Symptoms by Treatment with ORal Erdosteine in COPD) study was a prospective randomised, double-blind, placebo-controlled study, enrolling patients aged 40-80 years with Global Initiative for Chronic Obstructive Lung Disease stage II/III. Patients received erdosteine 300 mg twice daily or placebo added to usual COPD therapy for 12 months. The primary outcome was the number of acute exacerbations during the study.In the pre-specified intention-to-treat population of 445 patients (74% male; mean age 64.8 years, forced expiratory volume in 1 s 51.8% predicted) erdosteine reduced the exacerbation rate by 19.4% (0.91 versus 1.13 exacerbations·patient(-1)·year(-1) for erdosteine and placebo, respectively; p=0.01), due to an effect on mild events; the reduction in the rate of mild exacerbations was 57.1% (0.23 versus 0.54 exacerbations·patient(-1)·year(-1) for erdosteine and placebo, respectively; p=0.002). No significant difference was observed in the rate of moderate and severe exacerbations (0.68 versus 0.59 exacerbations·patient(-1)·year(-1) for erdosteine and placebo, respectively; p=0.054) despite a trend in favour of the comparison group. Erdosteine decreased the exacerbation duration irrespective of event severity by 24.6% (9.55 versus 12.63 days for erdosteine and placebo, respectively; p=0.023). Erdosteine significantly improved subject and physician subjective severity scores (p=0.022 and p=0.048, respectively), and reduced the use of reliever medication (p<0.001), but did not affect the St George's Respiratory Questionnaire score or the time to first exacerbation.In patients with COPD, erdosteine can reduce both the rate and duration of exacerbations. The percentage of patients with adverse events was similar in both the placebo and erdosteine treatment groups.

Th17 cytokines: novel potential therapeutic targets for COPD pathogenesis and exacerbations.

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease of the airways caused mainly by cigarette smoke exposure. COPD progression is marked by exacerbations of the disease, often associated with infections. Recent data show the involvement in COPD pathophysiology of interleukin (IL)-17 and IL-22, two cytokines that are important in the control of lung inflammation and infection. During the initiation and progression of the disease, increased IL-17 secretion causes neutrophil recruitment, leading to chronic inflammation, airways obstruction and emphysema. In the established phase of COPD, a defective IL-22 response facilitates pathogen-associated infections and disease exacerbations. Altered production of these cytokines involves a complex network of immune cells and dysfunction of antigen-presenting cells. In this review, we describe current knowledge on the involvement of IL-17 and IL-22 in COPD pathophysiology at steady state and during exacerbations, and discuss implications for COPD management and future therapeutic approaches.

Toll-like receptor 2 and 4 have Opposing Roles in the Pathogenesis of Cigarette Smoke-induced Chronic Obstructive Pulmonary Disease.

Chronic Obstructive Pulmonary Disease (COPD) is the third leading cause of morbidity and death and imposes major socioeconomic burdens globally. It is a progressive and disabling condition that severely impairs breathing and lung function. There is a lack of effective treatments for COPD, which is a direct consequence of the poor understanding of the underlying mechanisms involved in driving the pathogenesis of the disease. Toll-like receptor (TLR)2 and TLR4 are implicated in chronic respiratory diseases, including COPD, asthma and pulmonary fibrosis. However, their roles in the pathogenesis of COPD are controversial and conflicting evidence exists. In the current study, we investigated the role of TLR2 and TLR4 using a model of cigarette smoke (CS)-induced experimental COPD that recapitulates the hallmark features of human disease. TLR2, TLR4 and associated co-receptor mRNA expression were increased in the airways in both experimental and human COPD. Compared to WT mice, CS-induced pulmonary inflammation was unaltered in TLR2-deficient (Tlr2-/-), TLR4-deficient (Tlr4-/-) mice. CS-induced airway fibrosis, characterized by increased collagen deposition around small airways, was not altered in Tlr2-/- mice but was attenuated in Tlr4-/- mice compared to CS-exposed WT controls. However, Tlr2-/- mice had increased CS-induced emphysema-like alveolar enlargement, apoptosis and impaired lung function, whilst these features were reduced in Tlr4-/- mice compared to CS-exposed WT controls. Taken together, these data highlight the complex roles of TLRs in the pathogenesis of COPD and suggest that activation of TLR2 and/or inhibition of TLR4 may be novel therapeutic strategies for the treatment of COPD.

The patient with a complex chronic respiratory disease: a specialist of his own life?

The independent and central role of the patient with a complex chronic respiratory disease in targeted, personalized disease management strategies is becoming increasingly important. Patients are the ones living with the disease and are finally responsible for their lives underlining their role as essential members of the interdisciplinary treatment team. Areas covered: The present paper narratively reviews existing research and discusses the special, as well as specialized, role of the patient with a complex chronic respiratory disease in the healthcare system and highlights fundamental elements of the (future) relationship between patient and healthcare professionals. Expert commentary: Since the chronic respiratory disease at hand is part of the patient's entire life, we need holistic, personalized approaches optimizing patients' quality of life by not only treating the disease but considering the patients' whole environment and where healthcare professionals and patients are co-creating value care.

Cardiopulmonary interactions with beta-blockers and inhaled therapy in COPD.

Beta-blockers remain underused in patients with chronic obstructive pulmonary disease (COPD) and cardiovascular disease.