View clinical trials related to Chronic Obstructive Pulmonary Disease.
Filter by:In patients with chronic obstructive pulmonary disease (COPD) breaths at an abnormally high lung volume causes the inspiratory muscle to operate at non-optimal lengths, which reduce their maximal contractile forces. In addition, causes non thoraco abdominal synchronize, reduced inspiratory muscle strength and is associated with dyspnea and decreased exercise capacity. For these patients inspiratory muscle training (IMT) is a widely employed form of rehabilitation also targeting the respiratory muscle. In addition, patients often experience shortness of breath and a decline in exercise tolerance, resulting in disability in the performance of activities of daily living (ADL). The aims of this trial are to evaluate the effects of inspiratory muscle training associated with aerobic training on strength and endurance of inspiratory muscle, thoracic abdominal synchrony, exercise tolerance and quality of life patients with COPD. To compare the responses with the effects of aerobic training plus exercises of the trunk and upper limbs, and stretching of large muscle groups of the trunk. To compare difference in the perception of dyspnea during the ADL set (Borg Scale) with perception of dyspnea self-reported in the Medical Research Council (MRC), the London Chest Activity of Daily Living (LCADL) and the Pulmonary Functional Status and Dyspnea Questionnaire - Modified version (PFSDQ-M) before start the protocol. To investigate changes on perception of dyspnea (Borg scale), metabolic and ventilatory responses during a standard set of ADL tasks after a physical training and to evaluate and compare changes on perception of dyspnea. The hypothesis are that the ventilatory efficiency during the performance of ADL and the dyspnea reported from borg scale, the LCADL and the PFSDQ-M that quantifies the functional performance (change in activity levels) are improved during the IMT in conjunction with general exercise training in patients with COPD. The MIT increases the strength and endurance of inspiratory muscle, the exercise capacity and the quality of life compared to the general physical training. However, compared to the thorax abdominal synchronizes, higher modification is verified in the general physical training group with specific exercise to torso, limbs and stretching of the higher muscle group.
The investigators propose to study the efficacy and safety of three-week antifungal therapy with caspofungin in hospitalized patients with proven or probable IPA underlying chronic obstructive pulmonary disease.
Skeletal muscle is composed of two fibre types which are intertwined. Skeletal muscle weakness, particularly of the walking muscles, is an important complication of Chronic Obstructive Pulmonary Disease (COPD) but so far the investigators do not know what mechanisms drive the process. All existing studies have investigated signalling pathways in the whole muscle so they have been forced to consider type I and type II fibres together. It is possible that disease selectively affects one fibre type, most likely type I fibres which are in fact lost in COPD patients. For this reason mechanisms of disease may have been overlooked by current studies. The applicants have acquired the technology which allows type I and type II fibres in a muscle specimen to be split (by laser capture microdissection) and so signalling pathways can be assessed separately in type II and type I fibres which is what this proposal sets out to do. The proposal therefore aims to capture well characterised clinical data from 60 COPD patients and 20 age matched controls, from whom a biopsy of the main walking muscle, the quadriceps, will be taken. In the samples the investigators will assess at a fibre specific level inflammatory signalling. Surplus material will be retained for subsequent fibre specific analysis.
The purpose of this study is to characterize the safety and efficacy of the AeriSeal System in patients with advanced upper lobe predominant emphysema and significant collateral ventilation as determined by the Chartis System.
Although pulmonary hypertension (PH) is a quite frequent complication of advanced pulmonary diseases, and it is an independent prognostic factor, until now no evidence-based treatment approach exists for those patients. This study will address if the drug sildenafil can lower pulmonary vascular resistance in patients with significant pulmonary hypertension (high blood pressure in the lungs) associated to chronic obstructive pulmonary disease (COPD). It will see if this treatment can improve effort capacity, quality of life without causing a deterioration in pulmonary gas exchange (mainly arterial oxygenation). Patients 18 years of age and older with moderate COPD and pulmonary hypertension (mean pulmonary arterial pressure >30 mmHg) may be eligible for this study. Participants are randomly assigned to receive sildenafil or placebo (pill with no drug) for 16 weeks. Before starting treatment (baseline), and a the end of the study, the patients have a comprehensive assessment including: - a chest x-ray and CT scan (only at baseline); - pulmonary function tests to measure how much air the patient can breathe in and out, and the capacity of diffusion of gases; - arterial blood gases analysis (for safety reason this examination is performed at baseline, before the randomization after one hour from the administration of a tablet (20 mg) of sildenafil, and every month) - an echocardiogram (heart ultrasound) (only at baseline); - a 6-minute walk test to measure exercise capacity; - a quality-of-life assessment (SF-36 questionnaire) - a right heart catheterization to evaluate the severity of hypertension At the end of the 16-week period, patients may opt to continue to receive sildenafil and monitoring in an open-label phase of the study for up to 1 year.
Metabolomics is a large-scale approach to monitoring the compounds involved in cellular processes. It may reflect changes in biological function. Collection of exhaled breath is a newly developed, noninvasive method that may allow clinicians and researchers to assess biochemical profiles in the airway. This study is conducted for the metabolomic analysis of the exhaled gas in patients with Chronic Obstructive Pulmonary Disease (COPD) and bronchiectasis.
Chronic Obstructive Pulmonary Disease (COPD) is the cause of considerable deaths, and exacerbations (flare up of symptoms) are a major cause of hospital admission in the UK. Bacterial infections play an important role in the development of COPD, however, there is little information available about the use of long term antibiotics in the treatment of this disease. Therefore the purpose of this study is to identify the best antibiotic regime for treating patients with COPD who have persistent bacterial infection in their lung. We will test a variety of approaches including both older and newer regimes prescribed either on a daily basis at a lower dose or in "pulsed" courses (for example, every other day or five days every month). The three antibiotics tested in this study are: moxifloxacin, azithromycin and doxycycline. This is a 13 weeks study conducted at the Royal Free Hospital, London. It is expected that approximately 200 patients will be selected for this study. The information we get from this study may help us to treat future patients with COPD better.
This is a PI-initiated study taking place only at UCLA, sponsored by Sunovion. The investigators plan to enroll about 20 subjects who are at least 40 years old and have Chronic Obstructive Pulmonary Disease (COPD). The purpose of this study is to compare the effectiveness of Brovana and Serevent in helping relieve COPD symptoms. Specifically, the investigators are looking at how much and for how long the two drugs can open up the small airways in the lungs. This will be done with breathing tests on all subjects, and with high resolution CT scans on subjects who agree to this optional part of the study. Half of subjects will take Brovana (arformoterol tartrate inhalation solution) for 2 weeks and then Serevent (salmeterol xinafoate inhalation powder) for 2 weeks; the other half will take Serevent the first two weeks and Brovana the second two weeks. All subjects will also take Spiriva (tiotropium) and will be provided with albuterol for immediate relief of symptoms. After a Screening Visit to determine eligibility, subjects will be randomly assigned to receive Brovana or Serevent for the first 2 weeks, complete Test Visit 1, then receive the other study drug for 2 weeks, and finally complete Test Visit 2. Visits will include questionnaires, review of health and medications, and breathing tests before and after taking the study drug. Subjects who agree to be in the sub-study will also undergo CT scans before and after taking the study drug at both test visits.
Lung cancer is the leading cause of cancer death in Hong Kong. Lung adenocarcinomas is the most common type, accounting for 70% of lung cancer and the molecular target of epidermal growth factor receptor (EGFR) gene mutation at exons 18 - 21 is present in about 50% of lung adenocarcinomas. The v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (K-ras) mutations are commonly present in the other 50% that are EGFR wildtype. EGFR and K-ras mutations are found to be mutually exclusive in the same tumor. EGFR-tyrosine kinase inhibitor (TKI) can be used as treatment for EGFR mutated tumors while no specific targeted therapy can be recommended for EGFR wildtype tumors and these patients often receive chemoirradiation, which is toxic and clinical response is suboptimal. There is a need to find alternative molecular pathways/targets in EGFR wildtype lung adenocarcinomas. Even with EGFR mutations, good clinical response to EGFR-TKI is achieved in about 70% of these patients. This would mean suboptimal targeting of the EGFR gene or the presence of alternative pathways mediating tumor progression and susceptibility to therapy. Exploration of molecular pathways in lung cancer may allow for discovery of new molecular targets for therapeutic development. Neutrophil infiltration is frequently observed in lung cancer. Recognized similarities between neutrophils and cancer cells include (i) ability to circulate as single cells; (ii) target attachment via vascular system; (iii) target invasion. The major difference is that migrated neutrophils will undergo apoptosis while cancer cells can escape apoptosis. This led to the postulation that neutrophils and cancer cells may share similar inflammatory cascades by secreting a similar panel of proteases, and one of these could be neutrophil elastase (NE). Animal studies demonstrated that NE from neutrophils moves into lung tumor cells and mediates lung tumor growth via degradation of Insulin receptor substrate-1 (IRS-1), leading to activation of intracellular phosphoinositide-3-kinase (PI3k) and the v-akt murine thymoma viral oncogene homolog 1 (Akt) signaling pathways and the intracellular tyrosine kinase of the platelet-derived growth factor receptor (PDGFR). The aims of this study are to demonstrate NE activities and the subsequent signaling cascades activated in lung cancer cells, and to verify NE and its related pathway activation in clinical lung cancer specimen. This study will conclude the roles of NE and the therapeutic potential of NE/IRS-1/PI3K/PDGFR pathways in EGFR wildtype lung adenocarinomas.
The pathomechanisms of COPD are still not fully understood, and up to now there is no satisfying causal treatment inhibiting the progress of the disease. Available therapy is in most cases symptomatic. Experimental and clinical observations suggest that treatment with ASA might be beneficial in the treatment of COPD in terms of respiratory and lung-functional improvement. To evaluate the efficacy of ASA as add-on therapy in COPD in comparison to placebo a prospective, randomized, double-blind, placebo controlled study will be conducted. Adult male and female patients (n=74) with proven COPD GOLD grade II-III will be randomized to 2 groups (i.e. 37 patients per group, stratification according to smoking status and gender). They will receive either 500 mg ASA per day or matching placebo over 12 weeks. Primary efficacy endpoints are changes in the lung-functional parameter FEV1 (forced expiratory 1-second volume) after 12 weeks of treatment. Secondary endpoints are the health score of the St. Georges respiratory questionnaire (SGRQ) and Peak-flow (PEF).