Active clinical trials for "Lung Diseases"

Chronic obstructive pulmonary disease (COPD) is one of the UKs commonest chronic diseases and is responsible for a significant number of acute hospital admissions. COPD is characterised by progressive destruction in the elastic tissue within the lung, causing respiratory failure. The clinical course of COPD is characterised by recurrent acute exacerbations (AECOPD), causing considerable morbidity and mortality. Patients with moderate to severe acute exacerbations present with increased work of breathing and hypercapnia. The standard for respiratory support in this setting is non-invasive ventilation (NIV), a management strategy underpinned by a considerable evidence base. However despite NIV, up to 30% of patients with AECOPD will 'fail' and require intubation and mechanical ventilation. The mortality rate for patients requiring NIV is approximately 4%, if conversion to mechanical ventilation occurs the mortality is 29%. The last decade has seen an increasing interest in the provision of extracorporeal support for respiratory failure. The key element that has underpinned improving survival has been technological advancement. This has resulted in pumps causing less blood trauma and inflammatory response, better percutaneous cannulation techniques and coated circuits with reduced heparin requirements. Overall this has significantly reduced the complications associated with the provision of extracorporeal support. One variation of this technique (extra-corporeal CO2 removal ECCO2R) allows CO2 clearance from the blood. This approach has been the subject of a number of animal experiments and uncontrolled human case series demonstrating improved arterial CO2 and reduced work of breathing. Our own unpublished series demonstrates the same physiological changes. However to date the benefits of this approach have not been tested in a randomised controlled trial. The hypothesis is that the addition of ECCO2R to NIV will shorten the duration of NIV and reduce likelihood of intubation.

Study to obtain further information on the tolerability and efficacy of Atrovent® inhalets in the treatment of Chronic Obstructive Pulmonary Disease under conditions of daily practice

The inhaled Iloprost, approved for pulmonary hypertension, caused increase in oxygenation, and increase exercise tolerance in ARDS or chronic obstructive pulmonary disease. Inhaled iloprost has been researched in animal study, but not yet in human during one-lung ventilation. The investigators will enroll patients who diagnosed moderate to severe chronic obstructive pulmonary disease, preoperative pulse oximetry (SpO2) of below 95% at room air or PaO2 /FiO2 ratio< 150 mmHg after initiating one-lung ventilation. The primary outcome is pulmonary oxygenation expressed by PaO2 /FiO2 ratio. And secondary outcome is assessment of cardiac function including Tei-index during nebulizing iloprost. The investigators hypothesized inhaled iloprost will improve oxygenation and decrease the FiO2 in chronic obstructive pulmonary disease during one-lung ventilation.

The study is devoted to the comparative analysis of the data received in patients with lung pathology using new method of probe-based confocal laser endoscopy of distal airways and two reference methods: high resolution computed tomography and morphology.

The purpose of this study is to assess efficiency and safety of cryobiopsy compared to video-assisted thoracoscopic lung biopsy (VATS) in diagnosis of interstitial lung diseases (ILD). To that end, this non-interventional study prospectively collects data from patients undergoing routine diagnosis of ILD. In some of those patients less invasive diagnostic approaches do not yield a definitive diagnosis. Thus, they will ultimately be subjected to VATS if this procedure is reasonable. The information gained by this study will help to assess the significance of cryobiopsy in contrast to VATS in this particular disease group.

This was an observational pilot study to examine the usefulness of an electronic sensor that monitors short-acting beta-agonist inhaled medication use. The goals of this study were to: 1) test the feasibility of using the inhaler sensor to measure worsening symptoms and exacerbations, 2) characterize physical activity in patients with COPD, and 3) examine whether environmental factors can be linked to mild exacerbations measured by the inhaler sensor.

Title: Duplication in Chitotriosidase (CHIT1) Gene and the Risk for Aspergillus Lung Disease in CF Patients. Aim: To evaluate the link between CHIT1 duplication in CF patients and the predisposition to ABPA or persistent Aspergillus infection. Patients: 40 CF patients. Design: Observational, single visit. Methods: All patients will be assessed for pulmonary function tests (PFT), sputum cultures, and blood tests for: CHIT1 duplication, immunoglobulin E (IgE) and Eosinophils levels. Part of the patients will be assessed for RAST, skin prick test. Primary outcome measure is the difference in CHIT1 genotyping between the groups.

Recently, direct evidences point to the contributing role of peripheral muscle fatigue in exercise tolerance among patients with COPD. However, the physiological mechanisms by which peripheral muscle fatigue impairs exercise tolerance are still unknown, as factors regulating peripheral muscle fatigue in COPD may be complex. One possible link between limb muscle fatigue and exercise intolerance could be enhanced afferent signals from the active limb muscles to the central command, thereby limiting central motor output and eventually leading to exercise termination. A direct method to investigate the regulation of peripheral muscle fatigue during exercise in patients with COPD is the blockade of peripheral neural afferents via lumbar anesthesia. Consequently, investigating the interplay between the peripheral muscular component and the central motor command during self-paced exercise could shed light on the regulation of peripheral muscle fatigue in COPD and its implication in exercise intolerance.

COPD is a common, serious disease and is a major burden on patients and the National Health Service. Patients with COPD can develop worsening of their symptoms, known as an exacerbation, which can be severe enough to warrant hospital admission. There are currently no objective measurements available to patients and clinicians to predict exacerbation and monitor recovery. Detection of exacerbation by both patients and physicians is known to correlate poorly with onset of respiratory deterioration. Measurement of neural respiratory drive (NRD), or drive to breathe, using respiratory muscle electromyography (EMG) correlates with changes in patients' symptoms and physician defined deterioration during hospital admissions. This pilot study aims to identify whether daily measurement of NRD at home following admission to hospital with exacerbation of COPD can detect an exacerbation within 30 days of discharge (20% of patients are readmitted within this period). This technique could enable early detection of deterioration at home, facilitating earlier treatment compared to current practice, potentially avoiding hospital readmission. 30 patients admitted to St Thomas' Hospital because of an exacerbation of COPD aged 40-80, with a body mass index <35kg/m2, who can follow English instructions and give informed consent, who are discharged home will be recruited. If patients consent to participate, they will have assessments as inpatients and for 30 days at home following discharge, or until hospital readmission, whichever is sooner. Assessments include vital observations (heart rate, blood pressure, respiratory rate and oxygen saturations), NRD, and a symptom questionnaire. At the baseline assessment, age, height weight, a brief medical history, results of tests already taken by the clinical team (blood tests and chest x-ray) and lung function tests will be recorded. This study will take 12 months. Philips and its Affiliates are providing the NRD measuring equipment.

Smoking is one of the world's leading health hazards. Besides being a major risk factor in the etiology of COPD and lung cancer, cigarette smoke is also a causative agent lung diseases characterized by bronchiolar and interstitial inflammation. However, the associated lung pathology of smoking is not only a risk in the development of lung diseases, but also widely recognized as a major risk factor associated with perioperative respiratory and cardiovascular complications. Apart from the long term effects of cigarette smoke, acute effects of the inhalation of cigarettes smoke may influence the course of lung pathology. The inhalation of smoke causes inflammation in the lung by inducing chemotaxis and activation of neutrophils and macrophages and induces oxidative stress. As the acute inflammatory response to smoke inhalation seems to be the underlying mechanism for chronic diseases of smokers, exploring the field of the acute pulmonary changes after exposure to cigarette smoke is highly relevant. One reason for acute hypoxia and injury during smoking might be a severe mismatch of ventilation and perfusion of the lung. Using the multiple inert gas elimination technique (MIGET), a distribution of ventilation-perfusion ratios in the lung can be calculated by analyzing data on the retention and excretion of six infused inert gases. A saline solution containing the gases is infused intravenously. When passing through the lung the gases are either eliminated from the blood or retained depending on their partition coefficient and local V/Q ratio. The concentrations of the gases are measured in the mixed venous blood or the mixed expired gas and the arterial blood allowing for the calculation of retention and excretion and the derivation of V/Q distribution. MIGET is the experimental gold standard to determine the Ventilation-Perfusion ratio of the lung. The aim of this study is to show the acute effect of smoking on ventilation/perfusion ratio distribution in the lung in otherwise healthy smokers.