View clinical trials related to Chronic Obstructive Pulmonary Disease.
Filter by:Study purpose is to evaluate if subjects with chronic obstructive pulmonary disease (COPD) are more likely to be responsive to additional inhaled corticosteroids if they have a positive response to hyperosmolar challenge with mannitol than if their response is negative.
A biobank of Serum, plasma, DNA samples together with clinical information including specific questionnaires, complete pulmonary function and chest CT-scan, is prospectively collected in patients seen at the investigators' clinical service. The objective is to study candidate gene pathways in COPD and or lung cancer and to associate them with the clinical characteristics and phenotypes of COPD/emphysema and lung cancer. In subgroups of well characterised patients, other biological materials are also collected (lung tissue biopsies, peripheral blood mononuclear cells).
COPD is a progressive pulmonary disease that is characterized by an inflammatory process in the airways and the lungs which leads to progressive airway obstruction. The inflammation is associated with tissue loss and remodelling. The investigators hypothesized that doxycycline reduces neutrophilic airway inflammation in patients with COPD. Therefore the investigators will conduct a randomized trial of doxycycline in 30 patients.
This study was intended to assess how well inhaled NVA237 opens up the airways of patients with mild, moderate or severe COPD over a 24 hour period after a 14 day treatment period.
To test the compliance, tolerance, safety and to get preliminary insights into the efficacy of a new oral nutritional supplement (containing n-3 fatty acids, amino acids and antioxidants) designed to prevent or delay cachexia and anorexia in patients with chronic heart failure (CHF) or chronic obstructive pulmonary disease (COPD).
This study is an observational prospective pilot trial that utilizes finger cuff non invasive hemodynamic monitoring (NexfinHD Monitor) to assess 4 different groups (CHF/COPD, Trauma, Sepsis, Stroke) of patients on arrival to the Emergency Department and to document the changes seen in these hemodynamics with acute therapies.
COPD is ranked number 3 by the WHO list of important diseases worldwide and is the only disease with increasing mortality. The pathogenesis of cigarette smoke-induced COPD is obscure, therefore more insight is needed to design effective anti-inflammatory agents. Recently it has become clear that cigarette smoke-induced inflammation is not only present in the lungs but also in the blood, and that this systemic inflammation has important consequences for the clinical expression of COPD. The investigators hypothesize that healthy individuals who are susceptible to cigarette smoking demonstrate a higher and aberrant systemic inflammatory response to cigarette smoke. This susceptibility is caused by heterogeneous factors and is associated with various polymorphic genes that interact with each other and with the environment. Objective: - To study systemic inflammation in individuals who are or are not susceptible to develop COPD. - To characterize the switch to chronicity of the systemic inflmmatory response in COPD - To determine whether the type and severity of the systemic inflammation contributes to the clinical outcome of COPD - To compare between subjects who are or are not susceptible to develop COPD in peripheral blood, the corticosteroid responsiveness in vitro, and to unravel underlying mechanisms. - To study the role of candidate genes that may play a role in the development of fixed airway obstruction, and to identify clues for patient's responsiveness to specific drugs - To develop new biological and clinical markers for the early diagnosis and monitoring of COPD - To define possible mediators involved in the early induction of COPD in susceptible smokers, and to define new drug targets
The purpose of this study is: - To define The differences of bio-chemical phenotypes in chronic airway inflammatory diseases. - To identify novel biomarkers in chronic airway inflammatory diseases as a screening, diagnostic, or monitoring marker.
Asthma and chronic obstructive pulmonary disease (COPD) are chronic inflammatory airway diseases affecting millions of people worldwide. Inhaled corticosteroids (ICS) are by far the most effective treatment with a broad anti-inflammatory spectrum. Nevertheless, most COPD patients and a proportion of severe asthma patients are corticosteroid-resistant (CR) and to fail to respond to ICS even when higher doses are given. These corticosteroid-resistant patients suffer from persistent symptoms and repeated asthma exacerbations. It has been suggested that smoking and oxidative stress may induce corticosteroid-resistance. The reactive oxygen species (ROS) responsible for oxidative stress can be generated exogenously (air pollutants, cigarette smoke) and endogenously by metabolic reactions. After inhaling air pollutants or cigarette smoke, the bronchial epithelium is exposed. Preliminary data from our own lab suggest that smoking and oxidative stress may decrease epithelial cell-cell contact formation. This results not only in a decreased barrier function, but also in an increased production of pro-inflammatory mediators.
Smoking induces an inflammatory reaction in the airways which can ultimately result in persistent damage and the development of a Chronic Obstructive Pulmonary Disease (COPD). However, not all subjects who smoke end up with COPD. After long-term smoking, approximately 20% of subjects develop COPD. At this time, it is unclear why some subjects develop COPD, whereas others maintain a normal lung function. In addition, smoking has important consequences in asthma. Patients with asthma who smoke have a more severe asthma and more often experience an asthma exacerbation. In addition, it has been shown that inhaled corticosteroids are less effective in smoking asthmatics. With this research project, the researchers will investigate the effects of smoking on the airways. To this end, the researchers will compare markers of airway inflammation, lung function and symptoms between healthy smokers and non-smokers of varying age. In addition, the researchers will compare those healthy subjects with patients with asthma and COPD which are characterized in earlier studies.