View clinical trials related to Chronic Obstructive Pulmonary Disease.
Filter by:Highly active antiretroviral therapy (HAART) has considerably improved survival of HIV-infected patients. Opportunist diseases and cancers linked to immunodepression have largely regressed. Challenge is now the management of cardio-vascular diseases, nephrologic, neurologic, osteo-articular diseases, chronic hepatitis and cancer no linked to immunodepression. All this comorbidities are more reported in HIV-infected patients than in general non-HIV infected patients. Those are directly linked to the effect of chronic HIV-infection on ageing, metabolic effects of HAART, and way of life characterising this population. Chronic obstructive pulmonary disease (COPD) results from tobacco consumption. Bronchial chronic infection, immunity, and ageing are also involved in the physiopathology of COPD. This disease has never been evaluated in a large prospective cohort of HIV-infected patients whereas there is a known increase of tobacco consumption and pulmonary infection in this population regardless to the general population. Characterisation of COPD disease in HIV patients will allow us to make an hypothetic epidemiological link between HIV- HAART and COPD independently of tobacco consumption, and to study different physiopathologic hypothesis evocated in COPD genesis, like an accelerate pulmonary ageing.
The purpose of this study was to observe the Efficacy and safety of 400 μg twice daily of aclidinium bromide vs. placebo when administered to patients with moderate to severe chronic obstructive pulmonary disease (COPD).
To compare the efficacy, safety and pharmacokinetics of QMF149 delivered via Concept1 to salmeterol xinafoate/fluticasone propionate delivered via Accuhaler in adult patients with COPD
Objective: To characterize FeNO levels that may be indicative of eosinophilic airway inflammation in patients with chronic obstructive airways disease Number of participants: Approximately 200 subjects will be enrolled Reference product: NIOX MINO® Instrument (09-1100) Performance assessments: Fractional Exhaled Nitric Oxide (FeNO) Measurements will be performed according to the "Perform FeNO Measurement" guidelines on page 7 of the NIOX MINO® User Manual Safety assessments: The Investigator is responsible for the detection, reporting, and documentation of events meeting the definition of an Adverse Event (AE) and/or Serious Injuries as provided in this clinical investigation plan from the time that informed consent has been provided and during the study period Criteria for evaluations: This is an observational, pilot study and there are currently no plans for a formal statistical analysis. Information gained from this study may used to design subsequent studies in patients with chronic obstructive airways disease. Information collected will be summarized in a clinical study report but will not be subject to formal hypothesis testing
The investigators hypothesize that education will improve exercise capacity, symptoms and quality of life in patients with chronic obstructive pulmonary disease (COPD). In addition, the investigators are interested in determining how education might alter various chemicals in the blood and exhaled breath that reflect inflammation in the lungs and the body as a whole. The investigators plan to enroll 42 patients into this study, with half of them participating at each of the two sites, Vermont Lung Center at the University of Vermont in Burlington, Vermont, and at Baylor College of Medicine in Houston, Texas. Participants will undergo a series of measurements and tests at the beginning of the study, receive formal education about COPD over the next 2 weeks, return at 6 weeks for a brief refresher session, and finally return after 12 weeks for repeat measurement and testing as was done at the beginning. Participants will be asked to keep a diary of symptoms, medication, and exercise during the study.
Chronic obstructive pulmonary disease is associated with a low grade systemic inflammatory process. Systemic inflammation is hypothesized to maintain cardiovascular morbidity and mortality in COPD. Early changes of vascular integrity can be detected via markers of subclinical atherosclerosis. Selective Inhibition of phosphodiesterase subtype 4 describes a promising therapeutic option in COPD with beneficial impact on lung function and exacerbation rate. Moreover, an anti-inflammatory effect of phosphodiesterase-4 inhibition was confirmed by recent data. The aim of this study is to assess the effects of the phosphodiesterase-4 inhibitor Roflumilast on firstly surrogates of subclinical atherosclerosis and secondly markers of systemic inflammation in the peripheral circulation of patients with stable chronic obstructive pulmonary disease.
This is a multi-center, prospective, non-interventional study that aims to evaluate in daily clinical practice, the possible corelation between patIent perception of the ability to perform morning activities and physician evaluation; patients with COPD, grade C and D.
Aim The purpose of this study is to evaluate whether fuel subsidies reduce exacerbations of COPD among people aged over 55, and therefore whether providing such subsidies is a cost-beneficial policy initiative. The Warm Homes for Elder New Zealanders Study enrolled community-dwelling people aged over 55 with moderate or worse COPD. Prior to the study commencing the houses were insulated (if feasible, & the house-owner agreed). Data were collected on the health and energy use of the participants. The households randomly assigned to the "early" intervention group had a subsidy to their power account their first winter in the study. The subsidy was the intervention and was designed to enable the participants, if they chose to do so, to keep their house warmer during the winter.
To access the clinical usefulness of F1+2 in the diagnosis of PE in patients with AECOPD who require hospitalization. Specifically, to determine whether F1+2 may have an additional value in the subgroup of patients with an abnormal D-dimer,to determine whether it may increase the proportion of patients in whom PE can be safely ruled out and to determine the sensitivity, specificity and NPV of F1+2 at various cut-off values.
Loss of muscle protein is generally a central component of weight loss in Chronic Obstructive Pulmonary Disease (COPD) patients. Gains in muscle mass are difficult to achieve in COPD unless specific metabolic abnormalities are targeted. The investigators recently observed that alterations in protein metabolism are present in normal weight COPD patients. Elevated levels of protein synthesis and breakdown rates were found in this COPD group indicating that alterations are already present before muscle wasting occurs. The investigators recently observed that in order to enhance protein anabolism, manipulation of the composition of proteins and amino acids in nutrition is required in normal-weight COPD. Intake of casein protein resulted into significant protein anabolism in these patients. The anabolic response to casein protein was even higher than after whey protein intake. A substantial number of COPD patients, underweight as well as normal weight to obese, is characterized by an increased inflammatory response. This group failed to respond to nutritional therapy. Previous experimental research and clinical studies in cachectic conditions (mostly malignancy) indicate that polyunsaturated fatty acids (PUFA) are able to attenuate protein degradation by improving the anabolic response to feeding and by decreasing the acute phase response. Eicosapentaenoic acid (EPA) (in combination with docosahexaenoic acid (DHA)) has been shown to effectively inhibit weight loss in several disease states, however weight and muscle mass gain was not present or minimal. Until now, limited research has been done examining muscle protein metabolism and the response to EPA and DHA supplementation in patients with COPD. It is the investigator's hypothesis that supplementation of 2g/day EPA+DHA in COPD patients during 4 consecutive weeks will increase the muscle anabolic response to a high quality protein supplement as compared to a placebo, and supplementation of 3.5g/day EPA+DHA will increase the anabolic response even further. In the present study both the acute and chronic effects of EPA+DHA versus a placebo on muscle and whole body protein metabolism will be examined. The principal endpoint will be the extent of stimulation of net fractional muscle protein synthesis as this is the principal mechanism by which the effect of EPA+DHA on muscle anabolism can be measured. The endpoint will be assessed by isotope methodology which is thought to be the reference method.