Active clinical trials for "Bronchitis"

This study is evaluating the effectiveness of a dose counter for an inhaler device used to deliver medication to people diagnosed with asthma or COPD.

Cigarette smoking is the major risk factor for chronic obstructive pulmonary disease (COPD, commonly known as chronic bronchitis and emphysema). Despite this clear link, only 15-20% of smokers develop COPD suggesting that genetic factors affect the lung's susceptibility to the stress of cigarette smoke. The cells lining the airways (epithelium) and cells that help defend the lung (alveolar macrophages) of smokers develop gene expression changes that are different from that of nonsmokers. In the investigators' previous studies they have demonstrated that there are greater than 200 genes that are responsive to cigarette smoke in these cells. But the investigators do not know whether the gene expression is static or changes as a function of time. Genes that show significant changes over time may be relevant to the progression of the disease. Even though quitting smoking reduces the rate at which the lungs decline, many-smokers still go on to develop COPD. This study will provide insights into the natural history of smoking-related gene expression of the lung cells in health and disease.

Patients with chronic obstructive pulmonary disease (COPD) that have frequent chest infections are the patients most likely to become worse over time. Why these people are more susceptible to chest infections is not known. One reason might be that the white cells in their lungs called macrophages do not work properly. Normally, these cells remove all the debris inhaled into the lung. This can also include bacteria. In patients with COPD, these macrophages are not able to remove these particles. The research question addresses why this happens

The purpose of this study is to: 1) describe drug utilization for Fluoroquinolone(FQ), Azithromycin (AZ) and Sulfamethoxazole/Trimethoprim(ST) in the entire Truven MarketScan Commercial Claims and Encounters database (CCAE) database, and specifically among individuals in the Health and Productivity Management (HPM) during the observation period; 2) describe the rate of disability associated with 2 or more System Organ Class adverse events (SOC AEs) and exposure to FQs for several acute, uncomplicated indications; and 3) compare the rates of disability for 2 or more SOC AEs and exposure to FQs and AZ/ST for the same indications.

This is a pilot, observational and multicentric study of safety of sulfamethoxazole + trimethoprim + guaifenesin (Balsamic Bactrim) in adult participants with acute bronchitis. Adult participants with acute bronchitis eligible for treatment with Balsamic Bactrim will be enrolled. Administration of Balsamic Bactrim will be according to physician's recommendation under local labeling.

Evaluation of immunogenicity, safety and persistence of the subjects aged 60 years and above with chronic bronchitis and chronic obstructive pulmonary disease received the third dose of inactivated COVID-19 vaccine .

To evaluate the effect of a prophylactical therapy with a cough medicine containing ivy leaves dry extract on the frequency of recurrent wheezy bronchitis in toddlers, on the duration of the bronchitis episodes, on the severity and the additional drug demand. A prolonged asymptomatic episode between each wheezy bronchitis due to the therapy is assumed.

There is suggestive evidence for a role of dietary in the etiology of asthma and chronic bronchitis. However, there are few prospective data. We propose to expand our collaboration with the Singapore Chinese Health Study to examine dietary, environmental, and genetic factors, along with their interactions, in relation to the risk of developing asthma and chronic bronchitis. The Singapore Chinese Health Study is a cohort of 63,257 men and women of Chinese ethnicity in Singapore who were aged 45-74 years at enrollment from 1993 to 1998. Telephone follow-up of the cohort to update and outcome information began in 1999 and is ongoing. We expect to identify 538 cases of incident asthma and 672 cases of incident chronic bronchitis when the current follow-up questionnaire cycle is complete in 2004. In this proposal, we would validate self-reports of incident asthma, obtain follow-up data from the entire cohort to perform analyses of dietary and smoking in relation to these outcomes, and analyze genetic material on cases of incident asthma and chronic bronchitis and controls from the cohort. In this proposal we will examine the following hypotheses: Higher intake of fruits and/or antioxidant micronutrients decreases the risk of developing asthma and chronic bronchitis. a. Effects if fruit and/or antioxidant micronutrients may differ by smoking history. Common polymorphisms in genes involved in the response to oxidative stress influence the risk of asthma and chronic Bronchitis. We initially propose to examine polymorphisms in three genes--glutathione S-tranferase M1, glutahione S-transferase P1, and matrix metalloproteinase-1. However, we plan to examine additional relevant polymorphisms in the future, especially taking advantage of high throughput screens of candidate genes for asthma and chronic bronchitis. It is possible that by 2004 when the sample set will be available that more compelling candidates and high throughput screens may be available to us at a low cost. Thus we will re-evaluate our choice when the samples are available. Polymorphisms in these and other genes interact with fruit/antioxidant intake and/or smoking to influence the risk of asthma and chronic bronchitis.

A study to report the outcomes of patients who fail to respond to beta-lactam and macrolide antibiotics in the community

The aim of this study is to investigate the mechanisms whereby specific white cells called macrophages found in the lung release inflammatory mediators or chemicals together with enzymes that destroy the surrounding lung tissue. The hypothesis is that in diseases such as chronic obstructive pulmonary disease (COPD), lung macrophages release either more or different types of inflammatory mediators and/or destructive enzymes compared to subjects without COPD. We will isolate macrophages from small pieces of lung parenchyma. These samples are derived from lobes resected for carcinoma of the lung. We would aim to examine the responses of tissue derived macrophages in three groups of subjects, namely (i) non-smoking controls (lung carcinoma as secondary metastasis), (ii) smokers without clinical or histological signs of COPD and (iii) smokers with COPD. The resected lung tissue will be cut into small pieces and washed in order to release the macrophages from the tissue. The macrophages will then be isolated from other cell types in the washings. We will then use these isolated cells in vitro to examine the cell surface receptors in order to compare these macrophage cells with macrophages reported from bronchoalveolar lavage and monocyte derived macrophage models. We will then examine inflammatory mediator synthesis and release following stimulation of these cells. We will also examine the regulation and release of enzymes known to damage lung tissue. Using these two models we will then examine the signal transduction pathways that lead to this activation of the macrophages and investigate the effects of novel therapeutic agents to inhibit inflammatory mediator and/or enzyme synthesis and release. The objective is to identify the mechanisms whereby macrophages respond to pro-inflammatory conditions seen in COPD with a view to identify novel targets for drug therapy.