Expired Study
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Boston, Massachusetts 02115


Purpose:

Chronic obstructive pulmonary disease (COPD) and asthma are common respiratory diseases in which people experience long-term inflammation of the lungs. Exacerbations, or prolonged worsening of symptoms, of asthma and COPD are often life-threatening and can lead to frequent need for hospitalization. Even with the proper use of bronchodilators, corticosteroids, and other currently available medications, clinical responses among people with COPD and asthma are variable. There remains a significant unmet clinical need for new therapeutic approaches and insights, including the identification of biomarkers to accurately assess the presence of airway infection and intensity of airway inflammation. This study will investigate potential natural biological causes and new biomarkers for increased susceptibility to persistent airway infection in asthma and COPD.


Study summary:

COPD and asthma are chronic lung diseases that result in impaired air flow in the lungs, often causing coughing, wheezing, and shortness of breath. In uncontrolled COPD and asthma, people may experience a rapid worsening of symptoms, which may include fever, difficulty breathing, and chest pain. These exacerbations are the most serious expression of asthma and COPD and are usually caused by lung infections or air allergens. However, the biological basis for susceptibility to airway infection and inflammation is not well understood. Increased oxidative stress within the airways has been linked to several airway diseases. This increase in oxidative stress may reduce production of key fatty acid anti-inflammatory mediators. In turn, this may disrupt the airway's natural immune response mechanisms, making the airways more vulnerable to infection or inflammation during COPD and asthma exacerbations. This ancillary study will determine whether susceptibility to persistent airway infection in asthma and COPD stems from increased oxidative stress that impairs the natural formation of protective fatty acid mediators. This ancillary study will use data biological samples, including blood and sputum, from participants currently enrolled in the Macrolides in Asthma (MIA) and the Antileukotriene Therapy for COPD Exacerbations (LEUKO) trials. Biological samples will undergo fatty acid mediator analysis and RNA isolation. There will be no study visits for this study.


Criteria:

Inclusion Criteria: - No change from the MIA and LEUKO trials Exclusion Criteria: - No change from the MIA and LEUKO trials


NCT ID:

NCT00595114


Primary Contact:

Principal Investigator
Bruce D. Levy, MD
Brigham and Women's Hospital


Backup Contact:

N/A


Location Contact:

Boston, Massachusetts 02115
United States



There is no listed contact information for this specific location.

Site Status: N/A


Data Source: ClinicalTrials.gov

Date Processed: June 25, 2018

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