Clinical trial NCT00595114: Association Between Increased Oxidative Stress, Anti-Inflammatory Fatty Acid Formation, and Airway Infection in People With Asthma and Chronic Obstructive Pulmonary Disease
Official title: Ancillary Study of Oxidative Stress and Anti-Inflammatory Lipids in Airway Disease in the MIA (ACRN) and LEUKO (CCRN) Trials
Study type: OBSERVATIONAL
Overall status: COMPLETED
Conditions: Asthma
Pulmonary Disease, Chronic Obstructive
Keywords: COPD
Airway
Inflammation
Infection
Lipid Mediators
Oxidative Stress
Lead sponsor: Brigham and Women's Hospital
Sponsor class: OTHER
Collaborators: name: National Heart, Lung, and Blood Institute (NHLBI)
First posted: 2008-01-16
Enrollment: 43
Sex: ALL
Minimum age (years): 18
Standard ages: ADULT
OLDER_ADULT
Accepts healthy volunteers: no
Observational model: COHORT
Time perspective: RETROSPECTIVE
Sampling method: NON_PROBABILITY_SAMPLE
Study population: This ancillary study will use data and specimens previously collected in the Macrolides in Asthma (MIA) and the Antileukotriene Therapy for COPD Exacerbations (LEUKO) trials.

Brief summary: 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.

Detailed description: 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; NCT00318708) and the Antileukotriene Therapy for COPD Exacerbations (KIA; NCT01097694). Biological samples will undergo fatty acid mediator analysis and RNA isolation. There will be no study visits for this study.

Eligibility criteria: Inclusion Criteria:

* No change from the MIA and LEUKO trials

Exclusion Criteria:

* No change from the MIA and LEUKO trials

Primary outcomes:
measure: 8-isoprostane Levels as Biochemical Markers for Nonenzymatic Oxidative Stress in Asthma
timeFrame: Measured at completion of sample analysis
Secondary outcomes:
Other outcomes:
Locations:
city: Boston
country: United States
facility: Brigham and Women's Hospital
state: Massachusetts
Study officials:
affiliation: Brigham and Women's Hospital
name: Bruce D. Levy, MD
role: PRINCIPAL_INVESTIGATOR
References:
citation: Ono E, Dutile S, Kazani S, Wechsler ME, Yang J, Hammock BD, Douda DN, Tabet Y, Khaddaj-Mallat R, Sirois M, Sirois C, Rizcallah E, Rousseau E, Martin R, Sutherland ER, Castro M, Jarjour NN, Israel E, Levy BD; National Heart, Lung, and Blood Institute's Asthma Clinical Research Network. Lipoxin generation is related to soluble epoxide hydrolase activity in severe asthma. Am J Respir Crit Care Med. 2014 Oct 15;190(8):886-97. doi: 10.1164/rccm.201403-0544OC.