Association Between Increased Oxidative Stress, Anti-Inflammatory Fatty Acid Formation, and Airway Infection in People With Asthma and Chronic Obstructive Pulmonary Disease

NCT ID: NCT00595114

Last Updated: 2016-10-19

Study Results

Results available

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Basic Information

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Recruitment Status

COMPLETED

Total Enrollment

43 participants

Study Classification

OBSERVATIONAL

Study Start Date

2007-12-31

Study Completion Date

2009-08-31

Brief Summary

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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

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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.

Conditions

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Asthma Pulmonary Disease, Chronic Obstructive

Study Design

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Observational Model Type

COHORT

Study Time Perspective

RETROSPECTIVE

Study Groups

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MIA 1

Participants from the MIA trial who are polymerase chain reaction (PCR) negative and have received treatment with placebo

No interventions assigned to this group

MIA 2

Participants from the MIA trial who are PCR negative and have received treatment with the antibiotic clarithromycin

No interventions assigned to this group

MIA 3

Participants from the MIA trial who are PCR positive and have received treatment with placebo

No interventions assigned to this group

MIA 4

Participants from the MIA trial who are PCR positive and have received treatment with the antibiotic clarithromycin

No interventions assigned to this group

LEUKO 1

Participants from the LEUKO trial who have received treatment with placebo

No interventions assigned to this group

LEUKO 2

Participants from the LEUKO trial who have received treatment with zileuton

No interventions assigned to this group

Eligibility Criteria

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Inclusion Criteria

* No change from the MIA and LEUKO trials

Exclusion Criteria

* No change from the MIA and LEUKO trials
Minimum Eligible Age

18 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

No

Sponsors

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National Heart, Lung, and Blood Institute (NHLBI)

NIH

Sponsor Role collaborator

Brigham and Women's Hospital

OTHER

Sponsor Role lead

Responsible Party

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Bruce D. Levy

Principal Investigator

Responsibility Role PRINCIPAL_INVESTIGATOR

Principal Investigators

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Bruce D. Levy, MD

Role: PRINCIPAL_INVESTIGATOR

Brigham and Women's Hospital

Locations

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Brigham and Women's Hospital

Boston, Massachusetts, United States

Site Status

Countries

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United States

References

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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.

Reference Type DERIVED
PMID: 25162465 (View on PubMed)

Other Identifiers

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R01HL090927

Identifier Type: NIH

Identifier Source: secondary_id

View Link

HL090927

Identifier Type: -

Identifier Source: secondary_id

1421

Identifier Type: -

Identifier Source: org_study_id

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