Evaluation of Airway Gene Expression in COPD and Controlled Populations
|ClinicalTrials.gov Identifier: NCT00571792|
Recruitment Status : Unknown
Verified December 2007 by University of Nebraska.
Recruitment status was: Recruiting
First Posted : December 12, 2007
Last Update Posted : December 12, 2007
|Condition or disease|
Chronic Obstructive Pulmonary Disease(COPD) is currently the fourth leading cause of death in the United States. COPD is characterized by reduced airflow that is largely irreversible and progressive. Smoking is recognized as the most important cause of COPD contributing up to 80% of the cases. The disease does demonstrate a significant variability in airflow obstruction during the progression of the disease among those who are diagnosed and treated. This is probably due not only to the role of exposure of cigarette smoke and other noxious inhaled particles and gases but also to the individual's varied responses to those exposures.
COPD is characterized by an inflammatory response that does have a number of components that may be present in variable amounts. Recent data suggests that the cigarette exposure may cause several distinct pathophysiological processes that in turn may account for the variability demonstrated in altered lung structure that leads to functional impairment. Current therapies can help with alleviation of symptoms in individuals but not the unaltered course of loss in lung function that frequently leads to respiratory failure and death.
New strategies have been discussed as a means to new therapeutic approaches to altering the course of the disease. The use of genomic and proteomic methodologies offer promise to identify the pathways critical and relevant to the progression of COPD. To date approved medications target only the inflammatory response to the disease.
The study will explore metabolic pathways that could affect the remodeling process associated with the disease. Because of the heterogeneity of COPD, characteristics of the individual as well as between individuals must be identified in more detail. Mechanisms that enable this not only include physiological characterization by the current prescribed interventions but also imaging data which provides such ability to quantify airway wall thickness as well as via DNA that will be collected and save in order to gain a better understanding between the methodologies as they relate to the characterization of COPD. Currently, there may be a common understanding of how a particular drug affects a detailed molecular mechanism, however frequently it is not known why. The purpose of this study is to assist in discovery of the why.
|Study Type :||Observational|
|Estimated Enrollment :||30 participants|
|Official Title:||Evaluation of Airway Gene Expression in COPD and Controlled Populations|
|Study Start Date :||August 2006|
|Estimated Study Completion Date :||September 2008|
Individuals with normal lung function who do not smoke
Individuals who smoke but who do not demonstrate symptoms of chronic obstructive pulmonary disease
Individuals who smoke that demonstrate symptoms of COPD
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00571792
|United States, Nebraska|
|University of Nebraska Medical Center||Recruiting|
|Omaha, Nebraska, United States, 68198-2465|
|Contact: Kim Matthews, RN, APRN 402-559-8915 email@example.com|
|Contact: Stephen I Rennard, MD 402 559-7313 firstname.lastname@example.org|
|Principal Investigator: Stephen I Rennard, MD|
|Principal Investigator:||Stephen Rennard, MD||University of Nebraska|