Evaluating Genetic Factors That May Contribute to Elastin Function and the Development of Chronic Obstructive Pulmonary Disease

NCT00725309 | Completed DMC

• 1 other identifier: 576 -201108294
• Study Type: observational
• Target: 255
• Locations: 1 country
• Sites: 1

Brief Summary

Chronic obstructive pulmonary disease (COPD) is a lung disease that is primarily caused by cigarette smoking. The breakdown of elastin, a protein found in the lungs, can cause lung damage and may contribute to the development of COPD. Some people may be more prone to elastin damage and in turn to developing COPD than others. This study will examine whether genetic factors are responsible for altering elastin function and increasing the risk of developing COPD.

Conditions

Emphysema; Pulmonary Disease, Chronic Obstructive

Keywords

Chronic Obstructive Pulmonary Disease; COPD; Elastin; ELN

Eligibility Criteria

• Age: 18 Years+
• Sex: all
• Healthy Volunteers: No
• Age Groups: Adult (18-64), Older Adult (65+)
• Sampling Method: Non-Probability Sample

Study Population

This study will enroll people who undergo evaluation or follow-up at Barnes-Jewish Hospital for lung volume reduction surgery (LVRS). Researchers will also enroll eligible COPD patients from other Washington University Medical Center pulmonary clinics.

You may qualify if:

• Age equal to or greater than 18 years
• Ability to read and write in English
• Able to participate in the informed consent process
• Acceptable pulmonary function tests (PFTs) done at Barnes-Jewish Hospital within 1 month of study enrollment
• Relatively stable clinical status (not experiencing COPD exacerbation in the previous 6 weeks)
• Global Initiative for Chronic Obstructive Lung Disease (GOLD) class III or IV COPD (FEV1/FVC less than 70% and FEV1 less than 50% of predicted value)

You may not qualify if:

• Pregnant
• Prisoner
• Vulnerable populations
• Pi Z phenotype (i.e., alpha-1 antitrypsin deficiency)
• Significant lung disease, other than COPD / emphysema / chronic bronchitis (e.g., interstitial lung disease, asthma or other predominant airway disease, cystic fibrosis, active tuberculosis)
• Known active hepatitis B, hepatitis C, or HIV/AIDS (found in medical record review; not prospectively evaluated)

Sponsors & Collaborators

• Washington University School of Medicine: lead

Study Sites (1)

Washington University School of Medicine

St Louis, Missouri, 63110, United States

Location

Biospecimen

Retention: SAMPLES WITH DNA

Plasma, serum, isolated RNA and DNA, lung tissue (obtained from other substudies)

MeSH Terms

Conditions

Emphysema; Pulmonary Disease, Chronic Obstructive; Aortic Stenosis, Supravalvular

Condition Hierarchy (Ancestors)

Pathologic Processes; Pathological Conditions, Signs and Symptoms; Lung Diseases, Obstructive; Lung Diseases; Respiratory Tract Diseases; Chronic Disease; Disease Attributes; Aortic Valve Stenosis; Aortic Valve Disease; Heart Valve Diseases; Heart Diseases; Cardiovascular Diseases; Ventricular Outflow Obstruction

Study Officials

• Robert P. Mecham, PhD

  Washington University School of Medicine

  PRINCIPAL INVESTIGATOR

Study Design

• Study Type: observational
• Observational Model: CASE ONLY
• Time Perspective: CROSS SECTIONAL
• Sponsor Type: OTHER
• Responsible Party: SPONSOR

Study Record Dates

• First Submitted: July 29, 2008
• First Posted: July 30, 2008
• Study Start: November 1, 2007
• Primary Completion: December 1, 2017
• Study Completion: December 1, 2017
• Last Updated: June 18, 2018

Record last verified: 2018-06

Locations

US (1)