Format

Send to:

Choose Destination
See comment in PubMed Commons below
Clin Transl Sci. 2009 Apr;2(2):112-7. doi: 10.1111/j.1752-8062.2009.00095.x.

Noninvasive markers of airway inflammation in asthma.

Author information

  • 1Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, Ohio, USA.

Abstract

BACKGROUND:

Although airway inflammation plays a major role in the pathophysiology of asthma, quantitative markers of airway inflammation are limited in clinical practice.

OBJECTIVE:

To determine if levels of noninvasive markers of eosinophil-catalyzed oxidation, lipid peroxidation, and nitric oxide production are associated with asthma.

METHODS:

Participants were enrolled from academic medical centers participating in the Severe Asthma Research Program. Clinical characteristics, laboratory data, pulmonary function tests, and levels of the following noninvasive markers were obtained: urinary bromotyrosine, a marker of eosinophil-catalyzed oxidation; urinary F(2)-isoprostanes, markers of lipid peroxidation; and exhaled nitric oxide, a marker of airway inflammation

RESULTS:

Fifty-seven asthmatic participants and thirty-eight healthy participants were enrolled. Bromotyrosine, F(2)-isoprostanes, and exhaled nitric oxide were each significantly increased in asthmatic participants versus controls (p<0.01). An elevated level (greater than median) of any marker was associated with a significant 3- to 6-fold greater odds of having asthma. Participants with two or more elevated marker levels showed an 18-fold greater odds of having asthma. Relationships were also noted with airflow obstruction and bronchodilator response.

CONCLUSION:

Findings from this pilot study indicate that urinary levels of bromotyrosine and F(2)-isoprostanes, in addition to exhaled nitric oxide levels, are associated with asthma.

KEYWORDS:

Asthma; Biomarkers; Inflammation

PMID:
20234847
[PubMed - indexed for MEDLINE]
PMCID:
PMC2838203
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wiley Icon for PubMed Central
    Loading ...
    Write to the Help Desk