Abstract
We investigated whether the combination of increased exhaled nitric oxide fraction (FeNO) level and blood eosinophil count had an additive value in chronic airway disease in the general population.
We included 4677 individuals aged 20–100 years from the Copenhagen General Population Study. Based on pre- and post-bronchodilator spirometry, self-reported asthma and smoking history, participants were subdivided into healthy never-smokers (n=1649), healthy ever-smokers (n=1581), asthma (n=449), chronic obstructive pulmonary disease (COPD) (n=404), asthma–COPD overlap (ACO) (n=138) and nonspecific airflow limitation (n=456).
Compared to individuals with FeNO <25 ppb and blood eosinophils <0.3×109 cells·L−1, age- and sex-adjusted odds ratios (95% CI) for wheezing were 1.54 (1.29–1.84) for individuals with FeNO ≥25 ppb or blood eosinophils ≥0.3×109 cells·L−1 and 2.14 (1.47–3.10) for individuals with FeNO ≥25 ppb and blood eosinophils ≥0.3×109 cells·L−1. Corresponding odds ratios were 1.13 (0.91–1.41) and 1.83 (1.20–2.79) for sputum production, 1.54 (1.22–1.94) and 3.26 (2.16–4.94) for asthma, 1.03 (0.80–1.32) and 0.67 (0.36–1.27) for COPD and 1.32 (0.88–1.96) and 2.14 (1.05–4.36) for ACO. Among individuals reporting respiratory symptoms, predicting the type of chronic airway disease did not differ between the two biomarkers and did not improve by combining them.
Combination of FeNO and blood eosinophils may have an additive value in characterising chronic airway disease in the general population but still needs to be investigated further with regard to clinical application.
Abstract
Combination of exhaled nitric oxide and blood eosinophils may have an additive value in chronic airway disease http://ow.ly/jUmj30kod8B
Footnotes
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Author contributions: Y. Çolak and S. Afzal had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analyses. Study concept and design: Y. Çolak, S. Afzal, B.G. Nordestgaard, J.L. Marott and P. Lange. Acquisition, analyses, or interpretation of data: Y. Çolak, S. Afzal, B.G. Nordestgaard, J.L. Marott and P. Lange. Drafting of the manuscript: Y. Çolak. Critical revision of the manuscript for important intellectual content: Y. Çolak, S. Afzal, B.G. Nordestgaard, J.L. Marott and P. Lange. Statistical analyses: Y. Çolak and S. Afzal. Obtained funding: B.G. Nordestgaard and P. Lange. Administrative, technical, or material support: B.G. Nordestgaard. Study supervision: P. Lange.
Conflict of interest: Y. Çolak reports personal fees from Boehringer Ingelheim and AstraZeneca outside the submitted work.
Conflict of interest: P. Lange reports grants from AstraZeneca and GlaxoSmithKline, and personal fees from Boehringer Ingelheim, AstraZeneca, Novartis and GlaxoSmithKline, outside the submitted work.
Support statement: The Lundbeck Foundation, the Dept of Internal Medicine and Dept of Clinical Biochemistry at Herlev and Gentofte Hospital, and the Danish Lung Association. The funders had no role in the design and conduct of the study; collection, management, analysis or interpretation of the data; preparation, review or approval of the manuscript; or decision to submit the manuscript for publication. Funding information for this article has been deposited with the Crossref Funder Registry.
- Received June 20, 2017.
- Accepted June 4, 2018.
- Copyright ©ERS 2018
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