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Both allergic and nonallergic asthma are associated with increased FENO levels, but only in never-smokers
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
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2009 (English)In: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 64, no 1, 55-61 p.Article in journal (Refereed) Published
Abstract [en]

Allergic asthma is consistently associated with increased FENO levels whereas divergence exists regarding the use of exhaled nitric oxide (NO) as marker of inflammation in nonallergic asthma and in asthmatic smokers. The aim of this study is to analyze the effect of having   allergic or nonallergic asthma on exhaled nitric oxide levels, with special regard to smoking history. Exhaled NO measurements were performed in 695 subjects from Turin (Italy), Gothenburg and Uppsala (both Sweden). Current asthma was defined as self-reported physician-diagnosed asthma with at least one asthma symptom or attack recorded during the last year. Allergic status was defined by using measurements of specific immunoglobulin E (IgE).   Smoking history was questionnaire-assessed. Allergic asthma was associated with 91 (60, 128) % [mean (95% CI)] increase of FENO while no significant association was found for nonallergic asthma [6 (-17, 35) %] in univariate analysis, when compared to nonatopic healthy subjects. In a multivariate analysis for never-smokers, subjects with allergic asthma had 77 (27, 145) % higher FENO levels than atopic healthy subjects while subjects with   nonallergic asthma had 97 (46, 166) % higher FENO levels than nonatopic healthy subjects. No significant asthma-related FENO increases were noted for ex- and current smokers in multivariate analysis. Both allergic and nonallergic asthma are related to increased FENO   levels, but only in never-smoking subjects. The limited value of FENO to detect subjects with asthma among ex- and current smokers suggests the predominance of a noneosinophilic inflammatory phenotype of asthma among ever-smokers.

Place, publisher, year, edition, pages
2009. Vol. 64, no 1, 55-61 p.
Keyword [en]
asthma, atopy, European Community Respiratory Health Survey, exhaled nitric oxide, smoking history
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-97885DOI: 10.1111/j.1398-9995.2008.01835.xISI: 000261974400007PubMedID: 19076545OAI: oai:DiVA.org:uu-97885DiVA: diva2:172984
Available from: 2008-11-27 Created: 2008-11-27 Last updated: 2017-12-14Bibliographically approved
In thesis
1. Nitric Oxide Exchange in Central and Peripheral Airways: Determinants in Health and Respiratory Disease
Open this publication in new window or tab >>Nitric Oxide Exchange in Central and Peripheral Airways: Determinants in Health and Respiratory Disease
2008 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Background: Exhaled nitric oxide (NO) is a marker of eosinophilic steroid-sensitive inflammation in the airways of patients with respiratory disease. Moreover, information about the localization of inflammation in the respiratory tree is obtained by estimates of bronchial and alveolar contributions to exhaled NO.

Aims: The main aim of this thesis was to identify the determinants of exhaled NO, as well as determinants of bronchial and alveolar contributions to exhaled NO in health and disease. Smoking history, degree of IgE sensitization and effects of modulating the pharyngo-oral tract production of NO were specifically studied in this context. Other specific aims were to determine the association of exhaled NO with the presence of asthma and pulmonary hypertension (PH).

Methods: Both population-based studies and experimental studies have been performed within the frame of the thesis. The population-based studies are based on data from the European Community Respiratory Health Survey II. NO measurements at several exhalation flow rates were performed in order to estimate alveolar and bronchial contributions to exhaled NO.

Results: Both current and previous smoking were associated with decreased exhaled NO and bronchial NO flux levels. Alveolar NO concentrations were decreased in current smokers. The degree of IgE sensitization was positively related to the levels of exhaled NO and its bronchial contribution. Exhaled NO appeared to be a more specific marker of allergic inflammation than of rhinitis or asthma. Both allergic and non-allergic asthma were associated with increased exhaled NO levels, but only in never-smoking persons. The estimated alveolar NO increased after ingestion of nitrate in individuals with high nitrate turnover in the pharyngo-oral tract. Pulmonary arterial hypertension, but not other forms of PH, was associated with decreased bronchial NO flux, whereas PH of all etiologies was related to increased alveolar NO concentrations.

Conclusion: Smoking history and IgE sensitization, that are known determinants of exhaled NO, affected the bronchial and alveolar contributions to exhaled NO differently. The limitations of the simple NO pulmonary exchange models were highlighted by the paradoxical effects on estimated alveolar NO when modulating the NO production proximally, in the pharyngo-oral tract. Predominance of non-eosinophilic inflammation in ever-smoking patients with asthma could explain the poor association between the presence of asthma and exhaled NO in these patients. Different pathophysiological changes in terms of bronchial NO production and exchange were related to the etiology of pulmonary hypertension.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2008. 64 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 403
Keyword
exhaled nitric oxide, alveolar NO, bronchial NO flux, extended NO analysis, asthma, smoking, snus, IgE-sensitization, pharyngo-oral tract, nitrate, nitrite, pulmonary hypertension
Identifiers
urn:nbn:se:uu:diva-9416 (URN)978-91-554-7363-1 (ISBN)
Public defence
2008-12-19, Robergsalen, Akademiska Sjukhuset, Ingång 40, 4 tr., Uppsala, 09:15
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Available from: 2008-11-27 Created: 2008-11-27Bibliographically approved

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