Asthma, Rhinitis, Other Respiratory Diseases
Chronic sinusitis in severe asthma is related to sputum eosinophilia,☆☆

https://doi.org/10.1067/mai.2002.122458Get rights and content

Abstract

Background: Chronic rhinosinusitis and asthma are conditions that frequently coexist, particularly in severe asthma. The precise mechanism of the relationship between upper and lower airway inflammation is still a matter of debate. We hypothesized that the extent of inflammation in the nasal mucosa is related to lung function and inflammation in the bronchial mucosa in patients with severe asthma. Objective: We sought to investigate the relationship between sinonasal inflammation as assessed on computed tomography (CT) scanning, lung function, sputum eosinophilia, and nitric oxide (NO) in exhaled air in patients with severe asthma. Methods: Eighty-nine nonsmoking outpatients with severe asthma (29 men and 60 women; mean age 45 years; age range, 18-74 years) were included in this study. CT scans were scored (0-30) by a blinded investigator using a validated method. Lung function, NO in exhaled air, and sputum eosinophils were measured by using standard procedures. Results: CT scans showed abnormalities in 84% of patients. Extensive sinus disease (score 12-30) was found in 24% of patients. There was a significant positive correlation between CT scores and eosinophils in peripheral blood (Rs = 0.46) and induced sputum (Rs = 0.40) and level of exhaled NO (Rs = 0.45, P < .01). CT scores were also positively related to functional residual capacity and inversely related to diffusion capacity, particularly in patients with adult-onset asthma (Rs = 0.47 and Rs = −0.53, respectively). Conclusions: The results of this study show a direct relationship between sinonasal mucosa thickness and bronchial inflammation in severe asthma, particularly in patients with adult-onset disease. Whether sinus disease directly affects the intensity of bronchial inflammation is still an unanswered question. (J Allergy Clin Immunol 2002;109:621-6.)

Section snippets

Patients

Eighty-nine patients with severe bronchial asthma14 (age range, 18-74 years) were recruited from the outpatient pulmonary departments of 10 hospitals in the western part of The Netherlands. The patients had a history of episodic dyspnea and wheezing, a documented (recently or in the past) reversibility in FEV1 of greater than 12% of predicted value,15 or hyperresponsiveness to inhaled histamine (PC20 of <8 mg/mL).16

Design

This study was undertaken as part of a larger study on mechanisms of severe

Patient characteristics

In the whole group of 89 patients with severe asthma, the median CT-scan score was 5.0 (range, 0-29). According to the cut-off level, 21 (23.6%; 95% CI, 15%-33%) of the 89 patients had extensive paranasal sinus disease, with a median CT-scan score of 19.0 (range, 12-29), whereas 68 (76.4%) patients were classified as having limited sinus disease, with a median score of 3.0 (range, 0-11).

When comparing both groups, patients with extensive sinus disease were significantly older and had a shorter

Discussion

The present study shows that sinus CT-scan abnormalities are present in the vast majority of patients with severe asthma, even in the absence of nasal symptoms. The extent of sinus disease (as measured on CT scanning) is positively related to airway inflammation, as reflected by eosinophils in the lower airways and the systemic circulation, as well as the level of NO in exhaled air. Patients with extensive sinus disease more frequently have adult-onset asthma, and in these patients mucosa

Acknowledgements

We thank M. C. Timmers and H. van der Veen for technical assistance and the chest physicians of the participating hospitals for their cooperation (P. I. van Spiegel, G. Visschers, Slotervaart Hospital, Amsterdam; A. H. M. van der Heijden, Rode Kruis Hospital, Beverwijk; B. J. M. Pannekoek, Reinier de Graaf Gasthuis, Delft; H. H. Berendsen, K. W. van Kralingen, Bronovo Hospital, Den Haag; H. G. M. Heijerman, A. C. Roldaan, Leyenburg Hospital, Den Haag; A. H. M. van der Heijden, Spaarne Hospital,

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    Supported by the Netherlands Asthma Foundation (grant 97.24).

    ☆☆

    Reprint requests: Elisabeth H. Bel, MD, PhD, Department of Pulmonary Diseases, C3-P, Leiden University Medical Center, PO Box 9600, NL-2300 RC Leiden, The Netherlands.

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