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Protection of leukotriene receptor antagonist against aspirin-induced bronchospasm in asthmatics

Authors
Park, Jong SookJang, An SooPark, Sung WooLee, Young MokUh, Soo TaekKim, Yong HoonCha, Ji YeanPark, Se MinPark, Choon-Sik
Issue Date
Jan-2010
Publisher
대한천식알레르기학회
Keywords
Asthma; leukotriene antagonists; aspirin; eosinophils
Citation
Allergy, Asthma & Immunology Research, v.2, no.1, pp 48 - 54
Pages
7
Journal Title
Allergy, Asthma & Immunology Research
Volume
2
Number
1
Start Page
48
End Page
54
URI
https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/18111
DOI
10.4168/aair.2010.2.1.48
ISSN
2092-7355
2092-7363
Abstract
Purpose: Leukotriene receptor antagonists (LTRAs) are used to treat aspirin-intolerant asthma (AIA); however, the protective effects of long-term LTRA administration against aspirin-induced bronchospasm have not been evaluated. Objectives: We investigated the efficacy of a 12-week treatment with a LIRA in protecting against aspirin-induced asthma in AIA patients. Methods: Fifty-two adult patients with AIA underwent an aspirin challenge test just before administration of montelukast (10 mg/day) and just after 12 weeks of treatment. The protective effect was assessed as the disappearance of aspirin-induced bronchospasm after 12 weeks of treatment. The results were compared according to the patients' clinical and physiological parameters. Results: The decline in FEV1 following aspirin challenge was significantly reduced from 28.6 +/- 1.9% to 10.2 +/- 1.7% (P=0.0001) after 12 weeks of montelukast treatment. However, 14 subjects (30%) still showed a positive response (>15% decline in FEV1) to aspirin challenge. Grouping the subjects into good and poor responders according to post-treatment responses revealed that the pretreatment aspirin-induced FEV1 decline was significantly greater in the poor responders and that the triggering dose of aspirin and the induction time for a positive response were lower and shorter, respectively, in the poor responders. Histories of aspirin hypersensitivity and sinusitis were more prevalent among the poor responders than among the good responders. Conclusions: Twelve weeks of treatment with montelukast protected against aspirin-induced bronchospasm in 70% of the AIA cases. A poor response was associated with more severe aspirin-induced bronchospasms before treatment and a history of aspirin hypersensitivity or sinusitis. Clinical implications: A severe response to aspirin challenge may be a predictor of poor responsiveness to leukotriene antagonist treatment.
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