Cargando…

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

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 L...

Descripción completa

Detalles Bibliográficos
Autores principales: Park, Jong Sook, Jang, An Soo, Park, Sung Woo, Lee, Young Mok, Uh, Soo Taek, Kim, Yong Hoon, Cha, Ji Yean, Park, Se Min, Park, Choon-Sik
Formato: Texto
Lenguaje:English
Publicado: The Korean Academy of Asthma, Allergy and Clinical Immunology; The Korean Academy of Pediatric Allergy and Respiratory Disease 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831603/
https://www.ncbi.nlm.nih.gov/pubmed/20224678
http://dx.doi.org/10.4168/aair.2010.2.1.48
Descripción
Sumario: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 LTRA 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.