Division of Respiratory and Allergy Medicine, Soonchunhyang University Hospital, College of Medicine, Bucheon, Korea.
Allergy Asthma Immunol Res. 2010 Jan;2(1):48-54. doi: 10.4168/aair.2010.2.1.48. Epub 2009 Dec 30.
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.
We investigated the efficacy of a 12-week treatment with a LTRA in protecting against aspirin-induced asthma in AIA patients.
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.
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.
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.
A severe response to aspirin challenge may be a predictor of poor responsiveness to leukotriene antagonist treatment.
白三烯受体拮抗剂（LTRAs）用于治疗阿司匹林不耐受性哮喘（AIA）；然而，长期 LTRA 给药对阿司匹林诱导的支气管痉挛的保护作用尚未得到评估。
我们研究了 LTRA 治疗 12 周对 AIA 患者阿司匹林诱导性哮喘的保护作用。
52 例 AIA 成年患者在给予孟鲁司特（10mg/天）前和治疗 12 周后进行阿司匹林挑战试验。保护作用评估为治疗 12 周后阿司匹林诱导的支气管痉挛消失。结果根据患者的临床和生理参数进行比较。
孟鲁司特治疗 12 周后，FEV1 下降率从阿司匹林激发前的 28.6±1.9%显著降低至 10.2±1.7%（P=0.0001）。然而，仍有 14 名患者（30%）对阿司匹林激发呈阳性反应（FEV1 下降>15%）。根据治疗后反应将患者分为良好和不良反应者，发现治疗后不良反应者的阿司匹林激发前 FEV1 下降率显著更大，且阿司匹林的触发剂量和阳性反应的诱导时间分别更短。不良反应者的阿司匹林过敏史和鼻窦炎史更常见。
孟鲁司特治疗 12 周可预防 70%的 AIA 患者的阿司匹林诱导性支气管痉挛。不良反应与治疗前更严重的阿司匹林诱导性支气管痉挛和阿司匹林过敏史或鼻窦炎史相关。
阿司匹林激发试验的严重反应可能是对白三烯拮抗剂治疗反应不良的预测因素。
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