Martelli N A, Usandivaras G
Thorax. 1977 Dec;32(6):684-90. doi: 10.1136/thx.32.6.684.
Five patients with asthma and severe aspirin hypersensitivity were challenged on separate days with increasing doses of aspirin given by mouth, starting with 5 mg, until a reduction in FEV1 greater than 15% was obtained. Sodium cromoglycate in doses of 20-40 mg inhibited the bronchoconstrictive reaction not only when inhaled before the challenge but also after it, at a time when progressive reduction in FEV1 values was taking place. According to these results, it seems reasonable to postulate sequential mast cell degranulation and liberation of mediators of anaphylaxis as the mechanism through which aspirin induces bronchoconstriction in aspirin-sensitive asthmatics. The differences between bronchial provocation tests and oral challenge with aspirin are stressed.
五名患有哮喘且对阿司匹林严重过敏的患者在不同日期接受口服阿司匹林剂量递增的激发试验，起始剂量为5毫克，直至第一秒用力呼气量（FEV1）下降超过15%。剂量为20 - 40毫克的色甘酸钠不仅在激发试验前吸入时，而且在激发试验后、FEV1值逐渐下降时，均能抑制支气管收缩反应。根据这些结果，推测阿司匹林诱导阿司匹林敏感型哮喘患者支气管收缩的机制是肥大细胞相继脱颗粒并释放过敏介质似乎是合理的。文中强调了支气管激发试验与口服阿司匹林激发试验之间的差异。
