Seale J P
Med J Aust. 1983 Jun 11;1(12):585-7. doi: 10.5694/j.1326-5377.1983.tb136230.x.
The reported incidence of acute bronchospasm in patients with asthma who take aspirin varies from 2% to 28%, depending on the methods used to obtain data. Earlier surveys were conducted among adults, and recent studies have shown a similar incidence in children. Immunological mechanisms are unlikely to be responsible. A current hypothesis for the development of analgesic-induced asthma is based upon the inhibitory effect of aspirin on the cyclo-oxygenase pathway for the metabolism of arachidonic acid. This theory is supported by the observation that any non-steroidal anti-inflammatory drug which inhibits cyclo-oxygenase activity may precipitate attacks in subjects with asthma who are sensitive to aspirin. Since most of these drugs are structurally dissimilar to aspirin, any immunological crossreactivity is unlikely. It is possible that the bronchospasm which follows inhibition of cyclo-oxygenase activity is due either to decreased formation of cyclo-oxygenase products with bronchodilator properties and inhibitory effects on mediator release, or to increased formation of lipoxygenase products with bronchoconstrictor properties.
据报道，服用阿司匹林的哮喘患者中急性支气管痉挛的发生率在2%至28%之间，具体取决于获取数据的方法。早期的调查是在成年人中进行的，最近的研究表明儿童中的发生率相似。免疫机制不太可能是原因。目前关于镇痛剂诱发哮喘的假说基于阿司匹林对花生四烯酸代谢的环氧化酶途径的抑制作用。这一理论得到了以下观察结果的支持：任何抑制环氧化酶活性的非甾体抗炎药都可能在对阿司匹林敏感的哮喘患者中引发发作。由于这些药物中的大多数在结构上与阿司匹林不同，因此不太可能存在免疫交叉反应。环氧化酶活性受到抑制后出现的支气管痉挛，可能是由于具有支气管扩张特性并对介质释放有抑制作用的环氧化酶产物形成减少，或者是由于具有支气管收缩特性的脂氧合酶产物形成增加。
