阿司匹林诱发哮喘的中介分析。

A Szczeklik
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引用次数: 3

摘要

早期的研究推测阿司匹林敏感哮喘患者的血小板对阿司匹林和其他环加氧酶抑制剂有反应。同样,阿司匹林诱发哮喘患者血液白细胞中花生四烯酸氧化途径的调节也存在普遍异常。体外激活研究以及体内多形核白细胞的评估尚未确定代谢途径在阿司匹林敏感哮喘患者中诱导支气管痉挛。血清胰蛋白酶水平,肥大细胞活化的特异性标志物,似乎在支气管收缩期间增加服用口服阿司匹林。血清中嗜酸性阳离子蛋白(ECP)水平随之升高。白三烯拮抗剂可能部分保护个体与过敏原或阿司匹林引起的支气管收缩。
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Mediator assays in aspirin-induced asthma.

It had been postulated from earlier studies that platelets of aspirin-sensitive asthmatics reacted to aspirin and other cyclo-oxygenase inhibitors. Similarly, a generalized abnormality had been suggested in the regulation of arachidonic acid oxidative pathways in blood leukocytes of patients with aspirin-induced asthma. Studies of activation in vitro as well as in vivo assessment of polymorphonuclear leukocytes have not been conclusive of metabolic pathways inducing bronchospasm in aspirin-sensitive asthmatic patients. Serum levels of tryptase, a specific marker of mast cell activation, appear to increase during bronchoconstriction following ingestion of oral aspirin. Eosinophil cationic protein (ECP) levels in serum are concomitantly elevated. Leukotriene antagonists may partially protect individuals with allergen-provoked or aspirin-provoked bronchoconstriction.

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