Szczeklik Andrzej
Department of Medicine, Jagiellonian University Medical College, Cracow, Poland.
Chem Immunol Allergy. 2010;95:170-179. doi: 10.1159/000315950. Epub 2010 Jun 1.
Aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) are often incriminated in hypersensitivity reactions leading to anaphylaxis. Two populations are at the high risk of developing such reactions: patients with asthma and those with urticaria. In a subset of asthmatics, NSAIDs that inhibit cyclooxygenase-1 (COX-1) precipitate non-allergic, hypersensitivity reactions, characterized by violent attacks of dyspnea. These patients suffer from a distinct clinical syndrome, called aspirin induced asthma (AIA), which includes chronic eosinophilic rhinusinusitis and persistent asthma. Inpatients with chronic idiopathic urticaria, and less commonly in patients without chronic urticaria, NSAIDs usually acting through inhibition of COX-1 can induce or exacerbate skin eruptions. While alterations in eicosanoid biosynthesis characterized both AIA and aspirin-triggered urticaria, other patients may rarely manifest IgE-mediated reactions.
阿司匹林和其他非甾体抗炎药(NSAIDs)常被认为是导致过敏反应进而引发过敏症的原因。有两类人群发生此类反应的风险较高:哮喘患者和荨麻疹患者。在一部分哮喘患者中,抑制环氧化酶-1(COX-1)的非甾体抗炎药会引发非过敏性的过敏反应,其特征为剧烈的呼吸困难发作。这些患者患有一种独特的临床综合征,称为阿司匹林诱发哮喘(AIA),其中包括慢性嗜酸性粒细胞性鼻鼻窦炎和持续性哮喘。在慢性特发性荨麻疹患者中,以及较少见地在无慢性荨麻疹的患者中,通常通过抑制COX-1起作用的非甾体抗炎药可诱发或加重皮疹。虽然类花生酸生物合成的改变是AIA和阿司匹林诱发荨麻疹的共同特征,但其他患者可能很少表现出IgE介导的反应。