Joseph M, Capron A, Ameisen J C, Martinot J B, Tonnel A B
Allerg Immunol (Paris). 1987 Oct;19(8 Suppl):7-10.
Platelets isolated from patients with aspirin-induced asthma (ASA patients) react abnormally in vitro to aspirin and to non-steroid anti-inflammatory drugs (NSAID), by generating cytocidal molecules, that can kill parasitic larvae and to oxygen-dependent free radicles, which may be detected by chemiluminescence, although these drugs do not have a similar effect on platelets from normal donors or allergic asthmatics. The abnormality appears to be associated with the inhibiting properties of NSAID and aspirin on the cyclo-oxygenase pathway, that leads to a defect of the binding of prostaglandin endoperoxide PGH2 to its receptors on the platelet membrane. In addition, another metabolite from the lipoxygenase pathway which is at present poorly defined seems to participate in the anomaly. Sodium salicylate, a naturally produced catabolite of aspirin, that is well-tolerated by ASA patients, inhibits the abnormal response of the platelets and this opens new perspectives in the management of aspirin-sensitive intolerance.
从阿司匹林诱发哮喘患者(ASA患者)体内分离出的血小板,在体外对阿司匹林和非甾体抗炎药(NSAID)会产生异常反应,即生成可杀死寄生虫幼虫的杀细胞分子以及可通过化学发光检测到的氧依赖性自由基,不过这些药物对正常供体或过敏性哮喘患者的血小板并无类似作用。这种异常似乎与NSAID和阿司匹林对环氧化酶途径的抑制特性有关,该途径会导致前列腺素内过氧化物PGH2与其在血小板膜上的受体结合出现缺陷。此外,目前定义尚不明确的脂氧合酶途径的另一种代谢产物似乎也参与了这一异常现象。水杨酸钠是阿司匹林天然产生的分解代谢产物,ASA患者对其耐受性良好,它可抑制血小板的异常反应,这为阿司匹林敏感不耐受的治疗开辟了新的前景。