Christie P E, Tagari P, Ford-Hutchinson A W, Charlesson S, Chee P, Arm J P, Lee T H
Department of Allergy and Allied Respiratory Disorders, UMDS, Guy's Hospital, London, UK.
Am Rev Respir Dis. 1991 May;143(5 Pt 1):1025-9. doi: 10.1164/ajrccm/143.5_Pt_1.1025.
Urinary leukotriene E4 (LTE4) concentrations have been measured in six asthmatic patients with aspirin sensitivity and in five asthmatic subjects tolerant of aspirin, before and after provocation with aspirin or placebo. Aspirin-sensitive subjects showed an average 21% fall in FEV1 after aspirin challenge whereas control individuals had a 2% fall in FEV1 after ingestion of 100 mg aspirin. The resting urinary LTE4 concentrations in asthmatic subjects sensitive to aspirin were 243 pg/mg creatinine (range 50 to 1,041), and these were on average sixfold greater than those in control asthmatic subjects. Further, there was a mean fourfold increase in urinary LTE4 levels at 3 to 6 h after aspirin, but not placebo, challenge in aspirin-sensitive asthmatic subjects that was not seen in the control asthmatic individuals. Leukotriene release may play a central role in the mechanisms of asthmatic attacks produced by aspirin ingestion.
在六名对阿司匹林敏感的哮喘患者和五名对阿司匹林耐受的哮喘受试者中，分别在给予阿司匹林或安慰剂激发前后测量了尿白三烯E4（LTE4）浓度。对阿司匹林敏感的受试者在接受阿司匹林激发后FEV1平均下降21%，而对照组个体在摄入100mg阿司匹林后FEV1下降2%。对阿司匹林敏感的哮喘受试者静息尿LTE4浓度为243pg/mg肌酐（范围为50至1041），平均比对照哮喘受试者高六倍。此外，对阿司匹林敏感的哮喘受试者在接受阿司匹林而非安慰剂激发后3至6小时，尿LTE4水平平均增加四倍，而对照哮喘个体未出现这种情况。白三烯释放可能在阿司匹林摄入引发的哮喘发作机制中起核心作用。
