Slapke J, Hummel S
Wien Med Wochenschr. 1985 Apr 30;135(8):201-4.
Analgesics-induced asthma (AIA) is quite often unidentified and then is a severe danger to the patients affliced. In a case-control-study 1042 asthmatic patients selected by random were investigated. In 18.9% of patients the presence of AIA was recorded. Woman accounted for 71% of the AIA patients. Coincidence of AIA with nasal polyposis, paranasal sinus diseases, chronic rhinitis, alcohol intolerance and severe bronchial asthma was recorded with high significance. Chronic hyperplastic changes in the upper airways were exhibited by about 64% of the AIA patients. AIA is a non-allergic form of asthma, resembling immediate allergic type I reaction. Analgesics-based acute bronchoconstriction will typically develop within 45 min. following intake of the analgesic. Triggering threshold doses may differ strongly by individuals. Oral exposure test is connected with a high risk of complications. A case history usually is sufficient for save diagnosis. Analgesics without inhibiting action on cyclooxygenase usually are tolerated. The causes of AIA should be ascribed to changes in the release and conversion of arachidonic acid (Aa) from membrane phospholipids. The inhibition of Aa release (phospholipase-A2-reaction) by protease inhibitors or the inhibition of Aa transformation to bronchoconstrictive lipoxygenase products by lipoxygenase inhibitors were shown in vitro (isolated guinea pig lung strips and human bronchi). Paraaminomethylbenzoic acid also was found to be effective in clinical experiments preventing analgesics-induced bronchoconstriction. Both seem to be principal ways for modulation of bronchoconstriction.
镇痛药诱发的哮喘(AIA)常常未被识别,对患病患者构成严重威胁。在一项病例对照研究中,随机选取了1042名哮喘患者进行调查。在18.9%的患者中记录到了AIA的存在。女性占AIA患者的71%。AIA与鼻息肉、鼻窦疾病、慢性鼻炎、酒精不耐受和重度支气管哮喘的并发具有高度显著性。约64%的AIA患者出现上呼吸道慢性增生性改变。AIA是一种非过敏性哮喘形式,类似于即刻过敏I型反应。基于镇痛药的急性支气管收缩通常在摄入镇痛药后45分钟内发生。触发阈值剂量个体差异很大。口服激发试验伴有高并发症风险。通常详细询问病史就足以做出可靠诊断。对环氧化酶无抑制作用的镇痛药通常可耐受。AIA的病因应归因于膜磷脂中花生四烯酸(Aa)释放和转化的改变。蛋白酶抑制剂对Aa释放的抑制(磷脂酶A2反应)或脂氧合酶抑制剂对Aa转化为支气管收缩性脂氧合酶产物的抑制在体外(豚鼠离体肺条和人支气管)得到证实。对氨基甲基苯甲酸在预防镇痛药诱发的支气管收缩的临床试验中也被发现有效。两者似乎都是调节支气管收缩的主要方式。