Szczeklik A, Gryglewski R J, Czerniawska-Mysik G
Br Med J. 1975 Jan 11;1(5949):67-9. doi: 10.1136/bmj.1.5949.67.
Eleven patients with asthma and aspirin hypersensitivity have been challenged with eight non-steroidal anti-inflammatory drugs. Each drug was given by mouth in at least three different doses and the patients' symptoms and peak expiratory flow (PEF) rates were observed over a three-hour period. Indomethacin 5 mg caused bronchoconstriction in all patients. Therapeutic doses of mefenamic or flufenamic acid caused bronchoconstriction in most patients. Phenylbutazone 200-400 mg induced a moderate fall in PEF. There were no reactions to therapeutic doses of salicylamide, paracetamol, benzydamine, and chloroquine. Microsomal prostaglandin synthetase, activity was inhibited by aspirin, indomethacin, mefenamic acid, flufenamic acid, and phenylbutazone. The other four drugs had no inhibitory effect. We suggest that precipitation of attacks in asthmatic patients hypersensitive to certain anti-inflammatory drugs is related to drug's ability to inhibit prostaglandin biosynthesis.
11名患有哮喘和阿司匹林过敏的患者接受了8种非甾体抗炎药的激发试验。每种药物均经口服给予至少3种不同剂量，并在3小时内观察患者的症状和呼气峰值流速（PEF）。5毫克吲哚美辛可使所有患者出现支气管收缩。治疗剂量的甲芬那酸或氟芬那酸可使大多数患者出现支气管收缩。200 - 400毫克保泰松导致PEF中度下降。治疗剂量的水杨酰胺、对乙酰氨基酚、苄达明和氯喹未引起反应。微粒体前列腺素合成酶活性受到阿司匹林、吲哚美辛、甲芬那酸、氟芬那酸和保泰松的抑制。其他4种药物无抑制作用。我们认为，对某些抗炎药过敏的哮喘患者发作的诱发与药物抑制前列腺素生物合成的能力有关。
