Lainée R, Desaint M M, Godard S, Le Tessier G, Ertel M, Hooreman H, Sablon P, Bellorini M, Lévy M, Besse F
Arch Mal Coeur Vaiss. 1985 Jun;78(6):955-9.
The authors report the case of a 38 year old man who experienced at two month' interval, hypersensitivity reactions to the ingestion of 200 mg tablets of glafenine, complicated on the first occasion by a transmural anterior wall myocardial infarction as the first manifestation of coronary artery disease and on the second occasion by Prinzmetal angina due to posterior wall ischaemia. Coronary angiography was more or less normal. The timing of the symptoms in the context of an anaphylactic reaction and their repetition when the same molecule was reintroduced are strong arguments in favour of the pathogenic role of glafenine, even in the absence of biological criteria which are always variable. The mechanism of the coronary problems is discussed with reference to mediators released during the anaphylactic reaction: coronary vasoconstriction due to histamine and leukotriene release; inhibition of prostaglandin synthesis causing potentiation of the effects of histamine; lowering of the vasodilatory and antiaggregant prostacyclin enhancing the vasoconstrictor and platelet aggregant action of thromboxane A2. All the conditions favouring the initiation of coronary spasm with eventual coronary thrombosis, the one aggravating the other, are therefore present.
作者报告了一例38岁男性病例，该患者在两个月的间隔时间内，对服用200毫克格拉非宁片剂出现过敏反应，首次发作时并发透壁性前壁心肌梗死，这是冠状动脉疾病的首发表现，第二次发作时因后壁缺血导致变异型心绞痛。冠状动脉造影大致正常。过敏反应背景下症状出现的时间以及再次引入同一药物时症状的重复出现，有力地支持了格拉非宁的致病作用，即便缺乏始终多变的生物学标准。文中参照过敏反应期间释放的介质对冠状动脉问题的机制进行了讨论：组胺和白三烯释放导致冠状动脉血管收缩；前列腺素合成受抑制致使组胺作用增强；血管舒张和抗聚集的前列环素水平降低，增强了血栓素A2的血管收缩和血小板聚集作用。因此，所有有利于引发冠状动脉痉挛并最终导致冠状动脉血栓形成（二者相互加重）的条件均存在。
