Adam Albert, Cugno Massimo, Molinaro Giuseppe, Perez Melissa, Lepage Yves, Agostoni Angelo
Faculté de Pharmacie, Université de Montréal, Montréal, Canada.
Lancet. 2002 Jun 15;359(9323):2088-9. doi: 10.1016/S0140-6736(02)08914-6.
Angio-oedema is a rare but potentially life threatening side-effect of angiotensin-converting-enzyme (ACE) inhibitor treatment. Identification of individuals at risk of this adverse effect is not possible. Angio-oedema is associated with raised concentrations of bradykinin, which is mainly inactivated by ACE. We assessed the plasma activity of two other enzymes that catabolise bradykinin (aminopeptidase P and carboxypeptidase N) in 39 hypertensive patients with a history of angio-oedema during ACE inhibitor treatment and in 39 hypertensive patients who had never had ACE inhibitor associated side-effects. Patients with previous angio-oedema had a lower plasma activity of aminopeptidase P than did those who never presented with angio-oedema (p=0 003). Our data suggest that low plasma concentrations of aminopeptidase P could be a predisposing factor for development of angio-oedema in patients treated with ACE inhibitors.
血管性水肿是血管紧张素转换酶(ACE)抑制剂治疗罕见但可能危及生命的副作用。无法识别有这种不良反应风险的个体。血管性水肿与缓激肽浓度升高有关,缓激肽主要由ACE灭活。我们评估了39例有血管性水肿病史的高血压患者在接受ACE抑制剂治疗期间以及39例从未有过ACE抑制剂相关副作用的高血压患者中另外两种分解缓激肽的酶(氨肽酶P和羧肽酶N)的血浆活性。既往有血管性水肿的患者氨肽酶P的血浆活性低于从未出现过血管性水肿的患者(p = 0.003)。我们的数据表明,血浆氨肽酶P浓度低可能是接受ACE抑制剂治疗的患者发生血管性水肿的一个易感因素。