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血管紧张素转换酶抑制剂引发血管性水肿病史患者体内的氨肽酶P

Aminopeptidase P in individuals with a history of angio-oedema on ACE inhibitors.

作者信息

Adam Albert, Cugno Massimo, Molinaro Giuseppe, Perez Melissa, Lepage Yves, Agostoni Angelo

机构信息

Faculté de Pharmacie, Université de Montréal, Montréal, Canada.

出版信息

Lancet. 2002 Jun 15;359(9323):2088-9. doi: 10.1016/S0140-6736(02)08914-6.

Abstract

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.

摘要

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。

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