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首页> 外文期刊>Allergy >Angioedema induced by cardiovascular drugs: new players join old friends
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Angioedema induced by cardiovascular drugs: new players join old friends

机译：心血管药物引起的血管性水肿：新玩家加入老朋友

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摘要

During the last years, two new cardiovascular drug classes, namely inhibitors of DPP IV or neprilysin, have been developed. In both cases, there is clinical evidence for their potential to induce angioedema as known already from blockers of the renin-angiotensin-aldosterone system (RAAS). The majority of angioedema induced by DPP IV inhibitors occurs during concomitant treatment with ACEi and is therefore likely mediated by overactivation of bradykinin type 2 receptors (B2). In striking contrast, the molecular pathways causing angioedema induced by neprilysin inhibitors, that is, sacubitril, are unclear, although a contribution of bradykinin appears likely. Nevertheless, there is no clinical evidence suggesting that inhibition of B2 might relieve the symptoms and/or prevent invasive treatment including coniotomy or tracheotomy in angioedema caused by these drugs. Therefore, the risk of angioedema should always be considered, especially in ambulatory care situations where patients have no rapid access to intensive care.
机译：在过去的几年中，已经开发出两种新的心血管药物类别，即DPP IV或脑啡肽酶抑制剂。在这两种情况下，都有临床证据表明它们具有诱发血管性水肿的潜力，这已经从肾素-血管紧张素-醛固酮系统（RAAS）的阻滞剂中得知。 DPP IV抑制剂诱导的大多数血管性水肿发生在ACEi伴随治疗期间，因此可能由2型缓激肽受体（B2）的过度激活介导。与之形成鲜明对比的是，尽管可能存在缓激肽的作用，但尚不清楚由中性溶酶抑制剂（即沙必比尔）引起的引起血管性水肿的分子途径。然而，没有临床证据表明抑制B2可能减轻症状和/或阻止由这些药物引起的血管性水肿的侵入性治疗，包括锥切或气管切开术。因此，应始终考虑血管性水肿的风险，尤其是在患者无法快速获得重症监护的非卧床护理情况下。

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