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首页> 外文期刊>Polish Archives of Internal Medicine >Bradykinin-mediated angioedema
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Bradykinin-mediated angioedema

机译：缓激肽介导的血管性水肿

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Angioedema and urticaria often constitute a challenge in daily clinical practice. They may either co- -occur or present as independent conditions. They are characterized by a complex pathomechanism, and their symptoms may be triggered by diverse factors. These differences are crucial for developing a successful treatment regimen. Both conditions may have an allergic origin (immunoglobulin [Ig] E and non-IgE-related), usually induced by histamine, or a nonallergic one, such as bradykinin-mediated angioedema in patients with C1 inhibitor (C1-INH) deficiency or angioedema induced by certain drugs (eg, angiotensin-converting enzyme inhibitors). Currently, we distinguish 5 types of nonallergic angioedema: hereditary angioedema (HAE) due to C1-INH deficiency, acquired angioedema (AAE), and angioedema induced by the renin–angiotensin–aldosterone system, all of which are mediated by bradykinin, as well as pseudoallergic angioedema and idiopathic angioedema. Bradykinin-mediated angioedema (eg, laryngeal angioedema) may be life-threatening because of resistance to corticosteroids and antihistamine drugs. C1-INH concentrates are the drugs of choice in the treatment of HAE and AAE. In recent years, some new drugs have been introduced in the treatment of bradykinin-mediated angioedema, such as bradykinin B2-receptor antagonist, icatibant, and kallikrein inhibitor, ecallantide, which allow to improve treatment outcomes.
机译：在日常临床实践中，血管性水肿和荨麻疹经常构成挑战。它们可以同时出现，也可以作为独立条件出现。它们的特征是复杂的发病机制，其症状可能由多种因素触发。这些差异对于制定成功的治疗方案至关重要。两种情况都可能具有过敏源（免疫球蛋白[Ig] E和与非IgE相关），通常是由组胺引起的，或者是非过敏性源，例如缓激肽介导的C1抑制剂（C1-INH）缺乏或血管性水肿的患者由某些药物（例如，血管紧张素转换酶抑制剂）诱导。目前，我们区分出5种类型的非过敏性血管性水肿：由于C1-INH缺乏引起的遗传性血管性水肿（HAE），获得性血管性水肿（AAE）和由肾素-血管紧张素-醛固酮系统引起的血管性水肿，所有这些都由缓激肽介导如假性过敏性血管性水肿和特发性血管性水肿。缓激肽介导的血管性水肿（例如喉头血管性水肿）可能由于对皮质类固醇和抗组胺药的耐药性而危及生命。 C1-INH浓缩物是治疗HAE和AAE的首选药物。近年来，已经引入了一些新的药物来治疗缓激肽介导的血管性水肿，例如缓激肽B2受体拮抗剂，依卡替班和激肽释放酶抑制剂ecallantide，它们可以改善治疗效果。

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