Clinical Immunology, Mount Sinai School of Medicine, New York, NY 10029, USA.
Clin Exp Allergy. 2013 Apr;43(4):385-94. doi: 10.1111/cea.12019.
Angioedema is a result of increased vascular permeability, with subsequent extravasation of intravascular fluid into the surrounding tissues. Angioedema may be mediated by histamine, bradykinin or other mediators. Histaminergic angioedema generally presents with urticaria and/or pruritus and will respond to conventional treatment with antihistamines, corticosteroids or epinephrine. Bradykinin-mediated angioedema, which includes hereditary angioedema (HAE types I, II and III), acquired C1-INH deficiency, and angiotensin-converting enzyme inhibitor-induced angioedema does not typically present with urticaria/weals and does not respond to conventional agents such as antihistamines or corticosteroids. In recent years, several agents that prevent the generation or activity of bradykinin have been developed for the treatment of HAE types I and II and are also being evaluated in other types of bradykinin-mediated angioedema. These agents have the potential to improve outcomes for patients with different forms of bradykinin-mediated angioedema.
血管性水肿是由于血管通透性增加,随后血管内液体渗出到周围组织引起的。血管性水肿可能由组胺、缓激肽或其他介质介导。组胺能性血管性水肿通常表现为荨麻疹和/或瘙痒,可通过抗组胺药、皮质类固醇或肾上腺素等常规治疗来缓解。缓激肽介导的血管性水肿,包括遗传性血管性水肿(HAE 1 型、2 型和 3 型)、获得性 C1-INH 缺乏症和血管紧张素转换酶抑制剂诱导的血管性水肿,通常不表现为荨麻疹/风团,也不响应常规药物,如抗组胺药或皮质类固醇。近年来,已经开发出几种可预防缓激肽生成或活性的药物,用于治疗 HAE 1 型和 2 型,并且正在其他类型的缓激肽介导的血管性水肿中进行评估。这些药物有可能改善不同类型缓激肽介导的血管性水肿患者的预后。