缓激肽和组胺介导的血管性水肿的病理生理学。

IF 3.3 Q2 ALLERGY
Frontiers in allergy Pub Date : 2023-10-18 eCollection Date: 2023-01-01 DOI:10.3389/falgy.2023.1263432
Hermenio Lima, Jiayue Zheng, Dennis Wong, Susan Waserman, Gordon L Sussman
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引用次数: 0

摘要

血管性水肿的特点是皮下和粘膜下组织局部肿胀。这篇综述提供了血管性水肿的概述,包括不同类型、触发因素和潜在的病理生理机制。遗传性和获得性血管性水肿是由补体和激肽途径失调引起的。相反,药物诱导和过敏性血管性水肿涉及免疫系统的激活和血管活性介质的释放。血管性水肿病理生理学的最新进展导致了靶向治疗的发展,如单克隆抗体、缓激肽受体拮抗剂和补体抑制剂,有望改善这种具有挑战性的疾病患者的临床结果。为了准确诊断和治疗血管性水肿,了解这种情况复杂多样的病理生理学是必要的,也是至关重要的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Pathophysiology of bradykinin and histamine mediated angioedema.

Pathophysiology of bradykinin and histamine mediated angioedema.

Angioedema is characterized by swelling localized to the subcutaneous and submucosal tissues. This review provides an overview of angioedema, including the different types, triggers, and underlying pathophysiologic mechanisms. Hereditary and acquired angioedema are caused by dysregulation of the complement and kinin pathways. In contrast, drug-induced and allergic angioedema involve the activation of the immune system and release of vasoactive mediators. Recent advances in the understanding of the pathophysiology of angioedema have led to the development of targeted therapies, such as monoclonal antibodies, bradykinin receptor antagonists, and complement inhibitors, which promise to improve clinical outcomes in patients with this challenging condition. To accurately diagnose and manage angioedema, an understanding of this condition's complex and varied pathophysiology is both necessary and critical.

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来源期刊
CiteScore
2.80
自引率
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审稿时长
12 weeks
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