¿PLASMA LEVELS OF BRADYKININ AND CLEAVED HIGH MOLECULAR WEIGHT KININOGEN IN PATIENTS WITH IDIOPATHIC ANGIOEDEMA DURING ACUTE ATTACK¿
type: CreativeWork
description: Angioedema is a swelling of the subcutaneous and submucosal tissues that can involve lips, face, neck, extremities and/or submucosal tissues of the oral cavity, larynx and intestine. Patients with angioedema can be clinically critical and require urgent clinical evaluation, especially when angioedema affects the larynx (a life-threatening condition) or the gastrointestinal tract (mimicking an acute abdomen). Angioedema can be acquired or hereditary. The acquired forms may be histaminergic or non-histaminergic, drug-induced or due to an acquired C1-inhibitor deficiency; however, several cases remain idiopathic. The role of bradykinin in increasing vascular permeability has been demonstrated in angioedema due to C1-inhibitor deficiency and in angioedema due to the treatment with angiotensin converting enzyme (ACE) inhibitors, while its involvement in idiopathic angioedema is still unknown. Bradykinin derives from the cleavage of the high molecular weight kininogen and is catabolized mainly by ACE. During acute attacks of C1-inhibitor deficiency angioedema, high levels of cleaved high molecular weight kininogen (marker of bradykinin generation) were observed, thus indicating that the high concentrations of bradykinin detected in these patients are due to an excess of bradykinin production itself. Instead, during acute attacks of ACE inhibitor angioedema, the plasma levels of bradykinin are elevated without the presence of cleaved high molecular weight kininogen, thus indicating a reduction in bradykinin catabolism. Therefore, since in many cases of angioedema it is not possible to identify the underlying cause, a pathogenetic definition is necessary to adequately treat patients. Our preliminary data regarding 4 patients with non-histaminergic idiopathic angioedema demonstrated bradykinin production during acute attacks of the disease suggesting the potential role of this mediator in the pathogenesis of these forms of angioedema. Based on these observations, we planned …
abstract: Angioedema is a swelling of the subcutaneous and submucosal tissues that can involve lips, face, neck, extremities and/or submucosal tissues of the oral cavity, larynx and intestine. Patients with angioedema can be clinically critical and require urgent clinical evaluation, especially when angioedema affects the larynx (a life-threatening condition) or the gastrointestinal tract (mimicking an acute abdomen). Angioedema can be acquired or hereditary. The acquired forms may be histaminergic or non-histaminergic, drug-induced or due to an acquired C1-inhibitor deficiency; however, several cases remain idiopathic. The role of bradykinin in increasing vascular permeability has been demonstrated in angioedema due to C1-inhibitor deficiency and in angioedema due to the treatment with angiotensin converting enzyme (ACE) inhibitors, while its involvement in idiopathic angioedema is still unknown. Bradykinin derives from the cleavage of the high molecular weight kininogen and is catabolized mainly by ACE. During acute attacks of C1-inhibitor deficiency angioedema, high levels of cleaved high molecular weight kininogen (marker of bradykinin generation) were observed, thus indicating that the high concentrations of bradykinin detected in these patients are due to an excess of bradykinin production itself. Instead, during acute attacks of ACE inhibitor angioedema, the plasma levels of bradykinin are elevated without the presence of cleaved high molecular weight kininogen, thus indicating a reduction in bradykinin catabolism. Therefore, since in many cases of angioedema it is not possible to identify the underlying cause, a pathogenetic definition is necessary to adequately treat patients. Our preliminary data regarding 4 patients with non-histaminergic idiopathic angioedema demonstrated bradykinin production during acute attacks of the disease suggesting the potential role of this mediator in the pathogenesis of these forms of angioedema. Based on these observations, we planned …
author: DEPETRI, FEDERICA
language: eng
keywords: angioedema, C1-inhibitor, bradykinin, Settore MED/09 - Medicina Interna
date published: 2022-07-05
date modified: 2026-07-27T20:19:08Z
provider: Università degli Studi di Milano
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: Università degli Studi di Milano

PropertyValue
property ID: Handle
value: http://hdl.handle.net/2434/932626

PropertyValue
property ID: DOI
value: 10.13130/depetri-federica_phd2022-07-05