Related Experiment Video
Updated: Jul 4, 2026

07:21
Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice
Published on: September 28, 2015
[The multiple etiologies of angioedema]
S Petitpierre1, P A Bart, F Spertini
1Service d'immunologie et d'allergie, CHUV, 1011 Lausanne. Stephanie.Petitpierre@chuv.ch
Revue Medicale Suisse
|June 19, 2008
Summary
Angioedema has various causes, with some linked to histamine and others to bradykinin. Understanding the underlying mechanism is crucial for effective treatment, as therapies for histamine-mediated angioedema are ineffective for bradykinin-mediated types.
Area of Science:
- Immunology
- Pharmacology
- Genetics
Context:
- Angioedema is a common condition with diverse triggers.
- Histamine-mediated angioedema often co-occurs with urticaria.
- Bradykinin is implicated in specific angioedema subtypes, notably those related to ACE inhibitors and C1-inhibitor deficiency.
Purpose:
- To differentiate angioedema subtypes based on their underlying pathophysiology.
- To highlight the distinct treatment responses between histamine- and bradykinin-mediated angioedemas.
Summary:
- Angioedemas associated with urticaria are typically histamine-mediated, responding to antihistamines and adrenaline.
- Drug-induced (e.g., NSAID), physical, and recurrent idiopathic angioedemas often fall under the histamine-mediated category.
- Angioedemas linked to ACE inhibitors, ARBs, or C1-inhibitor deficiency (hereditary or acquired) are likely bradykinin-mediated, presenting without urticaria and unresponsive to standard treatments.
Impact:
- Clarifies diagnostic and therapeutic approaches for different angioedema types.
- Emphasizes the importance of identifying the specific angioedema pathway for appropriate clinical management.
- Guides clinicians in selecting treatments based on the suspected etiological mechanism, improving patient outcomes.
Related Concept Videos
Cerebral Edema l: Introduction
Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...
Cerebral Edema ll: Pathophysiology
Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
Pulmonary Edema II: Pathophysiology
Pulmonary edema is the accumulation of fluid in the interstitial and alveolar spaces of the lungs, impairing gas exchange and oxygen delivery. It may be cardiogenic or noncardiogenic, but both reduce oxygenation and lung compliance.Cardiogenic Pulmonary EdemaCardiogenic edema results from increased hydrostatic pressure in pulmonary capillaries, usually due to left ventricular dysfunction from myocardial infarction, heart failure, or valvular disease. Ineffective cardiac pumping causes blood to...
Cytotoxic Edema: Pathophysiology
Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
Allergic Reactions
Overview
Allergic Reactions: Anaphylaxis
Anaphylaxis is a severe, life-threatening hypersensitivity reaction mediated by Immunoglobulin E (IgE) antibodies. When IgE binds to allergens, it triggers the release of mediators– histamine, leukotrienes, and prostaglandins from mast cells and basophils. These mediators cause vasodilation, edema, and inflammation, leading to various symptoms.The primary allergens causing anaphylaxis include food items (e.g., peanuts, shellfish), drugs (e.g., penicillin, asparaginase, corticotropin, heparin),...
