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Related Concept Videos

Cerebral Edema l: Introduction01:19

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...
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Updated: May 14, 2026

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice
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Published on: September 28, 2015

[Hereditary angioedema].

Laura J Bouchard1, Heli Hyry, Seppo Meri

  • 1Helsingin yliopisto, Haartman-instituutti, bakteriologian ja immunologian osasto.

Duodecim; Laaketieteellinen Aikakauskirja
|February 12, 2013
PubMed
Summary
This summary is machine-generated.

Hereditary angioedema (HAE) is a rare genetic disorder causing swelling. Recent advancements offer new self-administered treatments targeting bradykinin, improving patient management.

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Area of Science:

  • Immunology
  • Genetics
  • Vascular Biology

Background:

  • Hereditary angioedema (HAE) is a rare autosomal dominant disorder.
  • Characterized by recurrent episodes of swelling in various body parts.
  • Caused by genetic mutations affecting C1 inhibitor or coagulation factor XII, leading to increased bradykinin levels.

Purpose of the Study:

  • To review the pathophysiology of HAE.
  • To discuss the different subtypes of HAE.
  • To highlight recent advancements in HAE treatment.

Main Methods:

  • Literature review of HAE pathogenesis and treatment.
  • Analysis of genetic causes for HAE types I, II, and III.
  • Overview of current therapeutic options.

Main Results:

  • HAE pathogenesis involves overproduction of bradykinin, increasing vascular permeability.
  • Types I and II HAE result from C1 inhibitor gene mutations.
  • Type III HAE is linked to a coagulation factor XII mutation.

Conclusions:

  • All HAE types share a common mechanism of increased bradykinin production.
  • Newer treatments, including self-administered C1 inhibitor concentrate and icatibant, have significantly improved HAE management.
  • The availability of targeted therapies marks a significant evolution in addressing HAE symptoms.