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Angioedema: etiology, pathophysiology, current and emerging therapies
1Division of Emergency Medicine, Washington University School of Medicine, St Louis, Missouri.
The Journal of Emergency Medicine
|September 3, 2013
Summary
Angioedema (AE) is swelling that can be life-threatening. Angiotensin-converting enzyme inhibitor-induced angioedema (ACEi-AE) shares a pathway with hereditary angioedema (HAE), suggesting HAE treatments may help ACEi-AE.
Area of Science:
- Immunology
- Pharmacology
- Internal Medicine
Background:
- Angioedema (AE) involves non-pitting edema, potentially affecting airways, with a 15% lifetime incidence.
- AE can be allergic or nonallergic, with common sites including the face, lips, and tongue.
- Nonallergic AE encompasses hereditary, acquired, and idiopathic forms.
Purpose of the Study:
- To review the etiology, pathophysiology, and treatment of nonallergic AE.
- To focus on angiotensin-converting enzyme inhibitor-induced angioedema (ACEi-AE), a common cause of AE in emergency departments.
- To explore potential therapeutic advancements for ACEi-AE.
Main Methods:
- Literature review of angioedema (AE) forms.
- Focus on angiotensin-converting enzyme inhibitor-induced angioedema (ACEi-AE) pathophysiology.
- Analysis of treatment strategies for hereditary angioedema (HAE) and their potential application to ACEi-AE.
Main Results:
- Angiotensin-converting enzyme inhibitor-induced angioedema (ACEi-AE) accounts for 30%-40% of AE cases in US emergency departments.
- Despite differing triggers, ACEi-AE shares the kallikrein-kinin system pathway with hereditary and acquired AE.
- Current ACEi-AE treatments are limited.
Conclusions:
- New hereditary angioedema (HAE) medications targeting the kallikrein-kinin system show promise for ACEi-AE treatment.
- Shared pathways suggest that advancements in HAE therapy may improve outcomes for ACEi-AE patients.
- Further research into kallikrein-kinin system modulation is warranted for ACEi-AE.
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