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J Emerg Med. 2013 Nov;45(5):789-96. doi: 10.1016/j.jemermed.2013.03.045. Epub 2013 Aug 29.

Angioedema: etiology, pathophysiology, current and emerging therapies.

Author information

1
Division of Emergency Medicine, Washington University School of Medicine, St Louis, Missouri.

Abstract

BACKGROUND:

Angioedema (AE) is characterized by nonpitting edema of the dermis and subcutaneous layers. The most common sites of involvement are the tongue, lips, face, and throat; however, swelling can also occur in the extremities, genitalia, and viscera. Life-threatening airway swelling can also occur. AE may be allergic or nonallergic. The overall lifetime incidence of AE is reported to be as high as 15%.

OBJECTIVE:

This article summarizes the etiology, pathophysiology, and current treatment of several forms of nonallergic AE (including hereditary, acquired, and idiopathic AE) and focuses on angiotensin-converting enzyme inhibitor-induced angioedema (ACEi-AE), which is responsible for 30%-40% of all AE seen in United States emergency departments.

DISCUSSION:

Although the triggers, which are primary biologic mechanisms, and treatments for ACEi-AE may differ from those of the hereditary and acquired forms of AE, the clinical effects of ACEi-AE are mediated through a shared pathway, the kallikrein-kinin system. Thus, although current therapeutic options for ACEi-AE are limited, recent advances in the treatment of hereditary AE (HAE) appear promising for improving the outcomes of patients with ACEi-AE.

CONCLUSIONS:

New HAE medications that correct imbalances in the kallikrein-kinin system may prove safe and efficacious in the treatment of ACEi-AE.

KEYWORDS:

angioedema; angiotensin-converting enzyme inhibitor–induced angioedema; ecallantide; icatibant; kallikrein-kinin system

PMID:
23992848
DOI:
10.1016/j.jemermed.2013.03.045
[Indexed for MEDLINE]

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