Abstract
Idiopathic angioedema is characterized by local edema involving the deeper dermis and subcutaneous tissue and triggered by the release of mediators that cause vasodilatation and increased capillary permeability.1 Acute attacks most commonly occur in the periphery, but patients also may experience laryngeal or bowel angioedema. Idiopathic angioedema shares some clinical features with hereditary angioedema (HAE) types I and II and is physiologically distinct in that patients with idiopathic angioedema exhibit normal C4 and C1 esterase inhibitor levels and function.
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