Idiopathic nonhistaminergic form of angioedema (AE) is a potentially life-threatening condition. It is characterized by local swelling involving the deeper dermis and subcutaneous tissue and results from the release of mediators that cause vasodilatation and enhanced capillary permeability. Normal C1 inhibitor (INH) antigenic levels and function and normal C4 levels are the hallmark. Up to now, epidemiological studies on this form of AE are missing, and the frequency in the general population is unknown. The clinical features of this form are similar to those of hereditary AE (HAE) and acquired C1 INH deficiency. Pathophysiological evidence suggests that bradykinin is involved in HAE, in angiotensin-converting enzyme (ACE) inhibitor-induced AE, and in idiopathic nonhistaminergic AE, whereas bradykinin is not involved in allergen-dependent or idiopathic histaminergic AE that is responsive to antihistamines. The synthetic decapeptide icatibant, a selective competitive antagonist at the bradykinin B2 receptor, is authorized in Europe for the treatment of acute attacks of HAE. Recently, its successful use in severe ACE inhibitor–induced AE has been described. Its mechanism of action makes icatibant a promising drug for the idiopathic nonhistaminergic form of AE. We describe here its successful use in this condition, in which pharmacological treatment with antihistamines, corticosteroids, and epinephrine is often poorly effective.
Annals of Allergy, Asthma & Immunology. Volume 108, Issue 6 , Pages 460-461, June 2012
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