Angioedema, hereditary angioedema, ACE inhibitor and Bradykinin
Posted: 23rd July 2013 | Posted by AdminMR
Angioedema is a result of increased vascular permeability, with subsequent extravasation of intravascular fluid into the surrounding tissues. Angioedema may be mediated by histamine, bradykinin, or other mediators. Histaminergic angioedema generally presents with urticaria and/or pruritus and will respond to conventional treatment with antihistamines, corticosteroids, or epinephrine. Bradykinin-mediated angioedema, which includes hereditary angioedema (HAE types I, II, and III), acquired C1-INH deficiency, and ACE inhibitor−induced angioedema, does not typically present with urticaria/wheals and does not respond to conventional agents such as antihistamines or corticosteroids. In recent years, several agents that prevent the generation or activity of bradykinin have been developed for the treatment of HAE types I and II and are also being evaluated in other types of bradykinin-mediated angioedema.
