Table 1.

Characteristics of different types of AEwW (modified from [12,13]).

	Types of Angioedema
	Mediated by Mast Cells	Mediated by Bradykinin	Mediated by Leukotrienes
Pathogenetic Mechanism	• IgE-mediated response to antigen exposure with the release of vasoactive mediators • Non-IgE-mediated (may be associated with chronic spontaneous urticaria) • Idiopathic (unidentifiable cause)	Complex interaction of complement, coagulation, and contact system • Hereditary angioedema with C1-INH deficiency or defect • Hereditary angioedema with normal C1-INH • Acquired angioedema with C1-INH deficiency • ACE inhibitor-induced angioedema	Inhibition of cyclooxygenase-1 determines a shunt of the arachidonic acid metabolism and causes an increase in 5-lipoxygenase activity • Induced by NSAIDs, aspirin
Response to antihistamine in 12 h	Yes	No
Urticaria	Frequent	Absent
Age of onset	Anyway	Often in the 1st or 2nd decade (40% within 5 years)	Anyway
Pruritus	Present	Slight
Duration of edema	Usually <48 h	Often >72 h	Variable
Preferred localizations	Face (eyelids, lips), neck	Face, abdomen, extremities	Periorbital, airways
Prodromal symptoms	No	Often
Trauma as a trigger	No	Yes
Development of signs and symptoms	Fast	Slower	Hours
Familiar history	Never	Often	Not known
Further investigations	Levels of serum tryptase (useful in the context of anaphylaxis/allergenic trigger)	Serum C4 Quantitative and qualitative levels of C1-INH (all normal in ACE inhibitor-induced angioedema)