Hereditary angioedema (HAE) is a rare genetic disease with potentially fatal consequences [1]. Its estimated occurrence ranges from 1 : 10,000 to 1 : 50,000 [2]. A few types of HAE have been differentiated. HAE types 1 and 2 are most common, with depleted C1 inhibitor esterase (C1-INH) in serum or its dysfunction caused by a mutated SERPING1 gene [3]. The illness is mainly inherited through autosomal dominance, with 20–25% of cases caused by de novo mutation [4]. C1-INH, a member of the serpin group proteins, is a natural inhibitor of the initial phase of the complement cascade. Disrupting its concentration or function causes uncontrolled bradykinin production and accumulation, due to non-physiological activation of the complement system, the coagulation pathway, fibrinolysis and kallikrein cascade. When bound to its specific type 2 receptors, bradykinin induces a rapid increase in subcutaneous and submucosal blood vessel permeability, manifested as recurrent episodes of subcutaneous and submucosal tissue oedema.