ABSTRACT
The presence of urticaria and/or angioedema requires considerations of allergic reactions to drugs and foods as part of the differential diagnosis. Among the pathogenic hallmarks of allergy are the degranulation of cutaneous mast cells due to bridging of IgE molecules by allergen that is, at minimum, bivalent, and also to infiltration of eosinophils as part of a latephase reaction. The same can occur as a result of mast cell activation by alternative mechanisms. such as occurs in the autoimmune subgroup of patients with chronic urticaria and angioedema, as well as the group whose condition remains idiopathic because an initiating stimulus has not yet been identified. When activation of mast cells is systemic, rather than being confined to the skin, the result can be idiopathic anaphylaxis. Other disorders are characterized by a proliferation of either mast cells or eosinophils, with symptoms resulting not only from tissue infiltration by such cells but also because there is abnormaL seemingly spontaneous, secretion of mediators by the cells with resulting constitutional symptoms or organ damage. Systemic mastocytosis and the hypereosinophilic syndrome can be characterized in this fashion.
