ABSTRACT
This chapter explains the structural, physiological, and molecular correlates of the symptoms and visible changes in the skin of the patient with urticaria and angioedema. The lesions of urticaria are, at first sight, straightforward. Localized vasodilatation causes redness; increased blood flow causes warmth; enhanced vascular permeability leads to swelling (edema). These are the features of Lewis's so-called 'triple response' (I), and itch is the dominant symptom. Similar processes underlie angioedema, but in this case increased vascular permeability predominates, leading to massive dermal and subcutaneous edema. Itching and visible redness are more variable. However, it is evident to anyone who deals with patients with these findings regularly that there is more to urticaria and angioedema than this. What determines the distribution of the lesions of urticaria and angioedema? Why do wheals of chronic so-called 'idiopathic' urticaria (other than delayed pressure urticaria and dermographism) often develop at sites of pressure such as around the waistband? Why does angioedema show a predilection for the eyelids and lips? Why do individual lesions in 'idiopathic' chronic urticaria last for ]2 h or more, in contrast with wheals of most physical
urticarias that last no more than an hour? Why is itching worse at night? Why do patients rub the itch of urticaria rather than scratch it? Why does chronic urticaria characteristically flare at times of stress? We cannot answer definitively these and other puzzling questions to the readers' (or our own) entire satisfaction, but we will address them.
