Urticaria and Angioedema at a Glance
- Occurs acutely at some time in 20% of the population; incidence of chronic urticaria/angioedema is approximately 0.5%.
- Acute urticaria/angioedema is caused by drugs, foods, occasionally infection in association with immunoglobulin E-dependent mechanisms (allergy), or metabolic factors.
- Chronic urticaria/angioedema is an autoimmune disorder in 45% of patients.
- In the absence of urticaria, angioedema can be due to overproduction or impaired breakdown of bradykinin.
- Treatment of acute urticaria/angioedemarelies on antihistamines and short courses of corticosteroids, and identification and elimination of endogenous and exogenous causes.
- Treatment of C1 inhibitor deficiency includes androgenic agents, antifibrinolytic agents, and C1 inhibitor (C1 INH) concentrates, a kallikrein inhibitor, and bradykinin receptor antagonist.
- Treatment of physical urticaria/angioedema includes high-dose antihistamine prophylaxis, except for delayed pressure urticaria.
- Treatment of chronic idiopathic or autoimmune urticaria/angioedema includes antihistamines (nonsedating preparations primarily), low-dose daily or alternate day corticosteroids, or cyclosporine.
Urticaria is defined as a skin lesion consisting of a wheal-and-flare reaction in which localized intracutaneous edema (wheal) is surrounded by an area of redness (erythema) that is typically pruritic. Individual hives can last as briefly as 30 minutes to as long as 36 hours. They can be as small as a millimeter or 6–8 inches in diameter (giant urticaria). They blanch with pressure as the dilated blood vessels are compressed, which also accounts for the central pallor of the wheal. The dilated blood vessels and increased permeability that characterize urticaria are present in the superficial dermis and involves the venular plexus in that location. Angioedema can be caused by the same pathogenic mechanisms as urticaria but the pathology is in the deep dermis and subcutaneous tissue and swelling is the major manifestation. The overlying skin may be erythematous or normal. There is less pruritus (fewer type C nerve endings at the deeper cutaneous levels) but there may be pain or burning.
Urticaria and angioedema are common. Age, race, sex, occupation, geographic location, and season of the year may be implicated in urticaria and angioedema only insofar as they may contribute to exposure to an eliciting agent. Of a group of college students, 15%–20% reported having experienced urticaria, while 1%–3% of the patients referred to hospital dermatology clinics in the United Kingdom noted urticaria and angioedema. In the National Ambulatory Medical Care Survey data from 1990 to 1997 in the United States, women accounted for 69% of patient visits. There was a bimodal age distribution in patients aged birth to 9 years and 30–40 years.1
Urticaria/angioedema is considered to be acute if it lasts less than 6 weeks. Most acute episodes are due to adverse reactions to medications or foods and in children, to viral illnesses. Episodes of urticaria/angioedema persisting beyond 6 weeks are considered chronic and are divided into two major subgroups: (1) chronic autoimmune urticaria (45%) and (2) chronic idiopathic urticaria (55%) with a combined incidence in the general population of 0.5%.2 Physically induced urticaria/angioedema is not included in ...