Chronic urticaria: Pathophysiology and treatment approaches

Abstract

Urticaria, a cutaneous reaction pattern, varies clinically and histopathologically. The origin of acute urticaria can be detected in some cases; in patients with chronic urticaria, however, the cause is rarely identified. Thus, most patients with chronic urticaria are considered to have idiopathic disease. The dermal mast cell and its mediators may play a central role in chronic idiopathic urticaria. Other inflammatory cells, including lymphocytes and polymorphonuclear cells, have also been implicated. Treatment is based on identification of the inflammatory cells within skin lesions and blockage of the effects of histamine in the skin. Urticaria in which a lymphocyte-predominant infiltrate is seen often responds to one or more H1 antihistamines. Recently, a new generation of nonsedating or mildly sedating H1 antihistamines has proved useful in the management of these cases. Antihistamine use alone may be unsuccessful in urticaria in which polymorphonuclear neutrophils predominate; frequently, the addition of agents that alter polymorphonuclear neutrophil function, such as colchicine or dapsone, is required. During the introduction of antihistamine and anti–polymorphonuclear neutrophil therapy, a simultaneous brief course of systemic corticosteroid therapy may be necessary, but the extended use of systemic corticosteroids should be avoided because of significant adverse effects. As the pathophysiologic mechanisms responsible for chronic urticaria are better defined, more effective therapeutic agents should become available. (J Allergy Clin Immunol 1996;98:S325-30.)