Antihistamines in asthma.

Substantial evidence indicates that airway hyperresponsiveness in asthma is associated with the inflammatory response directed toward the airway epithelium and submucosa. Endogenously released spasmogenic mediators interacting with smooth muscle have a greater effect on hyperresponsive than on normal airways. Histamine, a bronchoactive and vasoactive mediator, is released in patients with naturally occurring or allergen-induced asthma. It is clear that mast cells are activated as part of the asthmatic response, and they have now been implicated as effector cells of mediator secretion based on the results of provocative tests. The advent of more potent histamine antagonists selective for H1 receptors has led to a reappraisal of antihistamine therapy in asthma. Drugs such as terfenadine and azelastine inhibit early bronchoconstriction and to some extent the late-phase asthmatic response as well. The efficacy of other new antihistamines (e.g., ketotifen and cetirizine) may extend beyond H1-receptor blockade to inhibit some of the chronic (and perhaps more important) cellular events in asthma.