Antiallergic properties of antihistamines.

Histamine is a major mediator of the allergic reaction, and histamine H1-receptor antagonists have a long history of clinical efficacy in a variety of allergic disorders. The pathogenesis of allergic disease is complex, involving not only histamine and mast cell-derived tryptase, but also eosinophil and neutrophil derived mediators, cytokines, and intercellular adhesion molecules (ICAM-1). A number of "in vitro" and "in vivo" studies have been performed to assess the clinical effectiveness of antihistamines in inhibiting the allergen-induced inflammatory process in the skin and mucosa. In vitro human studies have shown that high concentration of second generation antihistamines can block inflammatory mediator release from basophils and mast cells, and reduce ICAM-1 expression in epithelial cell lines. In vivo studies have also shown an effect on the allergen-induced inflammatory reaction; both oral and intranasal antihistamines cause a reduction in nasal symptoms and inflammatory cell influx. Analysis of secretory fluids and tissues after challenge indicates that antihistamines interfere with mediator release. Recruitment of inflammatory cells to the site of the allergic insult is also disturbed by antihistamines of second-generation, suggesting that these drugs may inhibit upregulation of molecules involved in cell adhesion and migration, and perhaps they may interfere with the cytokine cascade through their ability of stabilizing mast cells and of limiting the incursion of inflammatory cells. This article reviews available human data on the antiallergic effects of antihistamines.