In addition to their increased potency as H1 blockers and their nonsedating effects, the
second-generation antihistamines have other unusual and potentially beneficial properties. Evidence is accumulating from several laboratories that at least one of these agents under investigation,
cetirizine, may be effective in inhibiting the late reaction. The Johns Hopkins group showed that during the cutaneous late phase response (LPR), histamine release was not altered by
cetirizine, 20 mg, pretreatment. The most dramatic effect of
cetirizine was attenuation of inflammatory cell migration into the chamber. Eosinophils, neutrophils, and basophils were reduced by about 75% during hours 6 to 8. It can be concluded that
cetirizine influences the LPR by causing a reduction in the inflammatory cell infiltrate.
Cetirizine, 10 mg, orally once a day also induced a significant decrease in the wheal and flare skin reactions caused by pollen,
histamine, and
compound 48/80.
Cetirizine inhibited eosinophil recruitment and
platelet-activating factor (PAF) in skin chambers 24 hours after pollen challenge. We and others have studied the mechanisms of this effect. The release of
eosinophil peroxidase induced by PAF and formyl-methionyleucyl/
phenylalanine was not attenuated by
cetirizine. At therapeutic concentrations, however,
cetirizine has a potent inhibitory action in vitro on eosinophil chemotaxis induced either by formyl-methionyleucyl/
phenylalanine or PAF and also on
IgE-dependent stimulation of platelets. In a separate study in patients with
chronic urticaria,
cetirizine markedly reduced both the immediate wheal and flare induced by PAF and the delayed reaction at six hours. These results suggest that
cetirizine acts on eosinophil migration to inhibit the late reaction.