Abstract
The major early phase clinical manifestations of allergic rhinitis are mediated by mast cell-derived histamine. This is followed by an eosinophil-dominated inflammatory cell influx, allergic inflammation—leading to changes in sensory neurone function—and development of nasal hyper-responsiveness. Thus, there are two distinct targets for drug therapy: (1) inhibition of the early phase response by blockade of the effects of histamine with H1-antihistamines and (2) reduction of allergic inflammation by intranasal corticosteroids.
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