Abstract
Nasal congestion, a defining symptom of seasonal allergic rhinitis (SAR), generally responds poorly to antihistamines and may require nasal corticosteroid or sympathomimetic therapy. The current understanding of the pathophysiology of SAR indicates that congestion is caused by persistent allergic inflammation of the nasal mucosa. Allergic inflammation is a complex immunological response that involves preformed (histamine, tryptase) and rapidly produced mediators (prostaglandin D2, leukotriene C4), neurotransmitters (kinins, substance P), cytokines [interleukin (IL)-4, IL-5, IL-13], chemokines (IL-8, eotaxin, RANTES), adhesion molecules (P-selectin, intercellular adhesion molecule-1) and cells (mast cells, eosinophils, basophils). Desloratadine, a potent H1 receptor antagonist that reduces symptoms of SAR, including nasal congestion, has also been shown to inhibit the production and release of many allergic inflammatory mediators in preclinical studies. The combination of potent H1 antagonism with these nonhistamine-related actions might help to explain the efficacy of desloratadine in treating the symptoms of SAR, including nasal congestion.
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