Immunologic Effects of Intranasal Corticosteroids

Intranasally administered corticosteroids have a wide margin of safety and are the mainstay of treatment for patients with moderate to severe allergic rhinitis, nonallergic rhinitis, and nasal polyposis. Long term use in recommended dosages has not caused nasal mucosal atrophy or hypothalamic-pituitary-adrenal (HPA) suppression. In practice, although fluticasone propionate and flunisolide appear to be twice as potent as beclomethasone dipropionate, there is little, if any, difference in therapeutic effectiveness (maximum achievable effect) among any of the currently available preparations. Intranasally administered corticosteroids can 1) inhibit the early and late (3–11 hour) responses following experimental allergen challenge, 2) reduce the number of eosinophils and basophils in nasal lavage samples, and 3) decrease the number of activated (CD₄+CD₂₅+) lymphocytes and presence of bioactive mediators. The number of interleukin 4 (IL-4) reactive cells is decreased in the nasal submucosa, which is of importance in that IL-4 participates in IgE synthesis, T cell activation, and vascular cell adhesion molecule (VCAM) upregulation. The beneficial immunologic actions and nasal protective properties of intranasal corticosteroids have resulted in widespread use and reduction in patient rhinitic symptoms. Nevertheless, intranasal corticosteroids are not a substitute for environmental control, cessation of smoking, or determination whether allergen immunotherapy is indicated.