Intranasally administered corticosteroids have a wide margin of safety
and are the mainstay of treatment for patients with moderate to sever
e allergic rhinitis, nonallergic rhinitis, and nasal polyposis. Long t
erm use in recommended dosages has not caused nasal mucosal atrophy or
hypothalamic-pituitary-adrenal (HPA) suppression. In practice, althou
gh fluticasone propionate and flunisolide appear to be twice as potent
as beclomethasone dipropionate, there is little, if any, difference i
n therapeutic effectiveness (maximum achievable effect) among any of t
he currently available preparations. Intranasally administered cortico
steroids call 1) inhibit the early and late (3-11 hour) responses foll
owing experimental allergen challenge, 2) reduce the number of eosinop
hils and basophils in nasal lavage samples, and 3) decrease the number
of activated (CD4+ CD25+) lymphocytes and presence of bioactive media
tors. The number of interleukin 4 (IL-4) reactive cells is decreased i
n the nasal submucosa, which is of importance in that IL-4 participate
s in IgE synthesis, T cell activation, and vascular cell adhesion mole
cule (VCAM) upregulation. The beneficial immunologic actions and nasal
protective properties of intranasal corticosteroids have resulted in
widespread use and reduction in patient rhinitic symptoms. Nevertheles
s, intranasal corticosteroids are not a substitute for environmental c
ontrol, cessation of smoking, or determination whether allergen immuno
therapy is indicated.