Nasal polyps affect approximately 4% of the population in the western world
. The etiology of this disease is unknown, although inflammatory mechanisms
may play an important role. In preceding studies we and others have shown
that besides H-1-antagonism, azelastine influences the immigration and infl
ammation of inflammatory cells. In this open label study in 16 patients wit
h nasal polyps and perennial mite-allergic rhinitis, the effect of azelasti
ne nasal spray hr ice daily 0.14 mg to each nostril on recurrence of nasal
polyposis after endonasal surgery was evaluated. One patient dropped out af
ter 3 months, unwilling to take further medication. Clinical and laboratory
data of 15 patients were recorded over 25 weeks in a total of seven visits
. Of these one patient needed nasal budesonide during the 4 weeks between v
isits 3 and 4. All other patients did not take any steroids before inclusio
n into the trial or during the 6-month observation period. Concentrations o
f eosin ophil cationic protein (ECP) far eosinophils, myeloperoxidase (MPO)
for neutrophils and tryptase for mast cells were determined in nasal secret
ions before and after eight and 25 weeks of treatment using double antibody
radioimmunoassays, because these have been demonstrated to be good inflamm
atory markers in nasal diseases. Mean concentrations of MPO decreased from
2724 ng/mL to 1610 ng/mL (p = 0.0015) over the entire treatment period. ECP
decreased from 458 ng/mL to 264 ng/mL (p = 00342). Tryptase decreased from
37.9 ng/mL to 22.4 ng/mL (I, = 0.0574). These data were consistent with a
significant decrease in clinical symptoms. Thus, azelastine seems to have a
n inhibitory effect on eosinophil and neutrophil activation in patients wit
h nasal polyps and mite allergy.