Aspirin (ASA) and several other nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit cyclo-oxygenase (COX) enzyme both isoforms 1 and 2, and can precipitate asthmatic attacks in aspirin-induced asthmatics. Rofecoxib (R) is a novel and specific COX-2 inhibitor which is caracterized by an highly selective COX-2 inhibition, and can be presumed as non cross-reactive with ASA. Aim of the study was to assess the bronchial and the nasal response to R in AIA.
Materials and methods: Nineteen subjects with AIA (21-54 years, 7 m, mean FEV1 85.1% pred. +/- 5.4 sd) performed two oral provocation tests: one with increasing doses of ASA and one other of R at a time interval of 2 weeks, according to a randomized, cross-over design. The bronchial and the nasal responses were measured by serial measures of FEV1, and of nasal resistences by acoustic rhinomanometry, respectively.
Statistics: Anova for trends was used, and p<0.05 accepted.
Results: Mean ASA PD20 was 68.3 mg +/- 12.4 sd. ASA induced a significant broncho-constriction in all patients with AIA: basal FEV1 dropped from 88.9% pred. +/- 6.2sd to 70.1% pred. +/- 6.9sd after 60 min. (Anova p = 0.001). Despite ASA, R was well tolerated: basal FEV1 remained unchanged during the period of observation following the R 25mg ingestion. ASA also precipitated a significant nasal response with increased nasal resistances (anova p < 0.001) and reduced volumes (anova p < 0.001). The nasal function was unchanged following R 25mg.
Conclusions: Despite ASA, Rofecoxib, largely due to its highly specificity for COX-2, proved a drug particularly safe in treating patients with AIA.