D1.164 - Evaluation of the use of cyclooxygenase-2 inhibitors in patients with AERD

Aspirin-exacerbated respiratory disease (AERD) is characterized by the triad of asthma, chronic rhinosinusitis with nasal polyps, and hypersensitivity to aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs). The literature reports that 5–20% of patients with severe asthma have AERD. One of the physiological actions of cyclooxygenase-1 (COX-1) is the production of prostaglandins, including prostaglandin E2 (PGE2), which inhibits lipoxygenase, thereby reducing leukotriene production. However, the main source of PGE2 is cyclooxygenase-2 (COX-2), whose activity is reduced in AERD.

Retrospective study of adult patients of both sexes with AERD followed at a tertiary hospital. Demographic data, asthma severity according to treatment step, and presence of anosmia were evaluated. All patients underwent an oral challenge with celecoxib 200 mg and were assessed for respiratory symptoms; in severe cases, vital signs, forced expiratory volume in one second (FEV₁), and peak nasal inspiratory flow were analyzed.

Objective: To demonstrate tolerance to COX-2 inhibitors (iCOX-2) in patients with AERD

Twenty patients were included, 70% female, with a mean age of 55.7 years and a mean disease duration of 14.9 years. Of these, 75% were in asthma step 5 (11 patients were using immunobiologic agents) and 75% had anosmia. Regarding the use of iCOX-2, three patients had reactions: two with bronchospasm and one with urticaria, at doses of 10% or 100%. One patient, after repeating the oral challenge following initiation of immunobiologic therapy, became tolerant to iCOX-2.

ur study observed that 15% of patients with AERD had hypersensitivity reactions to iCOX-2. Therefore, we suggest that in patients with severe clinical disease, oral provocation testing should be performed under medical supervision.