Nasal versus bronchial and nasal response to oral aspirin challenge: Clinical and biochemical differences between patients with aspirin-induced asthma/rhinitis.

BACKGROUND

Aspirin-induced asthma/rhinitis (AIAR) is characterized by the altered metabolism of leukotrienes and proinflammatory prostaglandins. The basal and postchallenge levels of eicosanoids might reflect the clinical and biochemical characteristics of patients with distinct types of hypersensitive responses to aspirin.

OBJECTIVE

We compared clinical and eicosanoid profiles of patients with AIAR showing both bronchial and nasal versus isolated nasal responses to aspirin challenge.

METHODS

Twenty-three patients with AIAR underwent the single-blind, oral, placebo-controlled aspirin challenge. The bronchial response (BR) was evidenced by dyspnea and spirometry, whereas the nasal response (NR) was evidenced by nasal symptoms and acoustic rhinometry and/or rhinomanometry. Urinary leukotriene E4 (uLTE4), serum and urinary stable prostaglandin D2 metabolite, and 9alpha,11beta-prostaglandin F2 (9alpha,11beta-PGF2), were determined at baseline and after the aspirin challenge.

RESULTS

Fifteen subjects showed BR and NR (BNR), whereas 8 showed NR only. Basal uLTE4 in the BNR group was significantly higher than in the NR group. After aspirin challenge, it increased significantly in both groups. Serum 9alpha,11beta-PGF2 increased after aspirin challenge in the BNR group only. The patients with BNR had more severe AIAR.

CONCLUSIONS

BNR to aspirin in AIAR indicates a more advanced disease and more profound underlying eicosanoid metabolism disturbances.