Aspirin intolerance and nasal polyposis.

Abstract

Chronic rhinosinusitis with nasal polyposis usually develops in aspirin-sensitive patients with asthma Arachidonic acid metabolism appears to be abnormal in the nasal polyps of aspirin-sensitive patients with asthma. These abnormalities an characterized by a low production of prostaglandin E2 (PGE2) and a high release of cysteinyl leukotrienes. Moreover, cyclooxygenase-2 is markedly downregulated in polyps from aspirin-sensitive patients with asthma. This abnormality may explain the low production of PGE2 in nasal polyps and may account for the increased susceptibility to the inhibitory effects of aspirin. Nasal instillation or ingestion of aspirin induces a nasal reaction in most aspirin-sensitive patients with asthma. This reaction is accompanied by the influx of eosinophils and a concomitant increase in cysteinyl leukotrienes, tryptase, and eosinophil cationic protein release. The aspirin nasal challenge is a very safe test with a moderate sensibility and high specificity that can be used in the diagnosis of aspirin intolerance. The similarities in the reaction between the nose and airways in aspirin-sensitive patients provide compelling evidence for common pathogenic mechanisms for nasal polyps, chronic rhinosinusitis, and bronchial asthma.