Rhinosinusitis and nasal polyposis in aspirin sensitive and aspirin tolerant patients: are they different?

Hypersensitivity to aspirin (acetylsalicylic acid; ASA) is present in 5–10% of asthmatic patients and is associated with chronic rhinosinusitis and nasal polyposis, a syndrome referred to as the aspirin triad. 2 The mechanism of the hypersensitivity reaction to aspirin is not immunological, but may be related to the inhibition of cyclo-oxygenase, an enzyme responsible for prostaglandin synthesis, by aspirin. A positive history of aspirin hypersensitivity, which is the hallmark of this syndrome, is a significant and reliable indicator of chronic intractable rhinosinusitis, persistent asthma of greater than average severity, and higher than ordinary medication requirements, including dependence on steroids. 3 In addition to bronchospasm, most aspirin sensitive asthmatic subjects challenged with aspirin develop nasal symptoms including rhinorrhoea, sneezing and nasal obstruction, but the nasal responses to aspirin are superimposed on the existing pathology of the upper respiratory tract. The incidence of sinusitis identified by radiography in aspirin sensitive asthmatics may be up to 96.2% and the frequency of nasal polyps may be as high as 70.8% 4 compared with 6.7% in the general asthmatic population. A subgroup of aspirin sensitive patients has a reaction exclusively in the upper respiratory tract. They do not have asthma but the clinical picture of nasal disease (hypertrophic rhinosinusitis) in these patients is similar to that observed in patients with the aspirin triad. This article reviews the similarities and diVerences in the severity, pathophysiology, and management of upper airway disease in aspirin sensitive and aspirin tolerant patients with asthma and chronic rhinosinusitis.