ABSTRACT
A subpopulation of asthmatic patients reacts to aspirin with an acute dyspnea, usually accompanied by nasal symptoms (rhinorrhea/nasal congestion) within two hours after ingestion of aspirin. These patients present a typical ‘‘aspirin triad,’’ which involves chronic rhinosinusitis complicated by polyp formation, severe bronchial asthma, and hypersensitivity reactions in response to aspirin and also other cross-reacting nonsteroidal anti-inflammatory drugs (NSAIDs). The first case of a hypersensitivity reaction to aspirin manifesting as dyspnea and angioedema was described in 1902 (two years after aspirin was marketed) by Hirschberg from Poznan´ in western Poland (1). The association of aspirin hypersensitivity, nasal polyposis, and asthma was noticed by Widal et al. (2) and the syndrome was characterized in a larger group of patients by Samter and Beers (3). Since that time, several various terms have been used to describe respiratory reactions to NSAIDs: aspirin sensitivity, pseudoallergy, idiosyncrasy, or intolerance (4). Having in mind the nonimmunological mechanism of respiratory reactions to aspirin and other NSAIDs, the term ‘‘hypersensitivity’’ seems to be the most appropriate and in agreement with current recommendations for nomenclature (5). The coexistence of aspirin hypersensitivity with upper airway (rhinosinusitis/nasal polyps) and lower airway (asthma) inflammatory disease was referred to as aspirin triad, asthma triad, Samter’s syndrome, aspirin-induced asthma, and aspirin-sensitive rhinosinusitis/asthma syndrome. More recently, the term ‘‘aspirin-exacerbated respiratory disease’’ (AERD) was proposed stressing the fact that the core issue in these patients is not acetylsalicylic acid (ASA) hypersensitivity but the underlying chronic inflammatory respiratory disease only occasionally exacerbated by aspirin or other NSAIDs (6). A subgroup of ASA-hypersensitive patients manifests a reaction exclusively in the upper respiratory tract; they do not have asthma, but the clinical picture of the nasal disease in these patients (hyperplastic rhinosinusitis with polyps) is similar to that observed in patients with ASA triad (7). Because the mechanism of the disease seems to be the same and some patients will evolve with time into full aspirin triad including bronchial asthma, it seems practical to discuss both subpopulations together as patients with AERD.
