• C Umbreit, J C Virchow, C Thorn, K Hörmann, L Klimek, and O Pfaar.
• Zentrum für Rhinologie und Allergologie, HNO-Universitätsklinik Mannheim, An den Quellen 10, 65183 Wiesbaden, Deutschland.
• Internist (Berl). 2010 Sep 1;51(9):1196-8, 1200-1.

AbstractThe full clinical picture of aspirin intolerance - the association of aspirin-induced bronchial asthma, aspirin sensitivity and nasal polyps - has been described as Morbus Widal or later as the "Samter triad". Today the term Aspirin-exacerbated respiratory disease (AERD) is preferred to account for the progressive nature of this inflammatory airway condition with its unrelenting course even in the absence of non steroidal anti-inflammatory drugs (NSAID). This acquired idiosyncrasy appears to be related to an abnormal arachidonic acid metabolism. Epidemiological data suggests that 10% of all asthmatics do react with life-threatening asthma-attacks after the ingestion of aspirin (ASA) or other NSAID. Some asthmatics with nasal polyposis have been reported to suffer from aspirin intolerance. Although the exact mechanism is still unclear, it is unlikely that the pathogenesis is IgE-mediated. Patients often report chronic nasal obstruction, hyposmia, chronic rhinorrhoea, orbital edema and urticaria with flushing after the ingestion of NSAID. While a typical history and endoscopic findings can be suggestive of AERD, a definite diagnosis relies on appropriate challenge tests. AERD is often refractory to standard asthma treatment with systemic and inhaled steroids, β(2)-agonists, leukotrien-antagonists. Adaptive desactivation can induce a reversible tolerance to NSAID which also leads to an improvement in signs and symptoms of the underlying AERD.

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