EDITORIALS
Aspirin sensitivity and eicosanoids
King’s College London, MRC and Asthma UK Centre in Allergic Mechanisms of Asthma, Guy’s Hospital, London, UK
Correspondence to:
Professor Tak H Lee, Department of Asthma, Allergy and Respiratory Science, 5th Floor, Thomas Guy House, Guy’s Hospital, London SE1 9RT, UK; tak.lee@kcl.ac.uk
| The first 150 words of the full text of this article appear below. |
Aspirin sensitive respiratory disease (ASRD) was first described in 1922 by the French physician Widal.1 It is characterised by asthma, chronic rhinosinusitis and nasal polyps on a background of aspirin sensitivity. The condition is a distinct, often aggressive, clinical syndrome, and it is rare in childhood with a peak age of onset in the early 30s.2 Rhinorrhoea and nasal congestion are typically the first symptoms with asthma usually manifesting 1–5 years after the onset of rhinitis.3 Once the disease is established, ingestion of aspirin induces the release of critical mediators that provoke an acute exacerbation of rhinosinusitis and asthma. It is estimated that 5–10% of all patients with asthma are aspirin sensitive.4 Often poorly responsive to treatment, patients with aspirin sensitivity are over-represented in the severe asthma group and 50% are steroid dependent.5
The aetiology of ASRD is complex, but most investigators are agreed that the reaction to aspirin is
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