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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 . . . [Full text of this article]