Article Text

Download PDFPDF
Aspirin sensitivity and eicosanoids
  1. Sophie Farooque,
  2. Tak H Lee
  1. King’s College London, MRC and Asthma UK Centre in Allergic Mechanisms of Asthma, Guy’s Hospital, London, UK
  1. 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{at}

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

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 not mediated by allergic mechanisms. Most evidence points towards an abnormality of arachidonic acid (AA) metabolism. AA is a substrate for both the production of leucotrienes (via the 5-lipoxygenase (5-LO) pathway) and prostanoids (via the cyclooxygenase (COX) pathway).

ASRD is characterised by excessive cysteinyl leucotriene (CysLT) production both in the steady state and for several hours after aspirin challenge.6 Urinary leucotriene E4 (LTE4) levels, as a measure of total body production of CysLTs, are a mean sixfold higher in patients with ASRD, increasing fourfold higher still after aspirin challenge.7 To date, the question of whether ASRD is associated with a fundamental predetermined abnormality in the production of CysLT8 or whether …

View Full Text


  • Competing interests: None.