Mechanisms of aspirin sensitivity

Curr Allergy Asthma Rep. 2006 May;6(3):198-202. doi: 10.1007/s11882-006-0035-2.


In some asthma patients, nonsteroidal anti-inflammatory drugs (NSAIDs) induce bronchospasm, rhinorrhea, and nasal obstruction. NSAID-induced reactions appear to be caused by the inhibition of cyclooxygenase-1 (Cox-1); this in turn activates the lipoxygenase pathway, which eventually increases the release of cysteinyl leukotrienes (Cys-LTs) that induces bronchospasm and nasal obstruction. With regard to the metabolism of arachidonic acid (AA) in NSAID-intolerant asthmatic patients, the following changes have been observed: 1) A low production of prostaglandin E2, seemingly due to deficient Cox-2 regulation; 2) an increased expression of leukotriene-C4 synthase; and 3) a reduced production of metabolites (lipoxins) released through the transcellular metabolism of AA. NSAID-intolerant asthmatics have higher basal levels of Cys-LT than NSAID-tolerant asthmatics. Moreover, Cys-LT levels in NSAID-intolerant asthmatics increase remarkably following NSAID provocation testing. There has been no explanation to date that connects all these findings, although an anomaly in the regulation of Cox-2 is probably accountable.

Publication types

  • Review

MeSH terms

  • Anti-Inflammatory Agents, Non-Steroidal / adverse effects*
  • Arachidonate 15-Lipoxygenase / metabolism
  • Arachidonate 5-Lipoxygenase / metabolism
  • Arachidonic Acid / metabolism
  • Aspirin / adverse effects*
  • Asthma / chemically induced
  • Asthma / metabolism*
  • Drug Hypersensitivity / metabolism*
  • Humans
  • Lipoxins / metabolism
  • Prostaglandin-Endoperoxide Synthases / metabolism


  • Anti-Inflammatory Agents, Non-Steroidal
  • Lipoxins
  • Arachidonic Acid
  • Arachidonate 15-Lipoxygenase
  • Arachidonate 5-Lipoxygenase
  • Prostaglandin-Endoperoxide Synthases
  • Aspirin