Crossreacting drugs and chemicals

Clin Rev Allergy Immunol. 2003 Apr;24(2):149-58. doi: 10.1385/CRIAI:24:2:149.


Aspirin and nonsteroidal antiinflammatory drugs (NSAIDs) exert their clinical effect through inhibition of prostaglandin H synthases 1 and 2, also known as cyclooxygenase. This shared effect of COX-inhibition is also the mechanism for shared adverse effects. Much of our understanding of cross-reacting drugs and chemicals with aspirin comes from studying asthmatics with aspirin-exacerbated respiratory disease (AERD). Aspirin exacerbated respiratory disease is characterized by recalcitrant sinusitis/polyposis, asthma and precipitation of asthma after ingestion of aspirin and most NSAIDs. Cross-reactions between ASA and NSAIDs occur with first exposure unlike IgE-mediated allergic drug reactions. Cross-reactions between aspirin and other drugs are dependent upon inhibition of the cyclooxygenase-1 isoenzyme. Desensitization to aspirin will result in cross-desensitization to all NSATDs that inhibit COX-1. Despite reports in the literature, there does not appear to he cross-reactions between food coloring, hydrocortisone succinate and monosodium glutamate in individuals with aspirin exacerbated respiratory disease. The new highly selective cyclooxygenase 2 inhibitors are well tolerated in AERD asthmatics who have not been desensitized to aspirin. Because low-dose ASA exerts a cardioprotective effect by irreversible inhibition of COX-1, AERD patients who are at risk for coronary artery disease should be considered for aspirin desensitization.

Publication types

  • Review

MeSH terms

  • Anti-Inflammatory Agents, Non-Steroidal / adverse effects*
  • Aspirin / adverse effects*
  • Cross Reactions / drug effects*
  • Cyclooxygenase 1
  • Cyclooxygenase 2
  • Cyclooxygenase 2 Inhibitors
  • Cyclooxygenase Inhibitors / adverse effects*
  • Drug Eruptions / enzymology
  • Drug Eruptions / etiology
  • Humans
  • Isoenzymes / drug effects
  • Membrane Proteins
  • Prostaglandin-Endoperoxide Synthases / drug effects
  • Respiratory Hypersensitivity / chemically induced
  • Respiratory Hypersensitivity / enzymology


  • Anti-Inflammatory Agents, Non-Steroidal
  • Cyclooxygenase 2 Inhibitors
  • Cyclooxygenase Inhibitors
  • Isoenzymes
  • Membrane Proteins
  • Cyclooxygenase 1
  • Cyclooxygenase 2
  • PTGS1 protein, human
  • PTGS2 protein, human
  • Prostaglandin-Endoperoxide Synthases
  • Aspirin