Pathogenesis, diagnosis, and treatment of aspirin intolerance

Ann Allergy Asthma Immunol. 2007 Jul;99(1):13-21. doi: 10.1016/S1081-1206(10)60615-1.

Abstract

Objectives: To provide an overview of aspirin intolerance (AI), to summarize the latest genetic and pathophysiologic findings, and to discuss the current therapeutic recommendations, including aspirin desensitization.

Data sources: Using the PubMed database, a systematic search of articles published between 1968 and 2006 was performed to evaluate the current literature on AI. The bibliographies of selected articles served as a source of additional literature.

Study selection: Included articles were selected for their relevance to the pathogenesis, diagnosis, and management of AI.

Results: The prevalence of AI is approximately 0.3% to 0.9%, but AI is often overlooked. It can display a wide range of clinical pictures, such as acute asthma attacks, urticaria, angioedema, chronic rhinitis, myocardial ischemia, and anaphylactic shock. Regarding the pathogenesis of AI, modifications of eicosanoid metabolism are supposed to underlie AI, including aspirin-induced asthma and aspirin-induced urticaria. However, the pathogenesis of AI has not yet been clearly elucidated. Associations of several HLA alleles with subtypes of AI, such as aspirin-induced urticaria and aspirin-induced asthma, and single nucleotide polymorphisms in genes encoding enzymes involved in arachidonic acid metabolism have been shown.

Conclusions: Because aspirin therapy should be avoided in AI patients, the use of alternative drugs is recommended. Patients intolerant of alternative drugs and those with therapy-resistant asthma or sinusitis benefit from aspirin desensitization.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Anti-Inflammatory Agents, Non-Steroidal / adverse effects
  • Aspirin / adverse effects*
  • Desensitization, Immunologic / methods
  • Diagnostic Techniques and Procedures
  • Drug Hypersensitivity / diagnosis*
  • Drug Hypersensitivity / etiology
  • Drug Hypersensitivity / therapy*
  • Humans
  • Models, Biological

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Aspirin