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What do we know about the genetics of aspirin intolerance?

Abstract
Although acetylsalicylic acid is prescribed for a broad range of diseases, it can induce a wide array of clinically recognized hypersensitivity reactions, including aspirin-intolerant asthma (AIA) with rhinitis and aspirin-intolerant urticaria (AIU) with anaphylaxis. Altered eicosanoid metabolism is the generally accepted mechanism of aspirin intolerance; the overproduction of cysteinyl leucotrienes has been suggested to play a causative role in both AIA and AIU. Genetic markers suggested for AIA include HLA-DPBI*0301, leucotriene C4 synthase (LTC4S), ALOX5, CYSLT, PGE2, TBXA2R and TBX21. Similarly, HLA-DB1*0609, ALOX5, FCER1A and HNMT have been identified as possible genetic markers for AIU. An additional low-risk genetic marker for AIA is MS4A2, which encodes the beta-chain of FCER1. Other single and sets of two or more interacting genetic markers are currently being investigated. Analyses of the genetic backgrounds of patients with AIA and AIU will promote the development of early diagnostic and therapeutic interventions, which may reduce the incidence of AIA and AIU.
AuthorsN S Palikhe, S-H Kim, H-S Park
JournalJournal of clinical pharmacy and therapeutics (J Clin Pharm Ther) Vol. 33 Issue 5 Pg. 465-72 (Oct 2008) ISSN: 1365-2710 [Electronic] England
PMID18834360 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Chemical References
  • Anti-Inflammatory Agents, Non-Steroidal
  • Genetic Markers
  • Aspirin
Topics
  • Anti-Inflammatory Agents, Non-Steroidal (adverse effects)
  • Aspirin (adverse effects)
  • Asthma (chemically induced, genetics)
  • Drug Hypersensitivity (etiology, genetics)
  • Genetic Markers
  • Humans
  • Polymorphism, Single Nucleotide
  • Urticaria (chemically induced, genetics)

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