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What do we know about the genetics of aspirin intolerance?

Authors
Palikhe, NS; Kim, SH; Park, HS
Citation
Journal of clinical pharmacy and therapeutics, 33(5):465-472, 2008
Journal Title
Journal of clinical pharmacy and therapeutics
ISSN
0269-47271365-2710
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.
MeSH terms
Anti-Inflammatory Agents, Non-Steroidal/adverse effects*Aspirin/adverse effects*Asthma/chemically inducedAsthma/geneticsDrug Hypersensitivity/etiologyDrug Hypersensitivity/genetics*Genetic MarkersHumansPolymorphism, Single NucleotideUrticaria/chemically inducedUrticaria/genetics
DOI
10.1111/j.1365-2710.2008.00961.x
PMID
18834360
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Allergy
Journal Papers > Research Organization > Regional Clinical Trial Center
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