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Genetic mechanism of aspirin-induced urticaria/angioedema.

Authors
Kim, SH; Ye, YM; Lee, SK; Park, HS
Citation
Current opinion in allergy and clinical immunology, 6(4):266-270, 2006
Journal Title
Current opinion in allergy and clinical immunology
ISSN
1528-40501473-6322
Abstract
PURPOSE OF REVIEW: Aspirin-induced urticaria/angioedema is a major aspirin-related hypersensitivity often associated with aspirin-intolerant asthma. Genetic studies on aspirin-intolerant asthma have shown chronic overproduction of cysteinyl leukotrienes. The genetic analysis of aspirin-induced urticaria/angioedema is limited, however.



RECENT FINDINGS: A recent study on HLA genotypes has suggested that the HLA alleles DRB11302 and DQB10609 may be genetic markers for aspirin-induced urticaria/angioedema. A polymorphism study that examined nine single-nucleotide polymorphisms of five leukotriene-related genes [ALOX5 (encoding 5-lipoxygenase), ALOX5AP (5-lipoxygenase-activating protein), PTGS2 (cyclooxygenase 2), LTC4S (leukotriene C4 synthase), and CYSLTR1 (cysteinyl leukotriene receptor 1)] found that promoter polymorphisms of ALOX5 (-1708A>G) and CYSLTR1 (-634C>T) were significantly different between aspirin-intolerant asthma and aspirin-induced urticaria/angioedema, suggesting different contributions to the lipoxygenase pathway. A second polymorphism study, conducted on histamine-related genes, did not find any significant associations with aspirin-induced urticaria/angioedema for the genes HNMT (encoding histamine N-methyltransferase), HRH1 or HRH2 (encoding histamine receptor types 1 and 2 respectively), or the gene encoding high-affinity IgE receptor Ibeta (FcepsilonRIbeta); however, the FcepsilonRIalpha gene promoter polymorphism was significantly associated with aspirin-induced urticaria/angioedema. This finding has been supported by in vitro functional studies.



SUMMARY: The HLA alleles DRB11302 and DQB10609, and the ALOX5 and FcepsilonRIalpha promoter polymorphisms, may contribute to the pathogenesis of aspirin-induced urticaria/angioedema. Further investigation to identify candidate genetic markers would help to elucidate the pathogenic mechanism of this condition.
MeSH terms
Angioedema/bloodAngioedema/chemically induced*Angioedema/genetics*Angioedema/immunologyAspirin/adverse effects*Drug Hypersensitivity/etiologyDrug Hypersensitivity/genetics*Drug Hypersensitivity/immunologyHLA-DQ Antigens/geneticsHLA-DQ Antigens/immunologyHLA-DR Antigens/geneticsHLA-DR Antigens/immunologyHistamine/geneticsHistamine/immunologyHumansUrticaria/chemically induced*Urticaria/genetics*Urticaria/immunologyUrticaria/microbiology
DOI
10.1097/01.all.0000235899.57182.d4
PMID
16825866
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Allergy
Journal Papers > Research Organization > Regional Clinical Trial Center
AJOU Authors
김, 승현예, 영민
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