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Genetic mechanism of aspirin-induced urticaria/angioedema.
DC Field | Value | Language |
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dc.contributor.author | Kim, SH | - |
dc.contributor.author | Ye, YM | - |
dc.contributor.author | Lee, SK | - |
dc.contributor.author | Park, HS | - |
dc.date.accessioned | 2011-03-31T05:48:13Z | - |
dc.date.available | 2011-03-31T05:48:13Z | - |
dc.date.issued | 2006 | - |
dc.identifier.issn | 1528-4050 | - |
dc.identifier.uri | http://repository.ajou.ac.kr/handle/201003/2099 | - |
dc.description.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. | - |
dc.language.iso | en | - |
dc.subject.MESH | Angioedema | - |
dc.subject.MESH | Aspirin | - |
dc.subject.MESH | Drug Hypersensitivity | - |
dc.subject.MESH | HLA-DQ Antigens | - |
dc.subject.MESH | HLA-DR Antigens | - |
dc.subject.MESH | Histamine | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Urticaria | - |
dc.title | Genetic mechanism of aspirin-induced urticaria/angioedema. | - |
dc.type | Article | - |
dc.identifier.pmid | 16825866 | - |
dc.identifier.url | http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=1528-4050&volume=6&issue=4&spage=266 | - |
dc.contributor.affiliatedAuthor | 김, 승현 | - |
dc.contributor.affiliatedAuthor | 예, 영민 | - |
dc.type.local | Journal Papers | - |
dc.identifier.doi | 10.1097/01.all.0000235899.57182.d4 | - |
dc.citation.title | Current opinion in allergy and clinical immunology | - |
dc.citation.volume | 6 | - |
dc.citation.number | 4 | - |
dc.citation.date | 2006 | - |
dc.citation.startPage | 266 | - |
dc.citation.endPage | 270 | - |
dc.identifier.bibliographicCitation | Current opinion in allergy and clinical immunology, 6(4). : 266-270, 2006 | - |
dc.identifier.eissn | 1473-6322 | - |
dc.relation.journalid | J015284050 | - |
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