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The human leucocyte antigen-DRB1*1302-DQB1*0609-DPB1*0201 haplotype may be a strong genetic marker for aspirin-induced urticaria.

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dc.contributor.authorKim, SH-
dc.contributor.authorChoi, JH-
dc.contributor.authorLee, KW-
dc.contributor.authorShin, ES-
dc.contributor.authorOh, HB-
dc.contributor.authorSuh, CH-
dc.contributor.authorNahm, DH-
dc.contributor.authorPark, HS-
dc.date.accessioned2011-06-23T05:38:53Z-
dc.date.available2011-06-23T05:38:53Z-
dc.date.issued2005-
dc.identifier.issn0954-7894-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/3011-
dc.description.abstractBACKGROUND: Urticaria/angioedema is a common aspirin-induced allergy; however, its pathogenic mechanism is not understood.



OBJECTIVE: In order to uncover the genetic mechanism, we studied the associations of the human leucocyte antigen (HLA) genotypes in patients with aspirin-induced urticaria compared with aspirin-intolerant asthma and normal control in a Korean population.



METHODS: Ninety-four aspirin-induced urticaria patients presenting urticaria/angioedema-induced by both ASA and NSAID (50 had underlying chronic urticaria) and showing positive responses on oral aspirin challenge test, 76 aspirin-intolerant asthmatics with positive responses on lysine-aspirin bronchoprovocation test, and 185 normal healthy controls were enrolled. HLA-DRB1, DQB1, and DPB1 genotypings were performed by direct DNA sequencing analysis.



RESULTS: The allele frequencies of HLA-DRB1(*)1302 (18.1%) and HLA-DQB1(*)0609 (10.1%) in aspirin-induced urticaria were significantly higher than in aspirin-intolerant asthma (5.3%, P=0.0004; 2.0%, P=0.0024) and in normal controls (8.1%, P=0.0005; 3.2%, P=0.0008), and they remained significant after correcting for multiple comparisons. The patients with these two HLA markers had a significantly younger age than patients without, while no associations were found in with respect to atopic status, a history of previous allergic diseases, total IgE level, or presence of underlying chronic urticaria (P>0.05, respectively). In haplotype analysis, the HLA-DRB1(*)1302-DQB1(*)0609-DPB1(*)0201 was significantly higher in the aspirin-induced urticaria (8.0%) than in the aspirin-intolerant asthma (0.7%, P=0.0014) and normal controls (2.0%, P=0.0006).



CONCLUSION: These findings suggest that the HLA-DRB1(*)1302-DQB1(*)0609-DPB1(*)0201 may be a strong genetic marker to determine the aspirin-induced urticaria phenotype.
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dc.language.isoen-
dc.subject.MESHAdult-
dc.subject.MESHAlleles-
dc.subject.MESHAnti-Inflammatory Agents, Non-Steroidal-
dc.subject.MESHAspirin-
dc.subject.MESHCase-Control Studies-
dc.subject.MESHFemale-
dc.subject.MESHGenetic Markers-
dc.subject.MESHHLA-DP Antigens-
dc.subject.MESHHLA-DQ Antigens-
dc.subject.MESHHLA-DR Antigens-
dc.subject.MESHHaplotypes-
dc.subject.MESHHumans-
dc.subject.MESHKorea-
dc.subject.MESHMale-
dc.subject.MESHMiddle Aged-
dc.subject.MESHUrticaria-
dc.titleThe human leucocyte antigen-DRB1*1302-DQB1*0609-DPB1*0201 haplotype may be a strong genetic marker for aspirin-induced urticaria.-
dc.typeArticle-
dc.identifier.pmid15784113-
dc.identifier.urlhttp://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0954-7894&date=2005&volume=35&issue=3&spage=339-
dc.contributor.affiliatedAuthor김, 승현-
dc.contributor.affiliatedAuthor서, 창희-
dc.contributor.affiliatedAuthor남, 동호-
dc.contributor.affiliatedAuthor박, 해심-
dc.type.localJournal Papers-
dc.identifier.doi10.1111/j.1365-2222.2004.02197.x-
dc.citation.titleClinical and experimental allergy-
dc.citation.volume35-
dc.citation.number3-
dc.citation.date2005-
dc.citation.startPage339-
dc.citation.endPage344-
dc.identifier.bibliographicCitationClinical and experimental allergy, 35(3). : 339-344, 2005-
dc.identifier.eissn1365-2222-
dc.relation.journalidJ009547894-
Appears in Collections:
Journal Papers > Hospital > Clinical Trial Center
Journal Papers > School of Medicine / Graduate School of Medicine > Rheumatology
Journal Papers > School of Medicine / Graduate School of Medicine > Allergy
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