{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T15:56:58Z","timestamp":1790006218109,"version":"4.0.1"},"reference-count":20,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2005,3,21]],"date-time":"2005-03-21T00:00:00Z","timestamp":1111363200000},"content-version":"vor","delay-in-days":20,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Experimental Allergy"],"published-print":{"date-parts":[[2005,3]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p><jats:bold>Background\n\t\t\t\t\t<\/jats:bold> Urticaria\/angioedema is a common aspirin\u2010induced allergy; however, its pathogenic mechanism is not understood.<\/jats:p><jats:p><jats:bold>Objective\n\t\t\t\t\t<\/jats:bold> In order to uncover the genetic mechanism, we studied the associations of the human leucocyte antigen (HLA) genotypes in patients with aspirin\u2010induced urticaria compared with aspirin\u2010intolerant asthma and normal control in a Korean population.<\/jats:p><jats:p><jats:bold>Methods\n\t\t\t\t\t<\/jats:bold> Ninety\u2010four aspirin\u2010induced urticaria patients presenting urticaria\/angioedema\u2010induced by both ASA and NSAID (50 had underlying chronic urticaria) and showing positive responses on oral aspirin challenge test, 76 aspirin\u2010intolerant asthmatics with positive responses on lysine\u2013aspirin bronchoprovocation test, and 185 normal healthy controls were enrolled. HLA\u2010DRB1, DQB1, and DPB1 genotypings were performed by direct DNA sequencing analysis.<\/jats:p><jats:p><jats:bold>Results\n\t\t\t\t\t<\/jats:bold> The allele frequencies of HLA\u2010DRB1<jats:sup>*<\/jats:sup>1302 (18.1%) and HLA\u2010DQB1<jats:sup>*<\/jats:sup>0609 (10.1%) in aspirin\u2010induced urticaria were significantly higher than in aspirin\u2010intolerant asthma (5.3%, <jats:italic>P<\/jats:italic>=0.0004; 2.0%, <jats:italic>P<\/jats:italic>=0.0024) and in normal controls (8.1%, <jats:italic>P<\/jats:italic>=0.0005; 3.2%, <jats:italic>P=<\/jats:italic>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 (<jats:italic>P<\/jats:italic>&gt;0.05, respectively). In haplotype analysis, the HLA\u2010DRB1<jats:sup>*<\/jats:sup>1302\u2010DQB1<jats:sup>*<\/jats:sup>0609\u2010DPB1<jats:sup>*<\/jats:sup>0201 was significantly higher in the aspirin\u2010induced urticaria (8.0%) than in the aspirin\u2010intolerant asthma (0.7%, <jats:italic>P<\/jats:italic>=0.0014) and normal controls (2.0%, <jats:italic>P<\/jats:italic>=0.0006).<\/jats:p><jats:p><jats:bold>Conclusion\n\t\t\t\t\t<\/jats:bold> These findings suggest that the HLA\u2010DRB1<jats:sup>*<\/jats:sup>1302\u2010DQB1<jats:sup>*<\/jats:sup>0609\u2010DPB1<jats:sup>*<\/jats:sup>0201 may be a strong genetic marker to determine the aspirin\u2010induced urticaria phenotype.<\/jats:p>","DOI":"10.1111\/j.1365-2222.2004.02197.x","type":"journal-article","created":{"date-parts":[[2005,3,21]],"date-time":"2005-03-21T22:25:09Z","timestamp":1111443909000},"page":"339-344","source":"Crossref","is-referenced-by-count":67,"title":["The human leucocyte antigen\u2010DRB1<sup>*<\/sup>1302\u2010DQB1<sup>*<\/sup>0609\u2010DPB1<sup>*<\/sup>0201 haplotype may be a strong genetic marker for aspirin\u2010induced urticaria"],"prefix":"10.1111","volume":"35","author":[{"given":"S.\u2010H.","family":"Kim","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.\u2010H.","family":"Choi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K.\u2010W.","family":"Lee","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S.\u2010H.","family":"Kim","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E.\u2010S.","family":"Shin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H.\u2010B.","family":"Oh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C.\u2010H.","family":"Suh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D.\u2010H.","family":"Nahm","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H.\u2010S.","family":"Park","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2005,3,21]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/0091-6749(84)90115-5"},{"key":"e_1_2_6_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/0021-8707(67)90076-7"},{"key":"e_1_2_6_4_2","doi-asserted-by":"publisher","DOI":"10.1385\/CRIAI:24:2:125"},{"key":"e_1_2_6_5_2","doi-asserted-by":"crossref","first-page":"588","DOI":"10.1183\/09031936.93.03050588","article-title":"The 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