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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
Author(s) -
Kim S.H.,
Choi J.H.,
Lee K.W.,
Kim S.H.,
Shin E.S.,
Oh H.B.,
Suh C.H.,
Nahm D.H.,
Park H.S.
Publication year - 2005
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/j.1365-2222.2004.02197.x
Subject(s) - aspirin , medicine , angioedema , human leukocyte antigen , asthma , immunology , population , allergy , haplotype , immunoglobulin e , antigen , genotype , gastroenterology , biology , antibody , genetics , environmental health , gene
Summary Background 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.