SummaryBackground 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 aspirinintolerant 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 5 0.0004; 2.0%, P 5 0.0024) and in normal controls (8.1%, P 5 0.0005; 3.2%, P 5 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 (P40.05, 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 5 0.0014) and normal controls (2.0%, P 5 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.
Background: There has been no study for evaluating the associations of human leukocyte antigen (HLA) class I and II alleles with toluene diisocyanate (TDI)‐induced asthma in an Asian population. Objective: The aim of this study was to investigate a susceptible or protective marker of HLA class I and II alleles in TDI‐induced asthma. Methods: Fifty‐five patients with TDI‐induced asthma patients (group I) showing positive responses on TDI bronchoprovocation test, 47 asymptomatic exposed subjects (group II) and 95 unexposed healthy nonatopic controls (group III) were enrolled in our study. HLA class I and II genotyping was done by the direct DNA sequencing method. Results: The allelic frequency of C*09 (15.5%) was significantly higher in group I than in group III (6.8%, P = 0.019), but this statistical significance disappeared after correction was made for multiple comparisons. On two‐locus and three‐locus haplotype analysis, the allelic frequency of HLA DRB1*15‐DPB1*05 in group I (10.6%) was significantly higher than that of group II (0%, P = 0.001) and group III (2.5%, P = 0.003). The allelic frequencies of HLA A*02‐DRB1*15, A*02‐DQB1*06, B*62‐C*09 and A*02‐DRB1*15‐DQB1*06 were significantly higher in group I (8.5%, 10.3%, 8.2% and 6.8%, respectively) than those allelic frequencies of group III (1.3%, P = 0.002; 1.6%, P = 0.001; 0.6%, P < 0.0001; 0%, P < 0.0001, respectively). The allelic frequencies of HLA DQB1*06‐DPB1*05 and DRB1*15‐DQB1*06‐DPB1*05 were significantly higher in group I (16.0% and 10.5%) than those in group II (2.5%, P = 0.001; 0%, P = 0.001), while the frequencies of DRB1*09‐DPB1*05 and DRB1*09‐DQB1*0303‐DPB1*05 were significantly lower in group I (0% and 0%) than those of group II (7.4%, P = 0.004; 7.5%, P = 0.004). These differences remained statistically significant even after the correction for multiple comparisons. Conclusions: The HLA haplotype DRB1*15‐DPB1*05 can be a susceptibility gene marker for the development of TDI‐induced asthma among the exposed workers in the Korean population.
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