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

S. H. Kim, J. H. Choi, K. W. Lee, Sangha Kim, E. S. Shin, H. B. Oh, C. H. Suh, D. H. Nahm, Haem Sim Park

Research output: Contribution to journalArticle

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Abstract

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.

Original languageEnglish
Pages (from-to)339-344
Number of pages6
JournalClinical and Experimental Allergy
Volume35
Issue number3
DOIs
Publication statusPublished - 2005 Mar 1

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Urticaria
HLA Antigens
Genetic Markers
Haplotypes
Aspirin
Angioedema
Asthma
Non-Steroidal Anti-Inflammatory Agents
DNA Sequence Analysis
Gene Frequency
Immunoglobulin E
Hypersensitivity
Genotype
Phenotype

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

Cite this

Kim, S. H. ; Choi, J. H. ; Lee, K. W. ; Kim, Sangha ; Shin, E. S. ; Oh, H. B. ; Suh, C. H. ; Nahm, D. H. ; Park, Haem Sim. / The human leucocyte antigen-DRB1*1302-DQB1*0609-DPB1*0201 haplotype may be a strong genetic marker for aspirin-induced urticaria. In: Clinical and Experimental Allergy. 2005 ; Vol. 35, No. 3. pp. 339-344.
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title = "The human leucocyte antigen-DRB1*1302-DQB1*0609-DPB1*0201 haplotype may be a strong genetic marker for aspirin-induced urticaria",
abstract = "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.",
author = "Kim, {S. H.} and Choi, {J. H.} and Lee, {K. W.} and Sangha Kim and Shin, {E. S.} and Oh, {H. B.} and Suh, {C. H.} and Nahm, {D. H.} and Park, {Haem Sim}",
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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. / Kim, S. H.; Choi, J. H.; Lee, K. W.; Kim, Sangha; Shin, E. S.; Oh, H. B.; Suh, C. H.; Nahm, D. H.; Park, Haem Sim.

In: Clinical and Experimental Allergy, Vol. 35, No. 3, 01.03.2005, p. 339-344.

Research output: Contribution to journalArticle

TY - JOUR

T1 - The human leucocyte antigen-DRB1*1302-DQB1*0609-DPB1*0201 haplotype may be a strong genetic marker for aspirin-induced urticaria

AU - Kim, S. H.

AU - Choi, J. H.

AU - Lee, K. W.

AU - Kim, Sangha

AU - Shin, E. S.

AU - Oh, H. B.

AU - Suh, C. H.

AU - Nahm, D. H.

AU - Park, Haem Sim

PY - 2005/3/1

Y1 - 2005/3/1

N2 - 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.

AB - 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.

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