J Korean Med Sci.  2005 Jun;20(3):367-372. 10.3346/jkms.2005.20.3.367.

Polymorphisms of High-Affinity IgE Receptor and Histamine-Related Genes in Patients with ASA-Induced Urticaria/Angioedema

• Choi JH
• Kim SH
• Suh CH
• Nahm DH
• Park HS

• KMID: 1778491
• DOI: http://doi.org/10.3346/jkms.2005.20.3.367

Abstract

The pathogenic mechanism of ASA-induced urticaria/angioedema (AIU) is still poorly understood, but it has been known that histamine releasing by cutaneous mast cell activation is considered to be an important role. Considering the importance of histamine in AIU, we speculated that a genetic abnormality of histamine-related genes such as a high-affinity IgE receptor, a metabolic enzyme of histamines and histamine receptors, may be involved in the development of AIU. Enrolled in the study were 110 patients with AIU, 53 patients without ASA hypersensitivity who had various drug allergies presenting as exanthematous skin symptoms, and 99 normal healthy controls (NC). Eleven single nucleotide polymorphisms (SNPs) of the beta chain of the high-affinity IgE receptor (FCER1B) and three histamine-related genes-histamine N-methyltransferase (HNMT), histamine H1 receptor (HRH1), histamine H2 receptor (HRH2)-were screened using the SNP-IT assay based on a single base extension method. No significant differences were observed in allele and genotype frequencies, and haplotype frequencies of all the SNPs of FCER1B, HNMT, HRH1, and HRH2 among the three groups (p>0.05, respectively). These results suggest that the polymorphisms of FCER1B and the three histamine-related genes may not contribute to the development of AIU phenotype in the Korean population.

Keyword

Aspirin; Hypersensitivity; Urticaria; Polymorphism, Genetic

MeSH Terms

Adult
Alleles
Angioneurotic Edema/chemically induced/*genetics/metabolism
Aspirin
Female
Gene Frequency
Genotype
Haplotypes
Histamine/*metabolism
Histamine Release/genetics
Humans
Linkage Disequilibrium
Male
Middle Aged
*Polymorphism, Single Nucleotide
Receptors, IgE/*genetics
Research Support, Non-U.S. Gov't
Urticaria/chemically induced/*genetics/metabolism

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