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Association of TNF-alpha promoter polymorphisms with aspirin-induced urticaria.

Authors :
Choi JH
Kim SH
Cho BY
Lee SK
Suh CH
Park HS
Source :
Journal of Clinical Pharmacy & Therapeutics; Apr2009, Vol. 34 Issue 2, p231-238, 8p
Publication Year :
2009

Abstract

OBJECTIVE: Although the pathogenesis of aspirin-induced urticaria (AIU) is not fully understood, mast cell activation has been noted in patients with AIU. Tumour necrosis factor (TNF)-alpha, a potent pro-inflammatory cytokine, is released by human skin mast cells and other inflammatory cells in patients with urticaria. To investigate the role of TNF-alpha promoter polymorphisms in the development of AIU, we performed an association study of TNF-alpha promoter polymorphisms with AIU phenotype. METHODS: Two hundred thirty-nine patients with AIU consisting of 120 patients with aspirin intolerant chronic urticaria (AICU) and 119 with aspirin-intolerant acute urticaria (AIAU), and 524 normal controls were enrolled. AIU was confirmed by oral aspirin challenge test. Five SNPs in the TNF-alpha gene (-1031T>C, -863C>A, -857C>T, -308G>A, -238G>A) were genotyped by a single-base extension method. Haplotype analyses were done. RESULTS: The genotype frequencies of TNF-1031T>C and TNF-863C>A were significantly higher in the AIU patients than in the normal controls in both co-dominant (P = 0.014, P = 0.007) and dominant (P = 0.007, P = 0.004) models. The frequency of TNF-ht2[CACGG] containing a genotype in the AIU group was significantly higher in the normal controls with both co-dominant (P = 0.004, Pc = 0.02) and dominant models (P = 0.002, Pc = 0.01). CONCLUSIONS: These findings suggest that the two promoter polymorphisms of TNF-alpha at -1031T>C and -863C>A may contribute to the development of AIU. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
02694727
Volume :
34
Issue :
2
Database :
Complementary Index
Journal :
Journal of Clinical Pharmacy & Therapeutics
Publication Type :
Academic Journal
Accession number :
105470505
Full Text :
https://doi.org/10.1111/j.1365-2710.2008.00979.x