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Original Article


A Possible Association Between ZNRD1 and Aspirin-Induced Airway Bronchoconstriction in a Korean Population


CFA Pasaje,1,* JS Bae,1,* B-L Park,2 HS Cheong,2 A-S Jang,3 S-T Uh,4 M-K Kim,5 J-H Kim,1 T-J Park,1 J-S Lee,1 Y Kim,1 C-S Park,4 HD Shin1,2

1Department of Life Science, Sogang University, Seoul, Republic of Korea
2Department of Genetic Epidemiology, SNP Genetics, Inc., Seoul, Republic of Korea
3Division of Allergy and Respiratory Medicine, Soonchunhyang University Seoul Hospital, Seoul, Republic of Korea
4Genome Research Center for Allergy and Respiratory Diseases, Division of Allergy and Respiratory Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Republic of Korea
5Department of Internal Medicine, Chungbuk National University, College of Medicine, Cheongju, Republic of Korea
*Both authors contributed equally to the manuscript

J Investig Allergol Clin Immunol 2012; Vol. 22(3): 193-200



Background: The etiology of aspirin-exacerbated respiratory disease (AERD) has been attributed to the combination of environmental and genetic risk factors. Although widely investigated in various diseases associated with immune dysfunction, the human zinc ribbon domain containing 1 (ZNRD1) gene is thought to play a role in the pathogenesis of AERD by altering the mechanisms involved in disease development.

Methods: We selected 6 single-nucleotide polymorphisms (SNPs) for genotyping from the International HapMap database in order to analyze the association between polymorphisms in ZNRD1 and AERD in a Korean asthma cohort. Genotyping was carried out using the TaqMan assay, and differences in genotype frequency distributions were analyzed using logistic regression models.

Results: Nominal associations were found between ZNRD1 rs1150740 and risk of AERD via codominant and dominant genetic inheritance (P=.03; odds ratio, 1.14 [1.14-10.16]). The same polymorphism was found to be significantly associated with a decrease in forced expiratory volume in the first second of expiration, an important diagnostic marker of AERD, even after multiple testing corrections (P=.006, Pcorr=.03 in codominant and dominant models).

Conclusions: These preliminary fi ndings suggest a possible relationship between ZNRD1 and aspirin-induced respiratory dysfunctions in a Korean population and provide essential information on the etiology of AERD.

Key words: Aspirin exacerbated respiratory disease. FEV1. Haplotype. Single-nucleotide polymorphism. ZNRD1.