Association of the Resistin Gene Promoter Region Polymorphism with Kawasaki Disease in Chinese Children. (8th April 2012)

• Record Type: Journal Article
• Authors: Liu, Ruixi; He, Bo; Gao, Fang; Liu, Qian; Yi, Qijian
• Other Names: Fantuzzi Giamila Academic Editor.
• Is Part Of: Mediators of inflammation. Volume 2012(2012)
• Publication Date: 2012-04-08
• Subjects: Inflammation -- Mediators -- Periodicals; Biological response modifiers -- Periodicals; Inflammation (Pathologie) -- Médiateurs; Immunomodulateurs; Biological response modifiers; Inflammation -- Mediators; Immunology; Autacoids; Immunologic Factors; Cell Adhesion Molecules; Cell Communication; Cytokines; Inflammation; Periodicals; Electronic journals; 616.0473
• DOI: 10.1155/2012/356362
• Languages: English
• ISSNs: 0962-9351

Abstract

Abstract : Objectives . The − 420 C > G polymorphism located in the resistin gene (RETN) promoter has recently been suggested to play a potential role in proinflammatory conditions and cardiovascular disease. This study investigated the association of the RETN promoter polymorphism with Kawasaki disease (KD) and its clinical parameters in Chinese children. Methods . We compared patients with complete KD to incomplete KD children. Genotyping of the RETN promoter polymorphism was performed using MassARRAY system, and serum resistin levels were estimated using the sandwich enzyme immunoassay method. Results . There was no significant difference in RETN (− 420 C > G ) genotypes between KD and control groups. However, the frequency of the G allele was higher in iKD patients than in cKD children due to a significantly increased frequency of the GG genotypes. Serum levels of resistin were significantly higher in KD patients than in controls regardless of the presence of coronary artery lesions (CALs). Conclusion . The present findings suggest that while resistin may play a role in the pathogenesis of KD, there is no apparent association between CAL and the RETN (− 420 C > G ) gene polymorphism in KD children. However, the diagnosis of iKD is challenging but can be supported by the presence of the G allele and the GG genotypes.