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.

Highlights

  • Kawasaki is an acute systemic vasculitis that predominantly affects infants and young children

  • Kawasaki disease (KD) patients, but the difference was not significant (Figure 3, P > 0.05). This is the first study to examine the association between the resistin gene (RETN) −420 C > G polymorphism and the risk of KD

  • We investigated whether the RETN −420 C > G promoter polymorphism could be associated with the development of coronary artery lesions (CALs) in KD patients

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Summary

Introduction

Kawasaki is an acute systemic vasculitis that predominantly affects infants and young children. More than 40 years have passed since the first description of KD [4], no specific laboratory markers have been identified to date, and the diagnosis rests on the clinical findings. Some patients fail to meet all the criteria [2] for KD but are at risk for the development of coronary artery disease. These incomplete forms of KD (iKD) are being increasingly reported, no clear definition has been developed [2, 5]. In patients with iKD, the diagnosis is challenging and therapeutic decisions are difficult

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