Kun Lin,1,2,* Linyuan Zhang,1,2,* Yishuai Wang,1– 3,* Jinqing Li,1 Yufen Xu,1 Di Che,1 Hanran Mai,4 Hongyan Yu,1 Lanyan Fu,1 Bing Wei,2 Zhiyong Jiang,2 Lei Pi,1 Xiaoqiong Gu1,2 1Department of Clinical Biological Resource Bank, Guangzhou Institute of Pediatrics, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou, Guangdong, 510623, People’s Republic of China; 2Department of Blood Transfusion and Clinical Lab, Guangzhou Institute of Pediatrics, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou, Guangdong, 510623, People’s Republic of China; 3School of Medicine, South China University of Technology, Guangzhou, Guangdong, 510006, People’s Republic of China; 4Department of Andrology, Guangzhou Women and Children’s Medical Center. Guangzhou Medical University, Guangzhou, Guangdong, 510623, People’s Republic of China*These authors contributed equally to this workCorrespondence: Xiaoqiong Gu; Lei Pi Email guxiaoqiong@gwcmc.org; pilei@gwcmc.orgBackground: A large number of studies demonstrated that the key to the occurrence and development of Kawasaki disease (KD) is the over-activation of immune cells and the generation of various inflammatory factors, leading to the imbalance of the immune system. Recently, mutations in the FNDC1 gene have been shown to be associated with inflammatory responses. However, there have been no reports on the relationship between FNDC1 gene and KD so far.Methods: We enrolled 1611 controls and 1459 patients with KD, including 372 patients with coronary artery aneurysm (CAA) and 179 patients with coronary artery lesion (CAL). The relationship between FNDC1 rs3003174 polymorphism and KD with CAA or without CAA was investigated.Results: This study showed no evidence that the association between FNDC1 rs3003174 C>T polymorphism and KD susceptibility was statistically significant (CT versus CC: adjusted odds ratio (OR) =0.897, 95% confidence interval (CI) =0.769– 1.045, P=0.162; TT versus CC: adjusted OR=0.995, 95% CI=0.786– 1.260, P=0.968; dominant model: adjusted OR=0.916, 95% CI=0.792– 1.059, P=0.235; and recessive model: adjusted OR=1.055, 95% CI=0.845– 1.316, P=0.638). However, our further stratified analysis in the control and KD group bore out that the incidence of TT genotype of FNDC1 rs3003174 C > T polymorphism was higher than that of CC/CT genotype in KD patients stratified by CAA (adjusted OR=1.437, 95% CI=1.034– 1.996, P=0.031). Moreover, a stratified analysis of age and gender in KD patients indicated that the rs3003174 TT genotype increased the risk of CAA formation in aged ≦60 months (CC/CT vs TT: adjusted OR=1.580, 95% CI=1.106– 2.259, P=0.012) and male (CC/CT vs TT: adjusted OR=1.653, 95% CI=1.101– 2.481, P=0.015) KD patients.Conclusion: The results of this study demonstrated that the FNDC1 rs3003174 C>T polymorphism may be a hazard factor in the formation of CAA in KD patients that was not disclosed before.Keywords: coronary artery aneurysm, Kawasaki disease, fibronectin type III domain containing 1, polymorphisms
