Lu Wen-Hsien, Huang Sin-Jhih, Yuh Yeong-Seng, Hsieh Kai-Sheng, Tang Chia-Wan, Liou Huei-Han, Ger Luo-Ping
Department of Pediatrics, Kaohsiung Veterans General Hospital, Kaohsiung.
National Yang-Ming University, Taipei.
Acta Cardiol Sin. 2017 May;33(3):273-284. doi: 10.6515/acs20161010a.
Kawasaki disease is the most common cause of pediatric acquired heart disease. The role of platelet endothelial cell adhesion molecule-1 in the inflammatory process has been documented. To date, no report has investigated the relationship between coronary artery lesions of Kawasaki disease and platelet endothelial cell adhesion molecule-1 polymorphisms.
A total of 114 Kawasaki disease children with coronary artery lesions and 185 Kawasaki disease children without coronary artery lesions were recruited in this study. The TaqMan assay was conducted to identify the genotype in this case-control study.
In three single nucleotide polymorphisms (Leu125Val, Ser563Asn, and Arg670Gly) of platelet endothelial cell adhesion molecule-1, we found that the Leu-Ser-Arg haplotype was associated with a significantly increased risk for coronary artery lesions in the chronic stage (odds ratio 3.05, 95% confidence interval 1.06-8.80, p = 0.039), but not for coronary artery lesions in the acute stage. Analysis based on the diplotypes of platelet endothelial cell adhesion molecule-1 also showed that Kawasaki disease with one or two alleles of Leu-Ser-Arg had a significantly increased risk of chronic coronary artery lesions (odds ratio 3.38, 95% confidence interval 1.11-10.28, p = 0.032) and had increased platelet counts after Kawasaki disease was diagnosed, as compared to those with other diplotypes.
The haplotype of platelet endothelial cell adhesion molecule-1 Leu-Ser-Arg might be associated with the increased platelet counts and the following risk of chronic coronary artery lesions in a dominant manner in Kawasaki disease.
川崎病是儿童获得性心脏病最常见的病因。血小板内皮细胞黏附分子-1在炎症过程中的作用已有文献记载。迄今为止，尚无报告研究川崎病冠状动脉病变与血小板内皮细胞黏附分子-1基因多态性之间的关系。
本研究招募了114例患有冠状动脉病变的川崎病患儿和185例无冠状动脉病变的川崎病患儿。在这项病例对照研究中采用TaqMan分析法确定基因型。
在血小板内皮细胞黏附分子-1的三个单核苷酸多态性（Leu125Val、Ser563Asn和Arg670Gly）中，我们发现Leu-Ser-Arg单倍型与慢性期冠状动脉病变风险显著增加相关（比值比3.05，95%置信区间1.06 - 8.80，p = 0.039），但与急性期冠状动脉病变无关。基于血小板内皮细胞黏附分子-1双倍型的分析还表明，与其他双倍型相比，具有一个或两个Leu-Ser-Arg等位基因的川崎病患儿慢性冠状动脉病变风险显著增加（比值比3.38，95%置信区间1.11 - 10.28，p = 0.032），且在川崎病确诊后血小板计数升高。
血小板内皮细胞黏附分子-1的Leu-Ser-Arg单倍型可能以显性方式与川崎病血小板计数增加及随后的慢性冠状动脉病变风险增加相关。
