Wen-Hsien Lu1,2,3, Sin-Jhih Huang4, Yeong-Seng Yuh5, Kai-Sheng Hsieh6, Chia-Wan Tang7, Huei-Han Liou4, Luo-Ping Ger4,8. 1. Department of Pediatrics, Kaohsiung Veterans General Hospital, Kaohsiung. 2. National Yang-Ming University, Taipei. 3. Fooyin University. 4. Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung. 5. Department of Pediatrics, Cheng Hsin General Hospital, Taipei. 6. Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung. 7. Department of Pediatrics, Antai Medical Care Corporation Antai Tian-Sheng Memorial Hospital, Pingtung. 8. Institute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan.
Abstract
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND: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. METHODS: A total of 114 Kawasaki diseasechildren with coronary artery lesions and 185 Kawasaki diseasechildren without coronary artery lesions were recruited in this study. The TaqMan assay was conducted to identify the genotype in this case-control study. RESULTS: 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. CONCLUSIONS: The haplotype of platelet endothelial cell adhesion molecule-1Leu-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.
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