The Relationship Between Kawasaki Disease With/Without Coronary Artery Lesion And SFractalkine

Objectives:To explore the pathogenesis of Kawasaki Disease(KD) and the relationship between KD with/without Coronary Artery lesion(CAL) and sFractalkine.Methods:According to the latest standard of diagnosis,thirty-four cases of children who were diagnosed with KD in the Children’s Hospital of Shanxi Province during the period between Mar. and Dec. 2014 were selected.They were classified into two groups based on the course of disease:the acute group(from the fitst day to the eleventh day of the course of the disease) and the subacute group(from the twelfth day to the twenty-first day of the course of the disease).They were divided into two groups by the damage of heart during the acute period:one was with CAL,the other was without CAL.Twenty healthy children who had medical examination over the same period in the Children’s Hospital of Shanxi Province were chosen as the healthy control group.The plasma concentration of sFractalkine in the research objects were determined with the aid of double antibody sandwich enzyme-linked immunosorbent assay(ABC-ELISA) method.Judge the damage of the coronary artery based on the results of UCG by the diameter of coronary artery.And choose the diameter of coronary artery as the criterion of the danmage of the coronary artery.At the same time,record the correlative clinical data.Results:1.Quantitative detections show that the plasma concentration of sFractalkine in theKD group is higher than that in the healthy control group(t=8.26,P<0.05);the plasma concentration of sFractalkine in the acute group is higher than that in the subacute group(t=2.51,P<0.05);the plasma concentration of sFKN of the CAL group is higher than the NCAL group(t=12.59,P<0.05).2.The correlation analysis shows that the plasma concentration of sFKN in KD is correlated with ESR and CRP(r=0.63,P<0.05;r=0.74,P<0.05),which is also correlated with the diameter of coronary artery(D)(r=0.66,P<0.05).Conclusions:The sFKN may partake the pathogenesis of KD and promote the formation of CAL.