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| Changes of plasma thrombospondin-1 and platelet activating factor in Kawasaki disease and their clinical significance |
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WANG Yang-ji, SHI Wei-qun, WANG Qian, WANG Yan, Lu Jin-quan |
（Department of Pediatrics， Affiliated Hospital of Jiangsu University, Zhenjiang Jiangsu 212001, China） |
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Abstract Objective: To investigate the level and significance of plasma thrombospondin1(TSP1) and the platelet activating factor(PAF) in children with Kawasaki disease (KD). Methods: A total of 53 children with KD were enrolled in this study, including 32 children with coronary artery lesion(CAL) and 21 children with non coronary artery lesion (NCAL).The level of plasma TSP1 and PAF was detected by ELISA assay. Twenty normal children were collected as the control group. Results: Plasma TSP1 in acute phase of KD group increased significantly than that of the control group and the convalescence of KD group(P＜0.05)，while there was no difference between the convalescence of KD group and the control group(P>0.05).Compared with the control group, the level of plasma PAF increased obviously both in acute phase of KD group and in the convalescence of KD group(P＜0.05).The level of plasma PAF in CAL group was significantly higher than that of NCAL group(P<0.05) during the acute phase group. Conclusion: The content of plasma TSP1 and PAF were associated with inflammation of KD in acute stage. The level of plasma PAF may be a biochemical index to predict the early coronary artery lesion in KD.
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Received: 22 January 2018
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| ［1］Kuo HC, Li SC, Guo MM, et al. Genomewide association study identifies novel susceptibility genes associated with coronary artery aneurysm formation in Kawasaki disease\[J\]. PLoS One, 2016, 11(5): e0154943.［2］Yeter D, Portman MA, Aschner M, et al. Ethnic Kawasaki disease risk associated with blood mercury and cadmium in U.S. children\[J\]. Int J Environ Res Public Health, 2016, 13(1) pii: E101: 101-104.［3］McCrindle BW, Rowley AH, Newburger JW, et al. Diagnosis, treatment, and longterm management of Kawasaki disease: a scientific statement for health professionals from the American Heart Association\[J\]. Circulcation，2017, 135(17): e927-999.［4］Kuwabara M, Yashiro M, Kotani K, et al. Cardiac lesions and initial laboratory data in Kawasaki disease: a nationwide survey in Japan\[J\]. J Epidemiol, 2015, 25(3): 189-193.［5］Dietz SM, Van Stijn D, Burgner D, et al. Dissecting Kawasaki disease: a stateoftheart review\[J\]. Eur J Pediatr, 2017, 176: 995-1009.［6］LopezDee Z,Pidcock K,Gutierrez LS.Thrombospondin1: multiple paths to inflammation\[J\]. Mediators Inflamm, 2011, 2011:296069.［7］Liu Z, Morgan S, Ren J, et al. Thrombospondin1 (TSP1) contributes to the development of vascular inflammation by regulating monocytic cell motility in mouse models of abdominal aortic aneurysm\[J\]. Circ Res, 2015, 117(2): 129-141.［8］Miller TW, Kaur S, IvinsO′Keefe K, et al. Thrombospondin1 is a CD47dependent endogenous inhibitor of hydrogen sulfide signaling in T cell activation\[J\]. Matrix Biol, 2013, 32(6): 316-324.［9］Suthar R, Singh S, Bhalla AK, et al. Pattern of subcutaneous fat during followup of a cohort of North Indian children with Kawasaki disease: a preliminary study\[J\]. Int J Rheum Dis, 2014, 17(3): 304-312.［10］Verouti SN, Fragopoulou E, Karantonis HC, et al. PAF effects on MCP1 and IL6 secretion in U937 monocytes in comparison with oxLDL and IL1β effects\[J\]. Atherosclerosis, 2011, 219(2): 519-525.［11］Vadas P. The plateletactivating factor pathway in food allergy and anaphylaxis\[J\]. Ann Allergy Asthma Immunol, 2016, 117(5): 455-457.［12］Kelesidis T, Papakonstantinou V, Detopoulou P, et al. The role of plateletactivating factor in chronic inflammation, immune activation, and comorbidities associated with HIV infection\[J\]. AIDS Rev, 2015, 17(4): 191-201.［13］Harayama T, Shindou H, Ogasawara R, et al. Identification of a novel noninflammatory biosynthetic pathway of plateletactivating factor\[J\]. J Biol Chem, 2008, 283(17): 11097-11106. |
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2018, Vol. 28 
