Correlation between ADAMTS13 and Kawasaki Disease
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Background The pathogenesis of kawasaki disease (KD) remains unclear, and its diagnosis lacks specific biomarkers. This research investigated changes in the antigen level of A disintegrin-like and metalloprotease with thrombospondin type 1 motif 13 (ADAMTS13), during the acute phase of KD, analyzing its correlation with markers of neutrophil extracellular traps (NETs). The aim was to explore the pathogenesis of KD and evaluate the predictive value of ADAMTS13 for KD and its complications. Methods This is a prospective study. 60 children with KD were selected as the KD group and further subdivided based on clinical type and complications. 60 children with infectious fever and 60 healthy children were randomly selected as the febrile control (FC) group and healthy control (HC) group, respectively. Clinical data were collected. Enzyme-lLinked immunosorbent assay (ELISA) was used to measure plasma levels of ADAMTS13 antigen and NETs markers [myeloperoxidase (MPO), neutrophil Elastase (NE), and citrullinated histone H3 (CitH 3 )]. Differences between groups were compared, and the correlation between ADAMTS13 and NETs markers was analyzed. Logistic regression analysis and receiver operating characteristic (ROC) curves were employed to assess their predictive efficacy for KD and KD complicated by hepatic dysfunction (HD). Results The ADAMTS13 antigen level in the KD group was significantly lower than in the FC and HC groups (p < 0.05), showing a negative correlation with Interleukin-6 (IL-6), NE, CitH 3 , and transaminase levels. ADAMTS13 levels increased at discharge compared to admission. Logistic regression indicated that decreased ADAMTS13 antigen level was an independent risk factor for both KD (OR = 0.939, p = 0.004) and KD complicated by HD (OR = 0.619, p = 0.002). ROC curve analysis showed the AUC for ADAMTS13 predicting KD complicated by HD was 0.863. The optimal cut-off value was 6.36 µg/mL, with a sensitivity of 70.8% and specificity of 91.7%. Conclusion ADAMTS13 may be involved in the inflammatory regulation of KD through interaction with NETs. ADAMTS 13 is conducive to the differential diagnosis between KD and infectious febrile diseases, and it can serve as a biomarker for predicting KD complicated by HD.