Abstract
Background and objective: Soluble ST2 (sST2), an interleukin (IL)-1 receptor family member, has been identified as a novel biomarker for cardiac stress. Although sST2 were reported to be elevated in acute Kawasaki disease (KD) and correlated with cardiac diastolic dysfunction, relation between sST2 levels and treatment resistance and risk of coronary artery abnormalities (CAAs) is not studied. The aim of this study is to evaluate clinical utility of sST2 in acute KD. Methods: We measured serum sST2 from 54 children (median age; 22 months, 29 boys and 26 girls) with acute KD before and after initial treatment, 10 febrile controls (FC) (median age; 14 months) and 2 healthy controls (HC). Using Kobayashi score from RAISE study, patients were divided into high (>score 5)and low risk group (≤score 4) for IVIG resistance. Results: Serum sST2 in KD significantly elevated compared with FC and HC (median; KD vs FC 0.81 vs 0.25 ng/ml, p<0.05, KD vs HC 0.81 vs 0.12 ng/ml, respectively, p<0.05). Compared with sST2 levels before treatment, sST2 decreased at 4 days after initial therapy, but it was not significant (median 0.81 vs 0.67 ng/ml). Statistically significant differences were observed in sST2 between high risk group and low risk group (median; 1.80 vs 0.54 ng/ml, respectively, p<0.05). Additionally, sST2 levels in non-responders to initial treatment were significantly higher than those in responders (median; 1.65 vs 0.64 ng/ml, respectively, p<0.05). There were no significant correlations between sST2 level at diagnosis and plasma brain natriuretic peptide (r = -0.05), C-reactive protein (r = 0.04), and AST (r = 0.07). Overall, 4 children (7%) had CAAs at 4 weeks of illness. sST2 levels at diagnosis were not significantly different between children with and without CAAs, median sST2 levels in children without CAAs (1.68 vs 0.79 ng/ml, respectively, p=0.07). At 4 days after initial therapy, median sST2 levels decreased in children without CAAs, (0.79 vs 0.65, p=0.1), whereas median sST2 levels increased in children with CAAs (1.68 vs 1.70, p=0.9). Conclusions: Elevated sST2 may be a potential risk factor of initial treatment resistance and developing CAAs in acute KD.
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