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We aimed to assess the kinetics of the release of proinflammatory cytokines and to clarify clinical usefulness as an indicator of the disease activity in human parechovirus type 3 virus (HPeV3)-induced sepsis-like syndrome. We measured serum levels of neopterin, interleukin (IL)-6 and the soluble forms of tumor necrosis factor (TNF) receptor types I (sTNF-RI) and II (sTNF-RII). Serum samples were obtained from 12 patients with HPeV3-induced sepsis-like syndrome and 28 healthy children. Disease course after onset was divided into 3 phases: early (day 1–2), peak (day 3–6) and recovery (day 9–16) phases. Serum IL-6 levels rapidly and markedly elevated in early phase and gradually decreased to those in healthy children in recovery phase. Furthermore, serum neopterin, sTNFR-I and sTNFR-II levels increased rapidly and markedly in onset phase and remained elevated in peak phase. These levels gradually decreased in recovery phase. Serum IL-18 levels increased from onset phase to peak phase and decreased in recovery phase. These results indicate that proinflammatory cytokines, in particular, interferon gamma, TNF-α and IL-18 are closely related to the development of HPeV3-induced sepsis-like syndrome. Serum levels of these cytokines might be a useful indicator of the disease activity.

BackgroundMacrophage activation syndrome (MAS) is a severe, potentially life-threatening complication of childhood systemic inflammatory disorders. MAS occurs most often in children with systemic juvenile idiopathic arthritis and less commonly in children with Kawasaki disease (KD).ObjectivesOur study aimed to assess the kinetics of cytokine release and compare the accuracy of serum biomarkers for diagnosis of MAS, including neopterin, IL-18, IL-6 and soluble TNF receptor type I (sTNFR-I) and sTNFR-II levels, we analysed these levels in patients with KD, including those with MAS, and compared them to the clinical features of KD and MAS.MethodsSerum neopterin, interleukin (IL)-18, IL-6 and soluble tumour necrosis factor receptor type I (sTNFR-I) and sTNFR-II levels were determined using enzyme-linked immunosorbent assay in 78 patients with KD, including five with MAS. Results were compared to the clinical features of MAS.ResultsSerum neopterin, IL-18, sTNFR-II levels and sTNFR-II/I ratio were significantly elevated in KD patients with MAS compared to those in the acute phase. Receiver operating characteristic curve analysis revealed areas under the curve and cutoff values of neopterin, IL-18, sTNFR-II levels and sTNFR-II/I ratio were 0.9750/30.0 nmol/L, 0.9813/1165 ng/mL, 0.9969/16,600 pg/mL and 0.9875/4.475, respectively. Serum sTNFR-II levels correlated positively with disease activity.ConclusionThese findings indicate that interferon (IFN)–γ and tumour necrosis factor-α (TNF-α) are closely associated with the pathogenesis of MAS associated with KD. Serum sTNFR-II levels might be a useful marker to diagnose the transition to MAS.References[1] García-Pavón S, et al. J Pediatr Hematol Oncol 2017;39:445-451.[2] Shimizu M, et al. Cytokine 2018;108:168-172.Disclosure of InterestsNone declared

Background: The gold standard for the diagnosis of acute pyelonephritis (APN) in children is the finding of both pyuria (P) and bacteriuria (B); however, some APN patients have neither of these findings [APN(P(−);B(−))]. Methods: In this study, we investigated APN patients who visited our hospital over 14 years to identify specific clinical characteristics of APN(P(−);B(−)). Results: A total of 171 APN patients were included in the study, and of these 29 were APN(P(−);B(−)). Of the APN(P(−);B(−)) patients, 25.9% had vesicoureteral reflux (VUR), the same percentage as the APN(P(+);B(+)) patients, and 69.0% of APN(P(−);B(−)) patients had already taken antibiotics before diagnosis. APN(P(−);B(−)) patients were older and had a longer duration between onset of fever and diagnosis than the patients with pyuria and/or bacteriuria. In addition, they showed higher C-reactive protein levels. APN(P(−);B(−)) patients had high levels of urinary α-1 microglobulin and urinary β-2 microglobulin. Conclusions: APN is difficult to diagnose in febrile patients who display neither pyuria nor bacteriuria, but as these patients have the same risk for VUR as APN patients with pyuria and bacteriuria, a detailed history establishing the clinical course as well as urinary chemistry investigations, may assist in diagnosis.