However, more reports emerged of a presentation in children much like Kawasaki disease or toxic shock syndrome [3, 4]

However, more reports emerged of a presentation in children much like Kawasaki disease or toxic shock syndrome [3, 4]. a novel coronavirus was recognized in Wuhan (China) as the cause of an atypical pneumonia which may cause severe acute respiratory distress syndrome. The computer virus rapidly spread around the world and became a global pandemic. The computer virus was named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) by the World Health Organization. The disease has been termed COVID-19 [1]. In Belgium, the first case was diagnosed in February 2020. During the following months, more information became available about the course of the disease. In children, a SARS-CoV-2 contamination is usually asymptomatic or moderate [2]. However, more reports emerged of a presentation in children much like Kawasaki disease or harmful shock syndrome [3, 4]. The syndrome has been named multisystem inflammatory syndrome in children (MIS-C), paediatric multisystem inflammatory syndrome, paediatric inflammatory multisystem syndrome temporarily associated with SARS-CoV-2 (PIMS-TS), or paediatric hyperinflammatory syndrome [5] and has been defined by the CDC (observe Table 1) and the WHO (observe Table 2) [6, 7]. Table 1 Definition of MIS-C by the CDC [6]. (1) An individual aged 21 years presenting with fever, laboratory evidence of inflammation, and evidence of clinically severe illness requiring hospitalization, with multisystem ( 2) organ involvement (cardiac, renal, respiratory, hematologic, gastrointestinal, dermatologic, or neurological)(2) AND no option plausible diagnoses(3) AND positive for current or recent SARS-CoV-2 contamination by RT-PCR, serology, or antigen test, or COVID-19 exposure within the 4 weeks prior to the onset of symptoms Open in a separate window Table 2 Definition of MIS-C by the WHO [7]. (1) Children and adolescents 0C19?years of age with fever 3 days(2) AND two of the following:?(i) Rash or bilateral nonpurulent conjunctivitis or mucocutaneous inflammation signs (oral, hands, or feet)?(ii) Hypotension or shock?(iii) Features of myocardial dysfunction, pericarditis, valvulitis, or coronary abnormalities (including ECHO findings or elevated troponin/NT-proBNP)?(iv) Evidence of coagulopathy (by PT, PTT, and elevated D3-βArr D-dimers)?(v) Acute gastrointestinal problems (diarrhoea, vomiting, or abdominal pain)(3) AND elevated markers of inflammation such as ESR, D3-βArr C-reactive protein, or procalcitonin(4) AND no other obvious microbial cause of inflammation, including bacterial sepsis and staphylococcal or streptococcal shock syndromes(5) AND evidence of COVID-19 (RT-PCR, antigen test, or serology positive) or likely contact with patients with COVID-19 Open in a separate window In our tertiary teaching hospital, we detected two cases of MIS-C that are worthwhile comparing, discussing, and sharing with the wider paediatric community, in order to optimize early acknowledgement and management of MIS-C. Both patients provided informed consent, and approval of the Ethical Committee was granted. 2. Case Presentation 1 The first case issues a 15-year-old young man, known with idiopathic end-stage kidney disease (ESKD) treated with peritoneal dialysis. He had no history of cardiac dysfunction. He was admitted on March 6th, 2020, for any deceased-donor kidney transplantation which was postponed because of fever for 3 days. He complained of fatigue, headaches, and loss of appetite. Characteristics and laboratory findings at admission and imaging results are noted in Table 3. A positive PCR for SARS-CoV-2 confirmed COVID-19 the day of admission. He was hospitalized for 10 days because isolation steps were not possible at home. He stayed paucisymptomatic and received supportive care with antipyretics besides his usual treatments for kidney failure. After 10 days, he was discharged home. Table 3 Comparing clinical signs and symptoms, lab and imaging, and treatment and end result for two cases of MIS-C. 0.314?g/L br / (viii) D-dimer 6943?ng/ml br / (ix) Fibrinogen 482?mg/dL(i) Lymphopenia (267/mm3) br / (ii) Thrombocytosis (808.000/mm3) br / (iii) Hemoglobin 7.6?g/dL br / (iv) CRP 304.3?mg/L (maximum) br / (v) Albumin 24?g/L br / (vi) Cardiac enzymes: br / ?(a) NT-proBNP 3228.0?ng/L br / ?(b) Cardiac troponin 0.01 mcg/L br / (vii) D-dimer 3584?ng/ml br / (viii) Fibrinogen 322?mg/dL hr / em Microbiology results /em (i) Nasopharyngeal swab: PCR SARS-CoV-2 positive(i) Nasopharyngeal swab: PCR SARS-CoV-2 unfavorable br / (ii) Heart biopsy: PCR SARS-CoV-2 unfavorable br / (iii) SARS-CoV-2 IgG ELISA positive (54.30 AE/mL)(i) Nasopharyngeal swab: PCR SARS-CoV-2 negative (twice) br / (ii) SARS-CoV-2 IgG ELISA positive (41.30 AE/mL) Open in a separate window Twenty-three days after discharge, he was readmitted because of dyspnea (NYHA grade HDAC7 III), D3-βArr orthopnea, and hemoptysis. Laboratory findings and imaging results are shown in Table 3. Because of suspected alveolar hemorrhage, bronchoscopy was performed the day after admission. Repeated bronchoalveolar lavage ruled out alveolar bleeding. SARS-CoV-2 PCR on lower respiratory samples was negative. Because of progressive oxygen requirements after bronchoscopy and severe myocardial dysfunction on echocardiography, the patient was transferred to the.