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Abstract Body

MIS-C was described during the first wave of the Covid-19 pandemic. Clinical features included features of systemic inflammation shared with Kawasaki disease in approximately half of patients, reduced left ventricular function requiring vasoactive support in approximately 75% of patients, coronary artery aneurysms in approximately 10% of patients, and gastrointestinal pain in most patients. Laboratory features included raised inflammatory markers, disordered coagulation and raised cardiac biomarkers. Most patients were respiratory PCR negative, but serum IgG positive for SARS-CoV-2. This, in addition to a time lag of approximately 4 weeks from peak SARS-CoV-2 transmission to peak MIS-C presentation, suggested that MIS-C was a post-infectious disease.

Immunologically, MIS-C is characterised by high numbers of activated immature neutrophils in peripheral blood, decreased antigen presentation, and widespread T and B cell lymphopaenia. B cells show a germinal centre independent B cell response. Some groups have suggested a role for auto-inflammation with the identification of self-reactive antibodies. Compelling data have identified a subset of activated T cells expressing specific T cell receptor sequences, which may be exploited to improve diagnosis of MIS-C and requires further investigation. Treatment includes intravenous IgG (IVIg), corticosteroids and monoclonal antibodies (to IL-1, IL-6 or TNF-alpha), and for differential diagnoses (e.g. toxic shock syndrome). There is no evidence of clinically important improvements in outcome between groups of children treated with IVIg, corticosteroids or both in propensity-score matched cohorts. Recent data suggest a decline in the incidence of MIS-C relative to SARS-CoV-2 infection in children; however, the Covid-19 pandemic continues to surprise us.