Health
COVID-19-related inflammatory syndrome in children described, MIS-C
COVID-19 (new coronavirus infectious disease) (# If there is no character limit, add parentheses when first appearing Often the child is asymptomatic and usually mild if symptoms occur. However, one complication that may arise from SARS-CoV-2 infection is multisystem inflammatory syndrome (MIS-C) in children. Little is known about MIS-C. MIS-C appears 4-6 weeks after infection with high fever, organ dysfunction, and inflammation. A team of researchers is currently mapping the immune response in children affected by MIS-C. Findings reveal that MIS-C shares some functions with Kawasaki disease, but the inflammatory response is different from Kawasaki disease and severe acute COVID-19.
“Our results show that MIS-C is a completely different inflammatory condition than Kawasaki disease, with some common features,” said Dr. Pero Brodin, pediatrician, and female. Said a researcher in the Children’s Health Division, a researcher at the Karolinska Institute. “The hyperinflammation and cytokine storms detected in children with MIS-C are also different from those seen in adult patients with severe acute COVID-19, which was recently described in another publication.”
The study is published in a journal cell “Immunology of multisystem inflammatory syndrome in children with COVID-19.. “
Researchers took blood samples from 13 MIS-C patients treated at the Karolinska University Hospital in Stockholm, Sweden and the Bambinojes Children’s Hospital in Rome, Italy, before COVID-19 from 2017 to 2018. We compared with a sample of 28 Kawasaki disease patients collected in Japan. The analysis also included samples from children with mild COVID-19.
Comparing MIS-C to these other inflammatory conditions, this study observed different frequencies of specific immune cell populations, inflammatory cytokines, and chemokines in the blood. More specifically, the authors stated that “the inflammatory response of MIS-C, unlike the severe acute COVID-19 cytokine storm, shares some features with Kawasaki disease, but the T cell subset, IL-17A, And biomarkers associated with arterial injury.”
Unlike children with Kawasaki disease and mild COVID-19, children with MIS-C lacked IgG antibodies to the common cold coronavirus. Researchers have also discovered several autoantibodies that target the body’s own proteins and may contribute to the pathogenesis of MIS-C. The authors note that these data suggest a “potential target for autoimmune attack.” The hypothesis that autoantibodies contribute to the pathology of MIS-C is supported, the authors write, “The effect of intravenous immunoglobulin on MIS-C activates and suppresses inhibitory Fc receptors. A general approach to prevent the membrane attack complex by somatic factors, which alleviates autoantibody pathologies.”
Researchers are currently investigating the genetic risk factors for developing MIS-C after SARS-CoV-2 infection. The authors state that the treatment of MIS-C is “most likely overlapping symptoms among these patient groups” according to the protocol used in atypical Kawasaki disease. Their data suggested, “We present a more complex diagram with both functional and shared features that should influence the therapeutic strategies of these conditions.”
“There is an urgent need to better understand why a small number of SARS-CoV-2 infected children develop MIS-C, and we are adding a piece to the puzzle,” Brodin said. “We need better knowledge of the etiology to develop optimal treatments that can suppress cytokine storms and hopefully save lives, and vaccines to avoid MIS-C caused by vaccination. It is important.”
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