PMC:7546716 / 28452-29861 JSONTXT

{"target":"http://pubannotation.org/docs/sourcedb/PMC/sourceid/7546716","sourcedb":"PMC","sourceid":"7546716","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7546716","text":"Similarities between COVID-19, Kawasaki disease, and Behçet's disease\nParallels between COVID-19 and rheumatic disorders can be made by referring to discrete autoinflammatory syndromes that share symptoms with COVID-19 such as fever, frequent conjunctivitis, and—most remarkably—vasculitic manifestations with neutrophilia, thrombosis, and aneurysmal dilations, involving coronary vessels (eg, Kawasaki disease in infants) or pulmonary vessels (eg, Behçet's disease in adults).\nCase series of children infected with SARS-CoV-2 who develop Kawasaki-like disease with MAS features have been described.68 GM-CSF produced by cardiac fibroblasts is key in disease progression in mouse models of Kawasaki disease, and significantly increased soluble ST2, E-selectin, CXCL10, IL-17F, and in some cases IL-9, have been reported in the circulation of patients with acute Kawasaki disease compared with other children who are febrile.69, 70, 71 Similarly, Behçet's disease has been associated with high concentrations of both soluble ST2 and IL-33, as well as increased CXCL10 and CCL2, Vγ9Vδ2 T-cell expansion, IL-17F gene polymorphisms, and intense recruitment of T cells producing IL-9 and IL-17 to the lungs.72, 73, 74, 75, 76 Some patients with either Behçet's disease77 or COVID-1978 also show positivity for antiphospholipid antibodies, which might further contribute to the coagulopathy seen in both 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