November 18 | Daily COVID-19 LST Report


· Pediatric cardiologists from the Association for European Pediatric and Congenital Cardiology's COVID-19 Rapid Response Team evaluated 286 children with symptoms of multisystem inflammatory syndrome in children (MIS-C) and found 65% had laboratory evidence of current or past COVID-19 infection, 93% had cardiac involvement, and all had elevated inflammatory markers, suggesting pediatric patients with MIS-C should be monitored for cardiovascular complications and rising biomarkers.

· A literature review conducted by an international panel of pediatric dermatologists describes documented skin manifestations of COVID-19 in children including chilblain-like lesions, erythema multiforme, urticaria (10-20% of cutaneous manifestation reports), vesicular exanthema, and Kawasaki disease-like inflammatory syndrome (pediatric inflammatory multisystem syndrome with nonspecific skin symptoms and cardiovascular involvement).

Understanding the Pathology

· A retrospective cohort study by cardiac pathologists from the Mayo Clinic of post-mortem reviews of 15 patients with COVID-19, six patients with influenza, and six patients with no viral pathology found patients with COVID-19 were significantly more likely to have fibrin microthrombi (12/12 [100%] of COVID-19 vs 2/6 [33%] of influenza and control patients; p=0.006) and that these were found in a higher proportion of arterioles (p=0.003). One-third (33%) of COVID-19 patients had evidence of myocarditis and 26.7% evidence of amyloidosis.

· Physiology researchers use mechanism-based reasoning to propose an explanation as to why COVID-19 can have varying clinical symptoms using three possible mechanisms: p38/MAPK pathway, JAK-STAT pathway, and the PGE2-EP receptors signaling pathway. From each of these pathways, the authors suggest the varying symptoms could be attributed to the level of prostaglandin E2 (PGE2) released, which causes a cytokine storm, and they further theorize that the amount of PGE2 could be directly correlated to disease severity.

· Investigators mainly from the Institute of Physiology in Berlin compared the respective plasma disruption to the lung epithelium between the plasma of 19 patients with severe COVID-19 (requiring intubation), 14 patients with moderate COVID-19 (requiring hospitalization but not intubation), and 15 healthy controls and found that addition of plasma from COVID-19 patients to healthy endothelial monolayers correlated with "significant endothelial gap formation and loss of junctional VE-cadherin". Additionally, when compared to the heathy control plasma, the plasma from COVID-19 patients not only resulted in increased severity of endothelial permeability but also rapid (within 1-2 hours) and long lasting (over 6 hours) effects, suggesting that endothelial-barrier-stabilizing adjunctive therapies administered to patients exhibiting signs of moderate to severe COVID-19 may delay progression to acute respiratory distress syndrome.


· Neurosurgeons at the Laboratory of Experimental Neurosurgery and Cell Therapy in Milan, Italy compared blood samples from 47 healthy patients to samples from 111 SARS-CoV-2 positive patients and found sphingosine-1-phosphate (S1P) and apolipoprotein M (apoM; a carrier of S1P) levels were significantly decreased in COVID-19 patients compared to healthy patients (p<0.0001). COVID-19 patients requiring intensive care unit (ICU) admission had significantly lower levels of apoM, S1P, albumin, and HDL compared to those not requiring ICU care (p<0.0001), suggesting that the SARS-CoV-2 induced cytokine storm and acute phase response lowers levels of these specific biomarkers, and low levels of S1P (<0.6uM) and apoM may be clinical predictors of severe disease and decreased survival.

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