Roberta L. DeBiasi, M.D., from The George Washington University School of Medicine and Health Sciences in Washington, D.C., and colleagues studied 124 children hospitalized and treated under the institutional MIS-C Task Force protocol. Of this cohort, 63 had the diagnosis of MIS-C (39 confirmed, 24 probable) and 61 had an alternative diagnosis (controls).
The researchers found that Black and Hispanic children were overrepresented in the MIS-C cohort (46 and 35 percent, respectively), with the highest risk for Black children (odds ratio, 4.62).
Compared with children not in the intensive care unit (ICU), children who were critically ill (in ICU) with MIS-C more frequently had cardiac complications (55 versus 28 percent), including systolic myocardial dysfunction (39 versus 3 percent) and valvular regurgitation (33 versus 7 percent).
In MIS-C cases, the median cycle threshold was 31.8, which was significantly higher (indicating lower viral load) than in primary severe acute respiratory syndrome coronavirus 2 infection. Compared with controls, in MIS-C patients, cytokine levels, including soluble interleukin 2 receptor, interleukin 10, and interleukin 6, were higher.
In phylogenetic analysis of viral genome sequences, there was a predominance of GH clade originating in Europe; no differences in viral sequencing were seen on comparison of MIS-C patients with primary COVID-19 patients.
“The fact that there were no notable sequencing differences between our MIS-C and primary COVID cohorts suggests that variations in host genetics and/or immune response are more likely primary determinants of how MIS-C presents itself, rather than virus-specific factors,” DeBiasi said in a statement.