RESUMEN
BackgroundMultisystem Inflammatory Syndrome in Children (MIS-C) is one of the most feared complications following SARS-CoV2 infection in children and adolescents. Few multinational multicenter studies from Latin America have been published.ObjectivesTo describe the clinical presentation, management, and outcomes of MIS-C in Latin America.MethodsObservational, prospective and retrospective, multicenter study to gather information from 84 participating centers across 16 Latin American countries, between August January 1, 2020 and June 30, 2022.ResultsOf the 1,239 reported cases of MIS-C, 84.2% were previously healthy. The most frequent clinical manifestation in our studied population was abdominal pain (N=804, 64.9%), followed by conjunctival injection (N=784, 63.3%). The median days of fever at the time of hospital admission was 5 and a significant number of subjects required admission to an intensive care unit (N=589, 47.8%). A total of 538 (47.2%) patients had an abnormal initial echocardiogram. Most of the subjects (N= 1,096, 88.7%) were treated with intravenous immunoglobulin (IVIG), while 76.7% (N= 947) were treated with steroids, of which 10.6% (N= 100) did not receive IVIG. The death rate attributed to MIS-C was 4.88%, with a rate of 3.39% for those initially diagnosed with MIS-C and 8.85% for those whose admission diagnosis was not MIS-C (P= 0.00001).ConclusionOne of the most significant findings from our study was the death rate, especially in those not initially diagnosed with MIS-C, in whom it was higher. This highlights the importance of increasing awareness and making an earlier diagnosis of MIS-C in Latin America.REFERENCES:NIL.Acknowledgements:NIL.Disclosure of InterestsNone Declared.
RESUMEN
Introduction: Multisystem Inflammatory Syndrome in Children (MIS-C) is a newly identified syndrome elicited by infection of acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although MIS-C shares several clinical features with Kawasaki disease (KD), a greater magnitude of systemic inflammation is usually associated with MIS-C. Inflammasome activation induces the secretion of pro-inflammatory cytokines, IL-1β and IL-18 and the inflammatory form of cell death, pyroptosis. To provide mechanistic insights into MIS-C and KD, we compared the expression and activation of the inflammasome in blood samples from MIS-C and KD patients. Methods: Expression levels of canonical and non-canonical inflammasome components, including NLRP3, CASP1, CASP4, CASP5, IL1B, and the inflammatory mediator, TIFA in whole blood from KD and convalescent patients were analyzed from microarray datasets. The expression of these inflammasomerelated genes was further examined in whole blood samples from MIS-C, KD, KD shock syndrome (KDSS) and convalescent patients using RT-qPCR. Inflammasome activation and TIFA expression were validated in granulocytes of febrile control, KD and MIS-C patients by Western blotting. Results:TIFA, NLRP3, CASP1, CASP4, CASP5, IL1B were upregulated in whole blood from MIS-C, KD, and KDSS patients as compared to convalescent patients. However, the differences were not significant among diseases. Although gene expression profiles were similar in KD, KDSS and MIS-C whole blood RNA, the processing of canonical and non-canonical inflammasome caspases, caspase-1, and caspase-4 were only observed in granulocytes isolated from MIS-C patients, but not KD and febrile controls. Moreover, TIFA was upregulated along with the activation of the inflammasome in granulocytes of MIS-C patients. Conclusions: Our results suggest that activation of inflammasomes, especially non-canonical inflammasome induction in granulocytes, is a hallmark of MIS-C, and differentiates it from KD.