Evidence map›Paper›PMID 41145634›Full record

Observational studyPediatric research2026

Multisystem inflammatory syndrome in children is a SARS-CoV-2 triggered Kawasaki disease.

Greta Mastrangelo, Paul Tsoukas, Ellen Go, Hua Lu, Arthur Hoi Hin Cheng, Amy Xu, Rae S M Yeung, SickKids MIS-C Working Group

Abstract readObservational Study
PubMed Full text at PMC Publisher
In one paragraph

Observational study in Pediatric research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Greta MastrangeloDivision of Rheumatology, Department of Paediatrics, The Hospital for Sick Children, University of Toronto, Toronto, ON, Canada.
Paul TsoukasDivision of Rheumatology, Department of Paediatrics, The Hospital for Sick Children, University of Toronto, Toronto, ON, Canada.
Ellen GoDivision of Rheumatology, Department of Paediatrics, The Hospital for Sick Children, University of Toronto, Toronto, ON, Canada.
Hua LuCell and Systems Biology Program, The Hospital for Sick Children Research Institute, Toronto, ON, Canada.
Arthur Hoi Hin ChengCell and Systems Biology Program, The Hospital for Sick Children Research Institute, Toronto, ON, Canada.
Amy XuCell and Systems Biology Program, The Hospital for Sick Children Research Institute, Toronto, ON, Canada.
Rae S M YeungDivision of Rheumatology, Department of Paediatrics, The Hospital for Sick Children, University of Toronto, Toronto, ON, Canada. rae.yeung@sickkids.ca.
SickKids MIS-C Working Group

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMultisystem Inflammatory Syndrome in Children (MIS-C) encompasses a spectrum of phenotypes: shock, Kawasaki disease (KD), and fever with hyperinflammation. Whether MIS-C is a new syndrome or SARS-CoV-2-triggered KD remains debated. To explore this, we investigated the relationship between clinical phenotypes and viral variants, and the contribution of pre-pandemic KD incidence to MIS-C reporting.

methodsSingle center, prospective, observational study of 384 patients with MIS-C, from March 2020 to September 2023. Clinical and laboratory features, complications, and outcomes were evaluated across the MIS-C waves.

resultsThree clinical phenotypes were identified: shock, KD, and fever with hyperinflammation. KD was most common across all variants, particularly during Omicron, while shock predominated in Delta cohort. Stratifying by phenotype outperformed the WHO MIS-C and RCPCH PIMS definitions in distinguishing subgroups. Countries with low pre-pandemic KD incidence identified MIS-C as a new syndrome, while countries with high KD incidence did not.

conclusionsMIS-C phenotypes vary accordingly to SARS-CoV-2 variants, with KD being most common. Stratification by clinical phenotypes out-performed MIS-C case definitions for patient identification, highlighting the value of clinical features in managing infection-triggered hyperinflammation. These findings, coupled with the inverse relationship between pre-pandemic KD incidence and MIS-C reporting, support the hypothesis that MIS-C is SARS-CoV-2-triggered KD. IMPACT: KD and MIS-C are not separate entities but different ends of the immune response spectrum. Among the hyperinflammation spectrum, each viral variant induces a distinct MIS-C phenotype, with the Omicron wave resembling KD. Clinical phenotype stratification outperformed MIS-C definitions in identifying patient subgroups, confirming the value of clinical features in managing infection-triggered hyperinflammation. The inverse relationship between pre-pandemic KD incidence and MIS-C reporting supports MIS-C being a SARS-CoV-2-triggered KD, underscoring critical equity and diversity considerations. A pathogen-agnostic approach to post-infectious hyperinflammation would recognize the full spectrum of phenotypes and complications and avoid confusion due to new naming conventions.

Indexed as

COVID-19Mucocutaneous Lymph Node SyndromeSARS-CoV-2Systemic Inflammatory Response SyndromeChildChild, PreschoolFemaleHumansIncidenceInfantMalePhenotypeProspective Studies

Identifiers

PMID41145634
PMCPMC13433241

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.