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Background <p>Multisystem 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.</p> Methods <p>Single 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.</p> Results <p>Three 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.</p> Conclusions <p>MIS-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.</p> Impact <p><UnorderedList Mark="Bullet"> <ItemContent> <p>KD and MIS-C are not separate entities but different ends of the immune response spectrum.</p> </ItemContent> <ItemContent> <p>Among the hyperinflammation spectrum, each viral variant induces a distinct MIS-C phenotype, with the Omicron wave resembling KD.</p> </ItemContent> <ItemContent> <p>Clinical phenotype stratification outperformed MIS-C definitions in identifying patient subgroups, confirming the value of clinical features in managing infection-triggered hyperinflammation.</p> </ItemContent> <ItemContent> <p>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.</p> </ItemContent> <ItemContent> <p>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.</p> </ItemContent> </UnorderedList></p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月27日

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  • Greta Mastrangelo,
  • Paul Tsoukas,
  • Ellen Go,
  • Hua Lu,
  • Arthur Hoi Hin Cheng,
  • Amy Xu,
  • Rae S. M. Yeung,
  • Nita Chahal,
  • Dilan Dissanayake,
  • Tala El Tal,
  • Jeremy N. Friedman,
  • Beth D. Gamulka,
  • Ellen Go,
  • Charlotte Moore Hepburn,
  • Linda T. Hiraki,
  • Julie Johnstone,
  • Andrea Knight,
  • Raphaël Kraus,
  • Ronald M. Laxer,
  • Deborah M. Levy,
  • Jayne M. MacMahon,
  • Brian W. McCrindle,
  • Luc Mertens,
  • Trent Mizzi,
  • Shaun K. Morris,
  • Laila Premji,
  • Lynn Spiegel,
  • Shirley M. L. Tse,
  • Rae S. M. Yeung

摘要

Background

Multisystem 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.

Methods

Single 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.

Results

Three 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.

Conclusions

MIS-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.