Plasma IL-17A is increased in patients with critical MIS-C and associated to in-hospital mortality

Emmerson C F de Farias1, Luciana M P P do Nascimento1, Manoel J C Pavão Junior1

  • 1Division of Pediatric Intensive Care, Department of Pediatrics, Fundação Santa Casa de Misericórdia do Pará, Belém, Brazil.

Frontiers in Immunology
|February 11, 2025
PubMed

Insights

Elevated Interleukin-17A (IL-17A) levels in children with Multisystem Inflammatory Syndrome (MIS-C) correlate with increased mortality risk. Early identification of high IL-17A may aid in managing critical MIS-C cases.

Area of Science:

  • Pediatric critical care medicine
  • Immunology
  • Infectious disease epidemiology

Background:

  • Multisystem Inflammatory Syndrome in Children (MIS-C) is a severe post-COVID-19 complication.
  • MIS-C presents with diverse clinical manifestations.
  • Understanding MIS-C pathogenesis is crucial for improving outcomes.

Purpose of the Study:

  • To investigate inflammatory biomarkers, specifically cytokines and oxidative stress markers, in critically ill MIS-C patients.
  • To determine the association between these biomarkers and mortality in MIS-C.

Main Methods:

  • A prospective, single-center study included 41 MIS-C patients (1 month to 18 years) admitted to a pediatric intensive care unit (PICU).
  • Inflammatory biomarkers were measured on days 1 and 3 post-hospitalization.
  • Survival analysis utilized Kaplan-Meier curves and Cox regression, with ROC analysis for predictive values.

Main Results:

  • 16 out of 41 MIS-C patients (39%) did not survive.
  • Higher levels of Interleukin-17A (IL-17A) on day 1 were significantly associated with increased mortality (p=0.012).
  • An IL-17A cutoff of 14.32 pg/mL predicted mortality, while other markers showed no significant association.

Conclusions:

  • Elevated IL-17A levels on day 1 of hospitalization are a significant predictor of mortality in critically ill MIS-C patients.
  • IL-17A may serve as a potential therapeutic target or prognostic marker in MIS-C.
  • Further research is warranted to explore the role of IL-17A in MIS-C pathophysiology and treatment.
Abstract