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Published on: January 27, 2019

Intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 are increased in the plasma of children with

M J Whalen1, L A Doughty, T M Carlos

  • 1Department of Anesthesiology/Critical Care Medicine, University of Pittsburgh, PA, USA.

Critical Care Medicine
|August 2, 2000
PubMed

Insights

In children with sepsis-induced multiple organ failure (MOF), elevated levels of vascular cell adhesion molecule (VCAM)-1 and intercellular adhesion molecule (ICAM)-1 indicate a proinflammatory state. These molecules predict organ failure and mortality in pediatric sepsis.

Area of Science:

  • Pediatric critical care medicine
  • Immunology
  • Sepsis research

Background:

  • Sepsis-induced multiple organ failure (MOF) is a critical condition in children.
  • Circulating adhesion molecules play a role in inflammatory processes and endothelial activation.

Purpose of the Study:

  • To measure concentrations of endothelial (E)-selectin, intercellular adhesion molecule (ICAM)-1, and vascular cell adhesion molecule (VCAM)-1 in children with sepsis-induced MOF.
  • To investigate the association between these adhesion molecules and clinical outcomes in pediatric sepsis.

Main Methods:

  • Prospective study conducted in a university pediatric intensive care unit.
  • Measured plasma E-selectin, ICAM-1, and VCAM-1 in 77 children with sepsis and 14 controls.
  • Utilized multivariate logistic regression to analyze associations with organ failure and mortality.

Main Results:

  • Children with sepsis showed increased E-selectin, ICAM-1, and VCAM-1 compared to controls.
  • Elevated VCAM-1 correlated with more severe organ failure (more than three organs).
  • ICAM-1 and VCAM-1 independently predicted the number of failed organs, mortality, and sequential MOF.

Conclusions:

  • Persistent elevation of VCAM-1 and ICAM-1 in pediatric sepsis with MOF suggests a proinflammatory endothelial phenotype.
  • Activated leukocytes may also contribute to increased adhesion molecule levels.
  • Further research is needed to elucidate the role of ICAM-1 and VCAM-1 in the pathogenesis of sepsis-induced MOF.
Abstract

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