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Published on: September 15, 2017
Soluble intercellular adhesion molecule-1 and E-selectin as markers of disease activity and endothelial activation in
Bradley J Bloom1, Sarah M Nelson, Daniel Eisenberg
1Department of Pediatrics, Hasbro Children's Hospital, and Brown Medical School, Providence, Rhode Island, USA.
Insights
Soluble intercellular adhesion molecule-1 (sICAM-1) and E-selectin levels are elevated in children with juvenile idiopathic arthritis (JIA), but do not reliably track disease activity for routine use as biomarkers.
Area of Science:
- Pediatric Rheumatology
- Immunology
- Biomarker Discovery
Background:
- Juvenile idiopathic arthritis (JIA) involves complex inflammatory pathways.
- Endothelial activation is increasingly recognized in JIA pathogenesis.
- Adhesion molecules like ICAM-1 and E-selectin may reflect endothelial status.
Purpose of the Study:
- To investigate the correlation between soluble intercellular adhesion molecule-1 (sICAM-1) and E-selectin levels and clinical markers of disease activity in children with JIA over time.
- To assess the utility of these adhesion molecules as potential biomarkers for JIA disease activity.
Main Methods:
- Longitudinal study of 28 children with JIA over 2 years, with assessments every 3 months.
- Serum analysis for sICAM-1 and sE-selectin, plasma analysis for fibrin d-dimer and von Willebrand factor (vWF).
- Clinical data collection including ESR, joint counts, and functional assessments; comparison with 30 healthy controls.
Main Results:
- Baseline sICAM-1 was elevated in JIA patients compared to controls.
- sE-selectin was higher in systemic JIA and correlated with ESR; sICAM-1 correlated with d-dimer.
- No consistent correlation was found between adhesion molecules and most clinical variables or disease course, except for increased sICAM-1 during flares in systemic JIA.
Conclusions:
- sICAM-1 is elevated in active JIA, and sE-selectin in active systemic JIA.
- These adhesion molecules do not consistently correlate with most clinical variables or parallel disease course in JIA.
- Routine use of sICAM-1 and sE-selectin as biomarkers for JIA disease activity is not recommended, though endothelial activation is crucial in JIA pathogenesis.
Objective:
To determine whether soluble forms of the adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and E-selectin correlate with clinical measures or other markers of endothelial activation in children with juvenile idiopathic arthritis (JIA) over time.
Methods:
A total of 28 children with JIA were studied every 3 months over 2 years. At each interval, serum was tested for soluble (s)ICAM-1 and sE-selectin, plasma for fibrin d-dimer and von Willebrand factor (vWF), and the following clinical variables were recorded: erythrocyte sedimentation rate (ESR), physician and parent global assessments, swollen and limited joint counts, and functional assessment by Childhood Health Assessment Questionnaire. Concentrations of the adhesion molecules were also determined once in 30 age matched healthy children.
Results:
Among all JIA subtypes, baseline sICAM-1 was elevated compared to controls; sE-selectin was higher in patients with systemic disease compared to other subtypes and controls. sE-selectin correlated with ESR, but there were no other correlations between concentrations of either adhesion molecule or any other clinical variables or vWF antigen. sICAM-1 was higher in those with elevated compared to normal d-dimer. There were no differences between mean sICAM-1 and sE-selectin before or during disease flare or improvement periods, except for an increase in sICAM-1 with flares in patients with systemic disease.
Conclusion:
sICAM-1 is elevated in children with active JIA. sE-selectin is only elevated in children with active systemic disease. Although some relationships were found between the adhesion molecules and other variables, they did not correlate with most variables, and did not parallel the disease course. Thus, we cannot recommend the routine use of these molecules as clinical biomarkers of disease activity. This study confirms that endothelial activation is key to the pathogenesis of JIA, especially in the systemic subtype.
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