Immature platelets and antiplatelet therapy response to aspirin in Kawasaki disease
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Published on: November 29, 2024
Lei Pi1, Di Che1, Haifeng Long2,3
1Department of Clinical Biological Resource Bank, Guangzhou Institute of Pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Insights
High levels of 11-dehydrothromboxane B2, soluble CD40 ligand, soluble P-selectin, and immature platelet fraction indicate a risk for coronary artery lesions in Kawasaki disease. These markers may predict treatment response to aspirin.
Area of Science:
- Pediatrics
- Cardiology
- Immunology
Background:
- Kawasaki disease is a vasculitis affecting children, leading to coronary artery lesions (CAL).
- Aspirin is a standard antiplatelet therapy, but its effectiveness varies individually.
- Immature platelet fraction (IPF) may influence aspirin's antiplatelet effect.
Purpose of the Study:
- To identify prognostic factors for vasculitis severity in Kawasaki disease.
- To evaluate the impact of antiplatelet therapy on disease markers.
- To correlate specific biomarkers with coronary artery damage.
Main Methods:
- Blood samples from 44 Kawasaki disease patients were analyzed before and after aspirin treatment.
- Immature platelet fraction (IPF) was quantified using a Sysmex XE-5000 instrument.
- Levels of 11-dehydrothromboxane B2 (11-DH-TXB2), soluble CD40 ligand (sCD40L), and soluble P-selectin (sP-selectin) were measured via ELISA.
Main Results:
- Elevated 11-DH-TXB2, sP-selectin, and sCD40L were observed in patients with CAL before treatment.
- Aspirin reduced 11-DH-TXB2, sCD40L, sP-selectin, and IPF in non-coronary artery lesion (NCAL) patients, but not in CAL patients.
- These markers showed a positive correlation with the degree of coronary artery damage.
Conclusions:
- High plasma concentrations of 11-DH-TXB2, sCD40L, sP-selectin, and IPF are risk factors for CAL in Kawasaki disease.
- These biomarkers may serve as experimental indicators for predicting CAL.
- Understanding these markers can aid in assessing vasculitis and antiplatelet therapy effectiveness.
Introduction:
Kawasaki disease is a kind of systemic vasculitis that mainly damages moderate and small-sized blood vessels, and is a leading cause of coronary artery lesions (CAL). Antiplatelet therapy is a routine component of Kawasaki disease treatment strategies. So it is important to evaluate the antiplatelet effect of aspirin because of the individual biological variability of antiplatelet effect of aspirin. The immature platelet fraction (IPF) has attracted particular attention as it may influence the antiplatelet effect of aspirin. This study investigated the prognostic factors for evaluating the degree of vasculitis and the effect of antiplatelet therapy in children with Kawasaki disease.
Materials And Methods:
Blood samples were collected from 44 patients with Kawasaki disease before aspirin treatment and 7 to 10 days after treatment. The IPF counts, percentage of the IPF, and highly fluorescent IPF were detected by a Sysmex XE-5000 instrument. The levels of 11-dehydrothromboxane B2 (11-DH-TXB2), soluble CD40 ligand (sCD40L), and soluble P-selectin (sP-selectin) were measured by ELISA. The correlation between the measured factors and the degree of coronary artery damage in Kawasaki disease was analyzed.
Results:
We found that 11-DH-TXB2, sP-selectin, and sCD40L levels were much more elevated in the CAL group than in the non-coronary artery lesions (NCAL) group before aspirin treatment. The concentrations of 11-DH-TXB2, sCD40L, sP-selectin, and IPF were reduced after aspirin treatment in the NCAL group but not the CAL group. This is related to the degree of coronary artery damage in Kawasaki disease patients. Additionally, 11-DH-TXB2, sCD40L, sP-selectin, and IPF were positively correlated with the degree of coronary artery damage in Kawasaki disease patients.
Conclusion:
The current study suggests that the presence of high plasma concentrations of 11-DH-TXB2, sCD40L, sP-selectin, and IPF can be considered a risk factor and experimental biomarker for CAL in Kawasaki disease patients.
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