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Published on: September 22, 2020
Platelet vascular endothelial growth factor is a useful predictor for prognosis in Kawasaki syndrome
Kentaro Ueno1, Yuichi Nomura, Teruto Hashiguchi
1Department of Paediatrics, Kagoshima University Graduate School of Medical and Dental Sciences, Japan. ukenta@m3.kufm.kagoshima-u.ac.jp
Insights
Platelet vascular endothelial growth factor (VEGF) is elevated in children with Kawasaki disease (KD) and correlates with coronary artery abnormalities (CAA). Platelet VEGF levels indicate treatment response, suggesting its role in KD vasculitis.
Area of Science:
- Pediatrics
- Immunology
- Cardiology
Background:
- Kawasaki syndrome (KS) is a childhood vasculitis.
- Coronary artery abnormalities (CAA) are a major complication of KS.
- Intravenous immunoglobulin (IVIG) reduces CAA occurrence.
Purpose of the Study:
- To evaluate the role of platelet vascular endothelial growth factor (VEGF) in Kawasaki syndrome vasculitis.
- To assess the relationship between platelet VEGF and IVIG treatment response.
- To determine if platelet VEGF correlates with coronary artery abnormalities.
Main Methods:
- Analysis of 80 KS patients (69 IVIG responders, 11 non-responders).
- Measurement of serum and platelet VEGF levels.
- Correlation analysis between VEGF levels, IVIG response, and CAA severity (z-score).
Main Results:
- Serum and platelet VEGF levels were significantly higher in KS patients compared to controls.
- Platelet VEGF decreased in IVIG responders but remained elevated in non-responders.
- Pre-treatment platelet VEGF levels, not serum VEGF, significantly correlated with maximum CAA z-score.
Conclusions:
- Platelet VEGF may indicate the severity of vasculitis and CAA development in Kawasaki syndrome.
- Platelet VEGF is a potential biomarker for KS pathophysiology and treatment response.
Abstract:
Kawasaki syndrome (KS) is an acute febrile vasculitis of childhood. Coronary artery abnormalities (CAA) are a significant problem in KS patients. High dose intravenous immunoglobulin (IVIG) is effective for reducing the occurrence of CAA. Clinical and histopathological findings suggest that vascular endothelial growth factor (VEGF) is involved in CAA. In circulating blood, newly activated platelets are the major source of VEGF, which is released in large amounts in vascular inflammation. The present study analysed 80 KS patients (69 IVIG responders and 11 IVIG non-responders) and evaluated the role of platelet VEGF in KS vasculitis. Serum VEGF and platelet VEGF levels were significantly higher in KS patients than controls (P < 0.001). Platelet VEGF reflected the reactivity of IVIG treatment and was decreased in responders (P < 0.001), but remained increased in non-responders (P = 0.01). Platelet VEGF levels, but not serum VEGF levels, before IVIG were significantly correlated with the maximum CAA z-score (r = 0.524, P = 0.02). Our findings demonstrate that platelet VEGF may reflect the severity of vasculitis related to the pathological development of CAA in KS. Platelet VEGF may be an important feature of KS pathophysiology.
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