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Published on: May 23, 2025
Absence of hypercoagulability in acute Kawasaki disease
Ming-Tsan Lin1, Lon-Yen Tsao, Ming-Lin Cheng
1Department of Pediatrics, Changhua Christian Hospital, Changhua 500, Taiwan. mtsy@ms18.hinet.net
Insights
This study found no evidence of hypercoagulability in acute Kawasaki disease (KD). Biomarkers of endothelial cell activation and clotting are not predictive of coronary aneurysms in KD patients.
Area of Science:
- Cardiovascular Research
- Pediatric Rheumatology
- Hematology
Background:
- Kawasaki disease (KD) is a vasculitis affecting children, often leading to cardiovascular complications.
- Endothelial cell (EC) damage is implicated in KD pathogenesis and coronary vascular disorders.
- Prethrombotic complications may arise from EC activation in KD.
Purpose of the Study:
- To investigate the role of EC activation and hypercoagulability in KD.
- To determine if plasma markers correlate with coronary aneurysm development in KD.
Main Methods:
- Assessed EC function and coagulation in 52 acute KD patients and 20 controls.
- Measured markers: thrombomodulin, tissue factor, tissue factor pathway inhibitor, von Willebrand factor (vWF), coagulation factor VII (FVII), activated FVII, prothrombin fragment 1 + 2 (F1 + 2), and D-dimer.
Main Results:
- Coronary artery dilatation occurred in 55.8%, aneurysms in 9.6% of KD patients.
- Elevated vWF, FVII, F1 + 2, and D-dimer in KD vs. healthy controls, but not febrile controls.
- No significant differences in EC/hypercoagulability markers between patients with/without cardiac complications.
Conclusions:
- Hypercoagulability is not evident during the acute phase of Kawasaki disease.
- EC damage and hypercoagulability markers do not predict coronary aneurysms in KD.
Background:
Kawasaki disease (KD) is a systemic vasculitis syndrome with the striking feature of cardiovascular involvement. Endothelial cell (EC) damage has been suggested to predispose individuals to the development of coronary vascular disorders. When EC are perturbed, prethrombotic complications ensue. The purpose of this study was to examine the clinical relevance of EC activation and hypercoagulability in the pathogenesis of KD and to determine if plasma levels of these markers are correlated with the development of coronary aneurysms.
Methods:
EC function and coagulation status were assessed in 52 patients with acute KD, 20 febrile control subjects, and 20 healthy control subjects. Biological markers of EC and hypercoagulability were measured and included thrombomodulin, tissue factor, tissue factor pathway inhibitor, von Willebrand factor (vWF), coagulation factor VII (FVII), activated factor VII, prothrombin fragment 1 + 2 (F1 + 2), and D-dimer.
Results:
Transient dilatation of coronary arteries was the most common complication (55.8%), and coronary aneurysm was noted in five patients (9.6%). Levels of vWF, FVII, F1 + 2 and D-dimer were higher in acute KD patients compared with healthy controls but not febrile controls. Markers of EC and hypercoagulability were not different between patients with cardiac complications and those without cardiac complications. Biological and immunological assays did not demonstrate the prethrombotic state in acute KD.
Conclusions:
Our results suggest that hypercoagulability does not occur during the acute stage of KD. Markers of EC damage and hypercoagulability are not predictive of coronary aneurysms in KD.
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