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Published on: February 28, 2012
Pro- and anticoagulatory factors under sodium valproate-therapy in children
M C Banerjea1, W Diener, G Kutschke
1Department of General Pediatrics, University Children's Hospital, Freiburg, Germany. m_banerjea@hotmail.com
Insights
Sodium valproate (VPA) therapy in children significantly reduces platelet counts and alters both procoagulatory and anticoagulatory factors. This VPA-induced hemostatic change may potentially lower bleeding risk in pediatric patients.
Area of Science:
- Pediatric Hematology
- Pharmacology
- Clinical Chemistry
Background:
- Sodium valproate (VPA) is widely used in pediatric epilepsy management.
- Hemostatic side effects are a known concern with VPA therapy.
- Understanding VPA's impact on coagulation is crucial for patient safety.
Purpose of the Study:
- To investigate the hemostatic side effects of sodium valproate (VPA) in children.
- To longitudinally assess procoagulatory and anticoagulatory parameters during VPA therapy.
Main Methods:
- Longitudinal study of 80 children undergoing VPA therapy.
- Measurement of platelet count, platelet function, von Willebrand factor (vWF) antigen and activity.
- Assay of procoagulatory factors (e.g., fibrinogen) and anticoagulatory factors (e.g., protein C, antithrombin).
Main Results:
- VPA significantly reduced platelet count (p=0.007) but did not impair platelet function.
- VPA therapy decreased vWF antigen but increased its in vivo activity (p=0.01).
- Significant reductions were observed in fibrinogen (p=0.001), protein C (p=0.005), and antithrombin (p=0.04).
Conclusions:
- Sodium valproate significantly impacts both procoagulatory and anticoagulatory systems in children.
- The observed alterations in hemostasis suggest a potential reduction in absolute bleeding risk.
- Further research is warranted to fully elucidate the clinical implications of VPA-induced hemostatic changes.
Objective:
To evaluate sodium valproate-induced hemostatic side effects in children.
Methods:
A variety of both pro- and anticoagulatory parameters were longitudinally investigated in 80 children before therapy and up to 720 days after initiation of sodium valproate (VPA) therapy.
Results:
VPA caused a significant reduction in platelet count (309,000/ micro l +/- 122,000 before treatment to 261,000/ micro l +/- 150,000 under VPA therapy, p = 0.007). However platelet function was not impaired. While vWF antigen was reduced during VPA therapy (1.05 U/ml +/- 0.4 U/ml before therapy, 0.95 +/- 0.4 U/ml under VPA therapy), the in vivo activity of vWF (ratio between function and antigen concentration) increased significantly (1.06 +/- 0.2 before therapy, 1.36 +/- 0.3 under VPA therapy, p = 0.01). Both procoagulatory and anticoagulatory factors were significantly reduced (fibrinogen: 264.5 +/- 64.5 mg/dl before therapy, 221.4 +/- 47.5 mg/dl under therapy, p = 0.001; protein C: 81.3 % +/- 18 before therapy, 65.6 % +/- 21.4 under VPA therapy, p = 0.005, antithrombin: 122.7 % +/- 23.7 before therapy, 101.7 % +/- 18 under VPA therapy, p = 0.04). With the exception of fibrinogen, these effects were identical in children treated either with monotherapy or with polytherapy.
Conclusions:
Besides already known alterations of a variety of procoagulatory parameters, a relevant influence of VPA on the anticoagulatory system is demonstrated. We hypothesize that this additional alteration of anticoagulatory parameters might reduce the absolute bleeding risk of children treated with VPA.
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