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Coagulation abnormalities and acquired von Willebrand's disease type 1 in children receiving valproic acid
Gül Serdaroglu1, Sarenur Tütüncüoglu, Kaan Kavakli
1Department of Pediatrics, Division of Child Neurology, Ege University Faculty of Medicine, Izmir, Turkey. gul.s@turk.net
Insights
Valproic acid can cause acquired von Willebrand
Area of Science:
- Pediatric Neurology
- Hematology
- Pharmacology
Background:
- Valproic acid is a common antiepileptic drug in children.
- Known hematologic side effects include bleeding issues, low platelets, and low fibrinogen.
- The impact on von Willebrand's factor (vWF) is less understood.
Purpose of the Study:
- To investigate coagulation parameters in children treated with valproic acid.
- Specifically, to assess the prevalence of acquired von Willebrand's disease.
- To determine if valproic acid dose or duration affects these parameters.
Main Methods:
- Studied 29 epileptic children (ages 2-18) on valproic acid for ≥6 months.
- Assessed platelet count, PT, aPTT, bleeding time, fibrinogen, platelet aggregation, vWF antigen, and ristocetin cofactor activity.
- Defined acquired von Willebrand's disease by decreased ristocetin cofactor activity.
Main Results:
- Six of 29 children (20.7%) developed acquired von Willebrand's disease.
- Decreased coagulation parameters were not linked to valproic acid dose or treatment length.
- Two patients experienced mild epistaxis, not requiring therapy cessation.
Conclusions:
- Valproic acid therapy can lead to acquired von Willebrand's disease in children.
- This potential side effect requires consideration, especially before surgery or trauma.
- Monitoring coagulation parameters is crucial for children on long-term valproic acid.
Abstract:
Valproic acid is commonly used in the management of childhood epilepsy. The known hematologic side effects of the drug are hemorrhagic diatheses, thrombocytopenia, and hypofibrinogenemia. We studied coagulation parameters in 29 epileptic children receiving valproic acid for at least 6 months. Their ages ranged between 2 and 18 years (10.2 +/- 4.9 years). The total valproic acid dose was 250 to 1000 mg/day equivalent to 20 to 30 mg/kg/day. Treatment duration ranged from 6 to 57 months. These children had not previously had a hemostatic defect and had no family history of bleeding disorders. Platelet count, prothrombin time, activated partial thromboplastin time, bleeding time, fibrinogen, platelet aggregation assays, and ristocetin cofactor activity levels were determined in all of the patients, but von Willebrand's factor antigen levels could be determined in only 14 patients. The values of von Willebrand's factor antigen ranged from 53 to 218% (104.1 +/- 42.3), and ristocetin cofactor activity levels ranged from 11.5 to 218% (94.5 +/- 43.1). Six of the 29 children (20.7%) had decreased values of ristocetin and cofactor activity and were considered to have acquired von Willebrand's disease. The decreases in coagulation parameters were not dependent on either valproic acid dose or treatment duration. Two patients with low ristocetin cofactor activity values had mild epistaxis, which did not require discontinuation of therapy. In patients receiving valproic acid therapy, this side effect must be considered, especially before surgical intervention and serious traumatic conditions.