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Protein C deficiency related to valproic acid therapy: a possible association with childhood stroke
R Gruppo1, A Degrauw, H Fogelson
1Divisions of Hematology/Oncology and Neurology, Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA.
Insights
Valproic acid (VPA) may cause acquired protein C deficiency in children, increasing stroke risk. Studies show reduced protein C levels in nearly half of children on VPA therapy.
Area of Science:
- Neurology
- Hematology
- Pediatrics
Background:
- Acquired protein C deficiency is a rare condition that can increase the risk of blood clots.
- Valproic acid (VPA) is a commonly used anticonvulsant medication in children.
Observation:
- A case of stroke in a child with acquired protein C deficiency while on VPA therapy prompted further investigation.
- Protein C levels were measured in pediatric patients receiving VPA monotherapy versus other anticonvulsants.
Findings:
- Reduced protein C levels were observed in up to 45% of children treated with VPA monotherapy.
- This suggests a potential association between VPA use and decreased protein C activity.
Implications:
- VPA may contribute to acquired protein C deficiency, potentially increasing thrombotic risk in pediatric patients.
- Monitoring protein C levels in children receiving VPA may be warranted.
- Further research is needed to confirm the causal link and elucidate the mechanism.
Abstract:
We report a case of stroke in a child with acquired protein C deficiency receiving valproic acid (VPA). To investigate the possible association of VPA with protein C deficiency, protein C levels were measured in 20 children receiving VPA monotherapy and 20 children receiving other anticonvulsants. Protein C levels were reduced in up to 45% of the VPA-treated subjects.