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Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
Published on: September 9, 2012
Factor XIII deficiency associated with valproate treatment
Martin Teich1, Elke Longin, Carl-Erik Dempfle
1Department of Pediatrics, Mannheim University Hospital, University of Heidelberg, Heidelberg, Germany. martin.teich@kikli.ma.uni-heidelberg.de
Insights
Valproate (VPA) treatment in children can lead to factor XIII deficiency, causing bleeding issues like epistaxis. Monitoring factor XIII activity is crucial before surgery in patients on VPA.
Area of Science:
- Pediatric Hematology
- Pharmacology
- Clinical Toxicology
Background:
- Valproate (VPA) is a widely used anticonvulsant and mood-stabilizing medication.
- Coagulation disorders are potential adverse effects of certain medications.
- Factor XIII deficiency is a rare bleeding disorder affecting hemostasis.
Observation:
- Two pediatric cases of factor XIII deficiency developed during valproate treatment are presented.
- Patients exhibited recurrent epistaxis as the primary clinical manifestation.
- Associated coagulation abnormalities included thrombocytopenia and decreased von Willebrand factor levels.
Findings:
- Factor XIII deficiency resolved upon reduction or discontinuation of valproate therapy.
- Valproate may impact hepatic synthetic function and megakaryocyte activity, potentially affecting factor XIII levels.
- The study suggests a causal or aggravating role of valproate in factor XIII deficiency.
Implications:
- Bleeding symptoms in children on valproate may indicate an acquired factor XIII deficiency.
- Pre-operative assessment of factor XIII activity is recommended for patients undergoing surgery while on valproate.
- This highlights the importance of recognizing drug-induced coagulation disorders for patient safety.
Purpose:
We present two children who developed a deficiency of factor XIII with valproate (VPA) treatment. This coagulation disorder has not been described in association with VPA treatment in children, and only very recently in one adult patient.
Results:
Both patients showed recurrent epistaxis as major clinical sign of a combination of decreased coagulation parameters (factor XIII deficiency with thrombocytopenia and decreased von Willebrand factor, respectively). A few days after reduction or withdrawal of VPA treatment, clinical symptoms disappeared, and laboratory findings were within normal range.
Conclusions:
VPA is known to influence the synthetic function of the liver and the number and function of megakaryocytes. Therefore an alteration of the factor XIII level by VPA is conceivable. Our case reports suggest that bleeding symptoms during VPA treatment may be caused or aggravated by a decreased factor XIII activity. A determination of factor XIII activity should be considered before surgical procedures during VPA treatment to minimize the risk of (severe) postsurgical bleeding complications.
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