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Some interactions between valproate and other antiseizure medications*

Some interactions between valproate and other antiseizure medications*
Interacting drugs Effects (probable mechanism) Management
Valproate, with:
Carbamazepine Decreased valproate effect and possible increased toxicity (increased metabolism by CYP 2C9, 2C19, glucuronidation, and formation of toxic metabolite) Monitor clinical status and valproate concentrations
Carbamazepine toxicity (increased concentration of active epoxide metabolite and displacement from binding sites) Monitor clinical status and carbamazepine and carbamazepine epoxide concentrations; carbamazepine dose may need to be adjusted
Ethosuximide Possible ethosuximide toxicity (decreased metabolism) Monitor clinical status and ethosuximide concentrations
Possible decreased valproate effect (mechanism not established) Monitor clinical status and valproate concentrations
Felbamate Possible decreased felbamate effect (mechanism unknown) Monitor clinical status
Possible valproate toxicity (decreased metabolism by CYP2C19) Monitor clinical status and valproate concentrations. A reduction in valproate dose is recommended when initiating felbamate. Specific dose adjustment recommendations are provided in the Lexicomp monograph.
Lamotrigine Lamotrigine toxicity (decreased metabolism; glucuronidation) Decrease lamotrigine dose by approximately 50%; monitor clinical status and lamotrigine concentrations. Specific lamotrigine dose adjustment recommendations for use with valproate are provided in the Lexicomp monograph.
Oxcarbazepine Possible decreased oxcarbazepine effect (increased metabolism) Monitor clinical status and oxcarbazepine concentrations
Phenobarbital Possible phenobarbital toxicity (decreased metabolism by CYP2C9 and glucuronidation) Monitor clinical status and phenobarbital concentrations
Possible decreased valproate effect (increased metabolism by glucuronidation and CYP oxidation) Monitor clinical status and valproate concentrations
Phenytoin Possible phenytoin toxicity (displacement from binding sites and decreased metabolism; complex time course) Monitor clinical status and phenytoin concentrations (unbound concentrations may be more helpful than total)
Possible decreased valproate effect and increased toxicity (increased metabolism and formation of toxic valproate metabolites) Monitor clinical status and valproate serum concentrations
Rufinamide Possible increased rufinamide toxicity (decreased metabolism) Monitor clinical status; a decrease in initial rufinamide dose is recommended. Specific rufinamide dose adjustment recommendations for use with valproate are provided in the Lexicomp monograph.
Topiramate Possible increased hepatotoxic effect of valproate and increased risk for hypothermia (mechanism not established) Monitor clinical status
  • Valproate is highly bound to plasma proteins and undergoes complex hepatic metabolism including glucuronidation (30 to 50%); the unbound fraction of valproate increases as valproate serum concentrations rise, causing wide inter-individual variability in the observed effect(s) of drug interactions.
  • Valproate effects can be altered by other antiseizure medications via multiple mechanisms, eg, altered protein binding and competitive inhibition at sites of hepatic drug metabolism (ie, glucuronidation).
CYP: cytochrome P450.
* Not all potential interactions are listed. Additional interactions of antiseizure medications and management suggestions may be determined using the drug interactions tool (Lexi-Interact) included within UpToDate.
¶ Routine carbamazepine serum measurements do not assess for accumulation of the active carbamazepine-epoxide metabolite, but this metabolite can be measured as a separate test; refer to accompanying text.
Adapted from: Drugs for Epilepsy. Treatment guidelines from The Medical Letter 2008; 6(70):37-46. Copyright © 2008 The Medical Letter. Additional data from: Lexicomp Online. Copyright © 1978-2024 Lexicomp, Inc. All Rights Reserved and Drugs for Epilepsy. Treatment guidelines from The Medical Letter 2013; 11(126):9-11. Copyright © 2013 The Medical Letter.
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