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Valproate-associated hyperammonemic encephalopathy.

Jim Wadzinski1, Ronald Franks, David Roane

  • 1Department of Family Medicine, East Tennessee State University, Johnson City 37604, USA.

Journal of the American Board of Family Medicine : JABFM
|September 8, 2007
PubMed
Summary
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Valproic acid (VPA) can cause serious hyperammonemic encephalopathy, even with normal VPA levels. Family physicians should monitor ammonia in patients with mental status changes.

Area of Science:

  • Neurology
  • Clinical Pharmacology
  • Toxicology

Background:

  • Valproic acid (VPA) is a widely prescribed anticonvulsant and mood stabilizer.
  • Elevated plasma ammonia is a known side effect of VPA treatment.
  • Hyperammonemic encephalopathy (HE) is a potentially severe complication linked to hyperammonemia.

Observation:

  • This study presents two cases of VPA-induced HE in patients with supratherapeutic VPA levels.
  • VPA-induced HE can occur even in individuals with normal liver function and normal VPA serum concentrations.
  • The condition has been documented in patients with both normal and elevated VPA levels.

Findings:

  • Valproic acid (VPA) can induce hyperammonemic encephalopathy (HE) irrespective of VPA dosage or serum levels.

Related Experiment Videos

  • Hyperammonemia and subsequent encephalopathy are significant risks associated with VPA therapy.
  • Early detection and intervention are crucial for managing VPA-induced HE.

    • Implications:

    • Family physicians must maintain a high index of suspicion for VPA-induced HE in patients presenting with altered mental status.
    • Monitoring plasma ammonia levels in patients on VPA is recommended, especially with neurological symptoms.
    • L-carnitine supplementation may be a beneficial therapeutic option for reducing ammonia levels in VPA-induced HE.