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DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
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[Valproate-induced hyperammonemic encephalopathy].

B Granel1, M Gavaret, X Le Baut

  • 1Service de médecine interne, hôpital Nord, Assistance publique des Hôpitaux de Marseille (AP-HM), chemin des Bourrely, Marseille cedex 15, France. bgranel@ap-hm.fr

La Revue De Medecine Interne
|July 17, 2010
PubMed
Summary
This summary is machine-generated.

Valproate can cause severe hyperammonemic encephalopathy, a brain condition. Discontinuing valproate rapidly improved consciousness and normalized brain activity and ammonia levels in a patient with liver disease.

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Area of Science:

  • Neurology
  • Psychiatry
  • Toxicology

Background:

  • Valproate is a widely used antiepileptic and psychiatric medication.
  • Hyperammonemic encephalopathy is a serious, albeit rare, complication associated with valproate use.
  • Patients with underlying liver conditions may be at increased risk.

Observation:

  • A 44-year-old male with epilepsy and alcoholic cirrhosis presented with drowsiness.
  • The patient was on valproate and gabapentin therapy.
  • Clinical examination, electroencephalogram (EEG), and blood tests confirmed valproate-induced hyperammonemic encephalopathy.

Findings:

  • Discontinuation of valproate resulted in rapid clinical improvement, including restored consciousness.
  • EEG abnormalities normalized quickly after valproate withdrawal.
  • Serum ammonia levels also returned to normal ranges following valproate cessation.

Implications:

  • This case highlights the potential for valproate to induce severe hyperammonemic encephalopathy, particularly in patients with compromised liver function.
  • The exact mechanisms underlying valproate-induced hyperammonemia remain unclear, with potential roles for carnitine deficiency or urea cycle defects.
  • Liver disease may exacerbate the risk and severity of valproate-induced encephalopathy, warranting careful monitoring in such patients.