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Related Experiment Videos

Valproic acid and the liver.

D Cotariu1, J L Zaidman

  • 1Assaf Harofeh Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Zerifin, Israel.

Clinical Chemistry
|May 1, 1988
PubMed
Summary
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Valproic acid (VPA) can cause liver damage, including reversible dysfunction or failure. This anticonvulsant affects fatty acid metabolism, gluconeogenesis, and urea synthesis, with mechanisms still under investigation.

Area of Science:

  • Biochemistry
  • Pharmacology
  • Hepatology

Background:

  • Valproic acid (VPA) is a widely prescribed anticonvulsant.
  • VPA therapy is linked to significant hepatotoxicity, ranging from reversible dysfunction to fatal hepatic failure.

Purpose of the Study:

  • To review the biochemical abnormalities associated with VPA-induced hepatotoxicity.
  • To explore potential mechanisms and risk factors for VPA hepatotoxicity.

Main Methods:

  • Review of clinical and experimental studies.
  • Analysis of biochemical pathways affected by VPA.

Main Results:

  • VPA inhibits hepatic fatty acid beta-oxidation and synthesis, gluconeogenesis, urea synthesis, and the glycine cleavage system.

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  • Observed abnormalities include altered mitochondrial membrane protein conformation, hyperammonemia, and increased bile flow.

    • Conclusions:

    • The precise mechanisms of VPA hepatotoxicity, whether by VPA or its metabolites, require further elucidation.
    • Factors like starvation, metabolic disorders, neurological conditions, and enzyme-inducing drugs may increase susceptibility to VPA-induced liver injury.