Changes in cerebral oxidative metabolism in patients with acute liver failure

    5 Citations (Scopus)

    Abstract

    Acute liver failure patients with a persistence of hyperammonemia are at an increased risk of intracranial hypertension due to development of brain oedema. In vitro studies of brain tissue and cell cultures that indicates that exposure to ammonium inhibits enzymatic activity in the tricarboxylic acid cycle, induces substrate depletion through marked glutamate utilization for glutamine synthesis and leads to mitochondrial dysfunction. In patients with acute liver failure cerebral microdialysis studies show a linear correlation between the lactate to pyruvate ratio and the glutamine concentration, as well as to some of the adenosine triphosphate degradation products. However, clinical observations of cerebral exchange rates of oxygen, glucose, lactate and amino acids challenge the interpretation of these findings. In this review the conflicting data of cerebral metabolism during acute liver failure is discussed.
    Original languageEnglish
    JournalMetabolic Brain Disease
    Volume28
    Issue number2
    Pages (from-to)179-82
    Number of pages4
    ISSN0885-7490
    DOIs
    Publication statusPublished - Jun 2013

    Keywords

    • Amino Acids
    • Ammonia
    • Animals
    • Brain
    • Brain Chemistry
    • Humans
    • Hyperammonemia
    • Lactic Acid
    • Liver Failure, Acute
    • Oxidation-Reduction
    • Pyruvic Acid

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