Changes in cerebral oxidative metabolism in patients with acute liver failure

• Published in: Metabolic brain disease Vol. 28; no. 2; pp. 179 - 182
• Main Authors: Bjerring, P. N., Larsen, F. S.
• Format: Journal Article
• Language: English
• Published: Boston Springer US 01-06-2013; Springer Nature B.V
• Subjects: Amino Acids - metabolism; Ammonia - metabolism; Animals; Biochemistry; Biomedical and Life Sciences; Biomedicine; Brain - metabolism; Brain Chemistry - physiology; Humans; Hyperammonemia - metabolism; Lactic Acid - metabolism; Liver Failure, Acute - metabolism; Metabolic Diseases; Neurology; Neurosciences; Oncology; Oxidation-Reduction; Pyruvic Acid - metabolism; Review Article; Pyruvate; Acute liver failure; Cerebral metabolism; Lactate; Hyperammonemia
• ISSN: 0885-7490; 1573-7365
• DOI: 10.1007/s11011-012-9346-2

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.