Ammonia, derived from the catabolism of amino acids and from the action of intestinal bacteria on dietary protein, is converted to urea in the liver hepatocytes and so rendered non-toxic. Studies have shown that excess ammonia can have a toxic effect on the central nervous system and clinical manifestations are typically neurological disturbances.
Elevated ammonia may also be observed in severe liver failure, as may occur in Reye’s Syndrome, viral hepatitis, or cirrhosis. Hyperammonemia occurs with genetic defects of the urea cycle and some other hereditary disorders. Therefore, elevated plasma ammonia may occur in the pediatric population. Elevated ammonia has also been reported due to administration of valproic acid.