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[Pathogenesis of cirrhotic hepatic encephalopathy. Treatment implications]
1Servico de Gastroenterología, Hospital Universitario, Universidad Autónoma de Nuevo León, Monterrey, México.
Background:
Hepatic encephalopathy (HE) is a neuropsychologic syndrome associated with multifactorial metabolic disruptions. Several physiopathogenic theories have been proposed.
Objectives:
To review the most important theories (ammonia, mercaptans, short chain fatty acids, false neurotransmitters, gamma-aminobutyric acid, endogenous benzodiazepines) and to analyze the different therapeutic modalities derived from these theories.
Methods:
An intensive bibliographic review was carried out using Med-Line and Current Contents data base. Randomized therapeutic trials published in the last ten years were particularly analyzed.
Results:
From all theories proposed, the revised ammonia theory better explains pathogenesis of HE based on the information about efficacy of anti-ammonia agents. Authors propose a theory in order to explain the effect of ammonia and serotonin in neurotransmission, particularly excitatory glutamatergic neurotransmission.
Conclusions:
It seems that ammonia has a predominant role in pathogenesis of HE. Some other agents may be involved but its nature is not actually defined. Glutamatergic neurotransmission un HE has been recently studied.