[Pathogenesis of cirrhotic hepatic encephalopathy. Treatment implications].
BACKGROUND
Hepatic encephalopathy (HE) is a neuropsychologic syndrome associated with multifactorial metabolic disruptions. Several physiopathogenic theories have been proposed.


OBJECTIVE
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.
D006501:Hepatic Encephalopathy / Q000178:diet therapy / Q000209:etiology* / Q000628:therapy*; D006801:Humans; D008103:Liver Cirrhosis / Q000150:complications; D016032:Randomized Controlled Trials as Topic
Fisiopatogenia de la encefalopatía hepática cirrótica. Implicaciones en el tratamiento.