The pathogenesis of Hepatic Encephalopathy (HE) is still unclear even though it is known that severe liver impairment and hepatic hemodynamic changes lead to reduced clearance of intestinal nitrogen substances. These substances cause an alteration of brain neurotransmission, inhibitory prevailing over excitatory complexes. Treatment of HE comprises two steps: first reduce the liver nitrogen load and second rebalance the neurotransmission. Reduced liver nitrogen load is obtained by decreasing intestinal absorption through administration of non-absorbable disaccharides or antibiotics, by moderating endogenous catabolism with nutritional support and by increasing nitrogen elimination through pathways that are alternative to urea synthesis. Branched chain amino acids and more recently benzodiazepine antagonist have been used to modulate the alteration in brain neurotrasmission. The use of the latter is however still at an experimental stage.
|Number of pages||9|
|Publication status||Published - 1997|
ASJC Scopus subject areas