Hepatic encephalopathy is a complex neuropsychiatric syndrome which may complicate acute or chronic live failure. It is characterized by changes in mental state including a wide range of neuropsychiatric symptoms ranging from minor signs of altered brain function to deep coma.
Treatment o hepatic encephalopathy aims at reducing the production and absorption of ammonia, which is involved in the pathogenesis. Reduction of absorption of neurotoxins from the gastrointestinal tract, low protein diet, non-absorbable disaccharides (lactulose and lactilol), and gut sterilizing antibiotics are the measures currently used in the management. Metabolic removal of ammonia through the use of L-ornithine, L-aspartate (LOLA) and benzoate have been added to the treatment regimen (J. McDonald, Evidence Based Gastroenterology and Hepatology, 1999). In cirrhotics, LOLA infusions prevented hyperammonemia after an oral protein load in a dose-dependent fashion. Benzoate, on the other hand, reacts with glycine to form hippurate, and for each mole of benzoate, one mole of waste nitrogen is excreted in the urine.
In this study, we performed a meta-analysis to assess the beneficial or harmful effects of LOLA for hepatic encephalopathy.
To assess the beneficial or harmful effects of LOLA for hepatic encephalopathy
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