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The main pathophysiological mechanism of HE are based upon evidence of the accumulation of toxic substances, including the ammonia, glutamine, manganese, false neurotransmitters, inflammation, short chain fatty acids, oxidative stress, mercaptanes, neurosteroids, or low grade edema.2 However, the most widely accepted is that accumulation of endogenous and gut-derived ammonia crossing the blood-brain barrier, and functional changes in various neurotransmitter systems.3 Thus, current therapies focus on pathogenesis previously accepted, and the roles of drugs were critically estimated through systematic review according to methodology of Evidence-based Medicine (EBM), such as non-absorbable disaccharides,4 rifaximin,5 L-ornithine-L-aspartate (LOLA),6 naloxone7 have been widespread used now
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