ABSTRACT
The pathogenesis of hepatic encephalopathy is mediated to a large extent by ammonia, mainly derived from the gut. Both bacterial and nonbacterial mechanisms of ammoniagenesis have been shown, but ammoniagenesis mediated by colonic bacteria is probably of clinical significance. The therapy of hepatic encephalopathy is based on the putative etiological agents, including ammonia. Non-absorbable disaccharides and antibiotics have been shown to modify gut flora and decrease blood ammonia levels, but these are not necessarily related (indicating nonbacterial sources of ammonia, which may also be decreased by these compounds). A combination of these has been suggested but not consistently demonstrated to be beneficial in hepatic encephalopathy. Sodium benzoate is an alternate method of nonbacterial, non-hepatic metabolic binding pathway for ammonia disposal. Other mechanisms of gut bacterial modification may be achieved albeit transiently by the use of resistant bacteria like Enterococcus faecium.