Hepatic encephalopathy (HE) is a brain dysfunction caused by liver insufficiency or portal systemic shunting. HE most commonly occurs in decompensated liver cirrhosis and incorporates a spectrum of manifestations that ranges from mild cognitive impairment to coma. Although its pathogenesis is not entirely understood, one of the main factors is thought to be ammonia. Apart from hyperammonemia, various other pathogenic mechanisms, such as the gamma-aminobutyric acid (GABA) theory, the benzodiazepine theory, the manganese theory, and the theory of oxidative/nitrosative stress, have been implicated in the development of HE. The pharmacological treatments that are currently used in clinical practice are directed toward reducing the production and absorption of gut-derived ammonia.
