Abstract  Hepatic encephalopathy (HE) is seen as a clinical manifestation of low grade chronic cerebral edema, which is accompanied by alterations in glioneural communication. Different factors such as ammonia, inflammatory cytokines, benzodiazepines and electrolyte imbalances may precipitate or aggravate glia edema, thereby explaining precipitation of HE episodes by a variety of unrelated factors. Recognition and rigorous treatment of these precipitating factors is the most important measure in HE therapy which may be augmented by dietary and medical approaches. Among these approaches, evidence for proven therapeutical efficacy in HE on the basis of placebo-controlled trials is existing only for transplantation, protein restriction, administration of vegetable proteins, ornithine-aspartate, oral branched-chain amino acid treatment as well as lactulose enemas. The efficacy of oral lactulose has not been demonstrated on the basis of placebo-controlled trials.

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