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Hepatic encephalopathy (HE) involves neurological and psychiatric issues due to liver insufficiency, often caused by ammonia buildup. Treatments focus on reducing ammonia and managing gut toxins, with liver transplantation as a last resort.

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Area of Science:

  • Hepatology
  • Neurology
  • Gastroenterology

Background:

  • Hepatic encephalopathy (HE) is a complex neuropsychiatric complication of liver dysfunction.
  • It presents as a spectrum from subtle cognitive changes to coma.
  • Pathophysiology involves hyperammonemia, neuroinflammation, and gut-brain axis disturbances.

Purpose of the Study:

  • To review the causes, types, and clinical staging of hepatic encephalopathy.
  • To discuss current understanding of HE's pathogenetic mechanisms.
  • To outline currently practiced therapeutic options for HE.

Main Methods:

  • Literature review of causes, mechanisms, and treatments of HE.
  • Analysis of current research on ammonia metabolism and neuroinflammation.
  • Discussion of therapeutic strategies including pharmacological and supportive measures.

Main Results:

  • HE encompasses covert and overt forms, with covert HE showing behavioral and cognitive impairment.
  • Hyperammonemia, neuroinflammation (TNF-α, IL-6, IL-17), gut dysbiosis, and metal deposition (manganese, zinc) contribute to HE.
  • Therapies include lactulose, rifaximin, L-ornithine L-aspartate (LOLA), and in refractory cases, liver transplantation or liver assist devices.

Conclusions:

  • HE pathogenesis is multifactorial, involving ammonia toxicity, neuroinflammation, and gut-derived toxins.
  • Therapeutic approaches aim to reduce ammonia production/absorption and mitigate neuroinflammation.
  • Management strategies are evolving, with advanced options like liver transplantation offering definitive treatment.