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Related Experiment Video

Updated: Apr 26, 2026

Electrochemically and Bioelectrochemically Induced Ammonium Recovery

Electrochemically and Bioelectrochemically Induced Ammonium Recovery

Published on: January 22, 2015

Pharmacotherapy for hyperammonemia.

Anna Hadjihambi¹, Varun Khetan, Rajiv Jalan

¹UCL Institute for Liver and Digestive Health, UCL Medical School , Upper Third Floor, Royal Free Campus, Pond Street, NW3 2PF, London , UK +44 207 4332 794 ; rjalan@ucl.ac.uk.

Expert Opinion on Pharmacotherapy

|July 18, 2014

Summary

Hepatic encephalopathy (HE) treatments focus on ammonia reduction. Lactulose and rifaximin are key for secondary prevention, while emerging therapies require further evidence for efficacy in managing HE.

Keywords:

acute liver failure chronic liver failure hepatic encephalopathy hyperammonemia ornithine phenylacetate

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Area of Science:

Hepatology
Neuroscience
Pharmacology

Background:

Hepatic encephalopathy (HE) is a severe neuropsychiatric complication of liver failure.
Ammonia accumulation is strongly implicated in HE pathogenesis and symptoms.
Current treatments primarily target ammonia detoxification pathways.

Purpose of the Study:

To review current therapeutic targets for hyperammonemia.
To discuss existing and emerging drugs for hyperammonemia treatment.

Main Methods:

Literature review of current therapeutic targets and drugs for hyperammonemia.
Analysis of established and novel treatment strategies for HE.

Main Results:

Lactulose and rifaximin are established for secondary prophylaxis of HE.
Molecular adsorbent recirculating system (MARS) shows efficacy in severe HE, independent of ammonia.
Challenges remain in defining appropriate endpoints for HE treatment trials.

Conclusions:

Lactulose and rifaximin are mainstays for HE secondary prophylaxis.
MARS offers a potential option for severe HE.
Further research is needed to validate emerging treatments and establish clear endpoints.