Evidence map›Paper›PMID 39251708›Full record

ReviewNature reviews. Gastroenterology & hepatology2024

Ammonia-induced stress response in liver disease progression and hepatic encephalopathy.

Rocío Gallego-Durán, Anna Hadjihambi, Javier Ampuero, Christopher F Rose, Rajiv Jalan, Manuel Romero-Gómez

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Gastroenterology & hepatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

44 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Five-decade prevalence of delirium in pneumonia, risk factors and associated mortality: a systematic review and meta-analysis.European respiratory review : an official journal of the European Respiratory Society · 2025
    Pooled it
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. The role of ammonia in chronic liver disease.Hepatology communications · 2026
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Cell-type-resolved transcriptomic landscape of human focal cortical dysplasia.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Rocío Gallego-Durán *UCM Digestive Diseases, Virgen del Rocío University Hospital. Instituto de Biomedicina de Sevilla (HUVR/CSIC/US), Department of Medicine, University of Seville, Seville, Spain.
Anna Hadjihambi *The Roger Williams Institute of Hepatology, Foundation for Liver Research, London, UK.
Javier AmpueroUCM Digestive Diseases, Virgen del Rocío University Hospital. Instituto de Biomedicina de Sevilla (HUVR/CSIC/US), Department of Medicine, University of Seville, Seville, Spain.
Christopher F RoseHepato-Neuro Laboratory, CRCHUM, Université de Montréal, Montreal, Canada.
Rajiv JalanInstitute for Liver and Digestive Health, Division of Medicine, UCL Medical School, Royal Free Hospital, London, UK.ORCID http://orcid.org/0000-0002-7747-4015
Manuel Romero-GómezUCM Digestive Diseases, Virgen del Rocío University Hospital. Instituto de Biomedicina de Sevilla (HUVR/CSIC/US), Department of Medicine, University of Seville, Seville, Spain. mromerogomez@us.es.ORCID http://orcid.org/0000-0001-8494-8947

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ammonia levels are orchestrated by a series of complex interrelated pathways in which the urea cycle has a central role. Liver dysfunction leads to an accumulation of ammonia, which is toxic and is strongly associated with disruption of potassium homeostasis, mitochondrial dysfunction, oxidative stress, inflammation, hypoxaemia and dysregulation of neurotransmission. Hyperammonaemia is a hallmark of hepatic encephalopathy and has been strongly associated with liver-related outcomes in patients with cirrhosis and liver failure. In addition to the established role of ammonia as a neurotoxin in the pathogenesis of hepatic encephalopathy, an increasing number of studies suggest that it can lead to hepatic fibrosis progression, sarcopenia, immune dysfunction and cancer. However, elevated systemic ammonia levels are uncommon in patients with metabolic dysfunction-associated steatotic liver disease. A clear causal relationship between ammonia-induced immune dysfunction and risk of infection has not yet been definitively proven. In this Review, we discuss the mechanisms by which ammonia produces its diverse deleterious effects and their clinical relevance in liver diseases, the importance of measuring ammonia levels for the diagnosis of hepatic encephalopathy, the prognosis of patients with cirrhosis and liver failure, and how our knowledge of inter-organ ammonia metabolism is leading to the development of novel therapeutic approaches.

Indexed as

AmmoniaDisease ProgressionHepatic EncephalopathyHumansHyperammonemiaLiver CirrhosisLiver DiseasesOxidative StressAmmonia

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.