Evidence map›Paper›PMID 30302044›Full record

ReviewJournal of clinical and experimental hepatology2018

Hyperammonemia in Hepatic Encephalopathy.

A R Jayakumar, Michael D Norenberg

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of clinical and experimental hepatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 3 pooled it
4.7field-weighted citation impact, top 4% of its field
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

54 citing papers in PubMed, 3 syntheses or guidelines pooled it, 108 citations in OpenAlex.

  1. Pooled it
  2. Meta-analysis of probiotics efficacy in the treatment of minimum hepatic encephalopathy.Liver international : official journal of the International Association for the Study of the Liver · 2024
    Pooled it
  3. Pooled it
  4. Trial
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Novel roles of ammonia in physiology and cancer.Journal of molecular cell biology · 2025
    Review
  14. Article
  15. Review
  16. Observational
  17. Review
  18. Observational
  19. 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

2 authors at 2 institutions in 1 country.

A R JayakumarGeneral Medical Research, Neuropathology Section, R&D Service, Veterans Affairs Medical Center, Miami, FL 33125, United States.
Michael D NorenbergDepartment of Pathology, University of Miami School of Medicine, Miami, FL 33125, United States.
Neurological Surgery · USSouth Florida Veterans Affairs Foundation for Research and Education · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The precise mechanism underlying the neurotoxicity of Hepatic Encephalopathy (HE) is remains unclear. The dominant view has been that gut-derived nitrogenous toxins are not extracted by the diseased liver and thereby enter the brain. Among the various toxins proposed, the case for ammonia is most compelling. Events that lead to increased levels of blood or brain ammonia have been shown to worsen HE, whereas reducing blood ammonia levels alleviates HE. Clinical, pathological, and biochemical changes observed in HE can be reproduced by increasing blood or brain ammonia levels in experimental animals, while exposure of cultured astrocytes to ammonium salts reproduces the morphological and biochemical findings observed in HE. However, factors other than ammonia have recently been proposed to be involved in the development of HE, including cytokines and other blood and brain immune factors. Moreover, recent studies have questioned the critical role of ammonia in the pathogenesis of HE since blood ammonia levels do not always correlate with the level/severity of encephalopathy. This review summarizes the vital role of ammonia in the pathogenesis of HE in humans, as well as in experimental models of acute and chronic liver failure. It further emphasizes recent advances in the molecular mechanisms involved in the progression of neurological complications that occur in acute and chronic liver failure.

Indexed as

AHE, Acute Hepatic EncephalopathyALF, Acute Liver FailureammoniaCHE, Chronic Hepatic EncephalopathyCNS, Central Nervous SystemCSF, Cerebrospinal FluidECs, Endothelial CellsHE, Hepatic Encephalopathyhepatic encephalopathyIL, InterleukininflammationLPS, LipopolysaccharideMAPKs, Mitogen-Activated Protein Kinasesmatricellular proteinsNCX, Sodium-Calcium ExchangerNF-κB, Nuclear Factor-kappaBNHE, Sodium/Hydrogen Exchanger-1 or SLC9A1 (SoLute Carrier Family 9A1)SUR1, The Sulfonylurea Receptor 1TDP-43 and tau proteinopathiesTDP-43, TAR DNA-Binding Protein, 43 kDaTLR, Toll-like ReceptorTNF-α, Tumor Necrosis Factor-AlphaTSP-1, Thrombospondin-1

Identifiers

PMID30302044
PMCPMC6175739
OpenAlexW2808917216

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.