Evidence map›Paper›PMID 26481639›Full record

ReviewMetabolic brain disease2016

The concept of "the inflamed brain" in acute liver failure: mechanisms and new therapeutic opportunities.

Roger F Butterworth

Abstract readReview
PubMed Publisher
In one paragraph

Review in Metabolic brain disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Observational
  8. Review
  9. Article
  10. Iranian journal of basic medical sciences · 2020
    Article
  11. Review
  12. Astrocytes and Glutamine Synthetase in Epileptogenesis.Journal of neuroscience research · 2019
    Review
  13. Review
  14. Hyperammonemia in Hepatic Encephalopathy.Journal of clinical and experimental hepatology · 2018
    Review
  15. Update in Hepatic Encephalopathy.Journal of clinical and experimental hepatology · 2018
    Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Brain Edema in Chronic Hepatic Encephalopathy.Journal of clinical and experimental hepatology
    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

1 author at 1 institution in 1 country.

Roger F ButterworthDepartment of Medicine, University of Montreal, Montreal, QC, Canada. roger.butterworth@umontreal.ca.
Université de Montréal · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The presence and severity of a systemic inflammatory response is a major predictor of brain edema and encephalopathy in acute liver failure (ALF) and polymorphisms of the gene coding for the proinflammatory cytokine TNF-alpha are known to influence the clinical outcome in ALF. Recent reports provide robust evidence for a role of neuroinflammation(inflammation of the brain per se) in ALF with the cardinal features of neuroinflammation including activation of microglial cells and increased production in situ of pro-inflammatory cytokines such as TNF-alpha and interleukins IL-1beta and IL-6. Multiple liver-brain signalling pathways have been proposed to explain the phenomenon of neuroinflammation in liver failure and these include direct effects of systemically-derived cytokines, recruitment of monocytes relating to microglial activation as well as effects of liver failure-derived toxins and altered permeability of the blood-brain barrier. Synergistic mechanisms involving ammonia and cytokines have been proposed. Currently-available strategies aimed at lowering of blood ammonia such as lactulose, probiotics and rifaximin have the potential to dampen systemic inflammation as does the anti-oxidant N-acetyl cysteine, mild hypothermia and albumin dialysis. Experimental studies demonstrate that deletion of genes coding for TNF-alpha or IL-1 leads to attenuation of the CNS consequences of ALF and administration of the TNF-alpha receptor antagonist etanercept has comparable beneficial effects in experimental ALF. Together, these findings confirm a major role for central neuroinflammatory mechanisms in general and mechanisms involving TNF-alpha in particular in the pathogenesis of the cerebral consequences of ALF and open the door to novel therapeutic interventions in this often fatal disorder.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalBrainBrain EdemaGenetic TherapyHepatic EncephalopathyHumansInflammation MediatorsLiver Failure, AcuteAnti-Inflammatory Agents, Non-SteroidalInflammation MediatorsAcute liver failureAmmoniaEncephalopathyMicrogliaMinocyclineNeuroinflammationProinflammatory cytokines

Identifiers

PMID26481639
OpenAlexW1768109898

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.