Evidence map›Paper›PMID 26041962›Full record

ReviewJournal of clinical and experimental hepatology2015

Pathogenesis of hepatic encephalopathy: role of ammonia and systemic inflammation.

Dominic R Aldridge, Edward J Tranah, Debbie L Shawcross

Open access · greenAbstract readReview
In one paragraph

Review in Journal of clinical and experimental hepatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 164 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
164citing papers in PubMed, 7 pooled it
6.1field-weighted citation impact, top 2% 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

164 citing papers in PubMed, 7 syntheses or guidelines pooled it, 298 citations in OpenAlex.

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104 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Dominic R AldridgeInstitute of Liver Studies, King's College London School of Medicine at King's College Hospital, King's College Hospital, Denmark Hill, London SE5 9RS, United Kingdom.
Edward J TranahInstitute of Liver Studies, King's College London School of Medicine at King's College Hospital, King's College Hospital, Denmark Hill, London SE5 9RS, United Kingdom.
Debbie L ShawcrossInstitute of Liver Studies, King's College London School of Medicine at King's College Hospital, King's College Hospital, Denmark Hill, London SE5 9RS, United Kingdom.
King's College Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The syndrome we refer to as Hepatic Encephalopathy (HE) was first characterized by a team of Nobel Prize winning physiologists led by Pavlov and Nencki at the Imperial Institute of Experimental Medicine in Russia in the 1890's. This focused upon the key observation that performing a portocaval shunt, which bypassed nitrogen-rich blood away from the liver, induced elevated blood and brain ammonia concentrations in association with profound neurobehavioral changes. There exists however a spectrum of metabolic encephalopathies attributable to a variety (or even absence) of liver hepatocellular dysfunctions and it is this spectrum rather than a single disease entity that has come to be defined as HE. Differences in the underlying pathophysiology, treatment responses and outcomes can therefore be highly variable between acute and chronic HE. The term also fails to articulate quite how systemic the syndrome of HE can be and how it can be influenced by the gastrointestinal, renal, nervous, or immune systems without any change in background liver function. The pathogenesis of HE therefore encapsulates a complex network of interdependent organ systems which as yet remain poorly characterized. There is nonetheless a growing recognition that there is a complex but influential synergistic relationship between ammonia, inflammation (sterile and non-sterile) and oxidative stress in the pathogenesis HE which develops in an environment of functional immunoparesis in patients with liver dysfunction. Therapeutic strategies are thus moving further away from the traditional specialty of hepatology and more towards novel immune and inflammatory targets which will be discussed in this review.

Indexed as

ammoniaAoCLF, acute-on-chronic liver failureATP, adenosine triphosphateBBB, blood–brain barrierCBF, cerebral blood flowCNS, central nervous systemGS, glutamine synthetaseHE, hepatic encephalopathyhepatic encephalopathyICH, intracranial hypertensioninfectioninflammationiNOS, inducible nitric oxide synthaseMHE, minimal hepatic encephalopathyMPT, mitochondrial permeability transitionPAG, phosphate-activated glutaminasePTP, permeability transition poresystemic inflammatory response syndromeTLR, toll-like receptor

Identifiers

PMID26041962
PMCPMC4442852
OpenAlexW2014782195

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.