Evidence map›Paper›PMID 32035166›Full record

ReviewNeuroscience letters2020

Cerebral edema and liver disease: Classic perspectives and contemporary hypotheses on mechanism.

Eric M Liotta, W Taylor Kimberly

Open access · greenAbstract readReview
In one paragraph

Review in Neuroscience letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
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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.

Eric M LiottaNorthwestern University-Feinberg School of Medicine, Department of Neurology, United States; Northwestern University-Feinberg School of Medicine, Department of Surgery, Division of Organ Transplantation, United States; Northwestern University Transplant Outcomes Research Collaboration, United States. Electronic address: Eric.liotta@northwestern.edu.
W Taylor KimberlyHarvard Medical School, Department of Neurology, United States. Electronic address: WTKIMBERLY@mgh.harvard.edu.
Harvard University · USNorthwestern University · US

Funding

NINDS NIH HHS L30 NS098427
6 · The paper itself

Abstract

Liver disease is a growing public health concern. Hepatic encephalopathy, the syndrome of brain dysfunction secondary to liver disease, is a frequent complication of both acute and chronic liver disease and cerebral edema (CE) is a key feature. While altered ammonia metabolism is a key contributor to hepatic encephalopathy and CE in liver disease, there is a growing appreciation that additional mechanisms contribute to CE. In this review we will begin by presenting three classic perspectives that form a foundation for a discussion of CE in liver disease: 1) CE is unique to acute liver failure, 2) CE in liver disease is only cytotoxic, and 3) CE in liver disease is primarily an osmotically mediated consequence of ammonia and glutamine metabolism. We will present each classic perspective along with more recent observations that call in to question that classic perspective. After highlighting these areas of debate, we will explore the leading contemporary mechanisms hypothesized to contribute to CE during liver disease.

Indexed as

AmmoniaAnimalsBrainBrain EdemaHepatic EncephalopathyHumansLiver Failure, AcuteAmmoniaCerebral edemaCirrhosisHepatic encephalopathyLiver failure

Identifiers

PMID32035166
PMCPMC7773170
OpenAlexW3004487619

What OpenQuestion holds

Textmetadata
LicenceTDM
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.