Evidence map›Paper›PMID 28106158›Full record

ArticleScientific reports2017

Transaminase abnormalities and adaptations of the liver lobule manifest at specific cut-offs of steatosis.

Andrew Hall, Claudia Covelli, Roberta Manuguerra, Tu Vinh Luong, Elena Buzzetti, Emmanuel Tsochatzis, Massimo Pinzani, Amar Paul Dhillon

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 16% 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, 23 citations in OpenAlex.

  1. Trial
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  4. A novel subset of hepatocytes is simultaneously gluconeogenic andbioRxiv : the preprint server for biology · 2026
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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

8 authors at 3 institutions in 1 country.

Andrew HallThe Department of Cellular Pathology, Royal Free London NHS Foundation Trust, London, NW3 2QG, UK.
Claudia CovelliThe Department of Cellular Pathology, Royal Free London NHS Foundation Trust, London, NW3 2QG, UK.
Roberta ManuguerraThe Department of Cellular Pathology, Royal Free London NHS Foundation Trust, London, NW3 2QG, UK.
Tu Vinh LuongThe Department of Cellular Pathology, Royal Free London NHS Foundation Trust, London, NW3 2QG, UK.
Elena BuzzettiInstitute for Liver and Digestive Health, UCL, Royal Free Campus, London, NW3 2QG, UK.
Emmanuel TsochatzisInstitute for Liver and Digestive Health, UCL, Royal Free Campus, London, NW3 2QG, UK.
Massimo PinzaniInstitute for Liver and Digestive Health, UCL, Royal Free Campus, London, NW3 2QG, UK.
Amar Paul DhillonThe Department of Cellular Pathology, UCL Medical School, Royal Free Campus, London, NW3 2QG, UK.
Royal Free London NHS Foundation Trust · GBUniversity College London · GBThe Royal Free Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is little documented evidence suggesting that liver fat is responsible for liver injury in the absence of other disease processes. We investigated the relationships between liver fat, aminotransferases and hepatic architecture in liver biopsies with simple steatosis. We identified 136 biopsies with simple steatosis from the Royal Free Hospital Archives with both clinical data and sufficient material. Digital image analysis was employed to measure fat proportionate area (mFPA). Hepatocyte area (HA) and lobule radius (LR) were also measured. There were significant increases in ALT (p < 0.001) and AST (p = 0.013) with increased fat content and evidence to suggest both 5% and 20% mFPA as a cut-off for raised ALT. In liver with increased fat content there were significant increases in HA (p < 0.001). LR also increased as mFPA increased to 10% (p < 0.001), at which point the lobule ceased to expand further and was counterbalanced with a decrease in the number of hepatocytes per lobule (p = 0.029). Consequently there are mechanisms of adaption in the liver architecture to accommodate the accumulation of fat and these are accompanied by significant increases in transaminases. These results support the generally accepted cut-off of 5% fat for steatosis and indicate 20% as a threshold of more severe liver injury.

Indexed as

AdultAlanine TransaminaseAspartate AminotransferasesBiopsyFatsFatty LiverFemaleHistocytochemistryHumansImage Processing, Computer-AssistedMaleMiddle AgedAlanine TransaminaseAspartate AminotransferasesFats

Identifiers

PMID28106158
PMCPMC5247698
OpenAlexW2573487838

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.