Evidence map›Paper›PMID 33190346›Full record

ReviewLiver international : official journal of the International Association for the Study of the Liver2021

Pathophysiological mechanisms of liver injury in COVID-19.

Alexander D Nardo, Mathias Schneeweiss-Gleixner, May Bakail, Emmanuel D Dixon, Sigurd F Lax, Michael Trauner

Open access · hybridAbstract readReview
In one paragraph

Review in Liver international : official journal of the International Association for the Study of the Liver, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 227 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
227citing papers in PubMed, 2 pooled it
7.5field-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

227 citing papers in PubMed, 2 syntheses or guidelines pooled it, 398 citations in OpenAlex.

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167 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

6 authors at 3 institutions in 1 country.

Alexander D NardoHans Popper Laboratory of Molecular Hepatology, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0000-0003-1895-7161
Mathias Schneeweiss-GleixnerMedical Intensive Care Unit 13H1. Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
May BakailCampus IT, Institute of Science and Technology Austria, Klosterneuburg, Austria.
Emmanuel D DixonHans Popper Laboratory of Molecular Hepatology, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Sigurd F LaxDepartment of Pathology, Hospital Graz II, Academic Teaching Hospital of the Medical University of Graz, Graz, Austria.
Michael TraunerHans Popper Laboratory of Molecular Hepatology, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Medical University of Vienna · ATInstitute of Science and Technology Austria · ATJohannes Kepler University of Linz · AT

Funding

Austrian Science Foundation F7310-B21
6 · The paper itself

Abstract

The recent outbreak of coronavirus disease 2019 (COVID-19), caused by the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) has resulted in a world-wide pandemic. Disseminated lung injury with the development of acute respiratory distress syndrome (ARDS) is the main cause of mortality in COVID-19. Although liver failure does not seem to occur in the absence of pre-existing liver disease, hepatic involvement in COVID-19 may correlate with overall disease severity and serve as a prognostic factor for the development of ARDS. The spectrum of liver injury in COVID-19 may range from direct infection by SARS-CoV-2, indirect involvement by systemic inflammation, hypoxic changes, iatrogenic causes such as drugs and ventilation to exacerbation of underlying liver disease. This concise review discusses the potential pathophysiological mechanisms for SARS-CoV-2 hepatic tropism as well as acute and possibly long-term liver injury in COVID-19.

Indexed as

SARS-CoV-2Viral TropismAngiotensin-Converting Enzyme 2CholestasisCOVID-19HumansLiverLiver DiseasesNon-alcoholic Fatty Liver DiseaseACE2 protein, humanAngiotensin-Converting Enzyme 2

Identifiers

PMID33190346
PMCPMC7753756
OpenAlexW3104434004

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.