Evidence map›Paper›PMID 32589264›Full record

ReviewEuropean journal of clinical investigation2020

COVID-19 and non-alcoholic fatty liver disease: Two intersecting pandemics.

Piero Portincasa, Marcin Krawczyk, Wiktor Smyk, Frank Lammert, Agostino Di Ciaula

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in European journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 4 pooled it
16.9field-weighted citation impact, top 1% 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

89 citing papers in PubMed, 4 syntheses or guidelines pooled it, 143 citations in OpenAlex.

  1. Pooled it
  2. Fibrosis-4 index and mortality in coronavirus disease 2019: a meta-analysis.European journal of gastroenterology & hepatology · 2021
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29 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

5 authors at 3 institutions in 3 countries.

Piero PortincasaClinica Medica 'A. Murri', Department of Biomedical Sciences and Human Oncology, University of Bari 'Aldo Moro', Bari, Italy.ORCID https://orcid.org/0000-0001-5359-1471
Marcin KrawczykDepartment of Medicine II, Saarland University Medical Center, Saarland University, Homburg, Germany.ORCID https://orcid.org/0000-0002-0113-0777
Wiktor SmykLiver and Internal Medicine Unit, Department of General, Transplant and Liver Surgery, Medical University of Warsaw, Warsaw, Poland.
Frank LammertDepartment of Medicine II, Saarland University Medical Center, Saarland University, Homburg, Germany.
Agostino Di CiaulaClinica Medica 'A. Murri', Department of Biomedical Sciences and Human Oncology, University of Bari 'Aldo Moro', Bari, Italy.ORCID https://orcid.org/0000-0002-5476-7376
Medical University of Warsaw · PLUniversity of Bari Aldo Moro · ITSaarland University · DE

Funding

FOIE GRAS #722619FOIE GRAS #734719mtFOIE GRAS #734719
6 · The paper itself

Abstract

backgroundInitial evidence from China suggests that most vulnerable subjects to COVID-19 infection suffer from pre-existing illness, including metabolic abnormalities. The pandemic characteristics and high-lethality rate of COVID-19 infection have raised concerns about interactions between virus pathobiology and components of the metabolic syndrome.

methodsWe harmonized the information from the recent existing literature on COVID-19 acute pandemic and mechanisms of damage in non-alcoholic fatty liver disease (NAFLD), as an example of chronic (non-communicable) metabolic pandemic.

resultsCOVID-19-infected patients are more fragile with underlying metabolic illness, including hypertension, cardiovascular disease, type 2 diabetes, chronic lung diseases (e.g. asthma, chronic obstructive pulmonary disease and emphysema) and metabolic syndrome. During metabolic abnormalities, expansion of metabolically active fat ('overfat condition') parallels chronic inflammatory changes, development of insulin resistance and accumulation of fat in configuring NAFLD. The deleterious interplay of inflammatory pathways chronically active in NAFLD and acutely in COVID-19-infected patients, can explain liver damage in a subgroup of patients and might condition a worse outcome in metabolically compromised NAFLD patients. In a subgroup of patients with NAFLD, the underlying liver fibrosis might represent an additional and independent risk factor for severe COVID-19 illness, irrespective of metabolic comorbidities.

conclusionsNAFLD can play a role in the outcome of COVID-19 illness due to frequent association with comorbidities. Initial evidences suggest that increased liver fibrosis in NAFLD might affect COVID-19 outcome. In addition, long-term monitoring of post-COVID-19 NAFLD patients is advisable, to document further deterioration of liver damage. Further studies are required in this field.

Indexed as

BetacoronavirusCoronavirus InfectionsCOVID-19Cytokine Release SyndromeHumansInflammationInsulin ResistanceLiverMetabolic SyndromeNon-alcoholic Fatty Liver DiseasePandemicsPneumonia, ViralSARS-CoV-2fatty livermitochondrianitrosative stressoxidative stressSARS-CoV-2

Identifiers

PMID32589264
PMCPMC7361203
OpenAlexW3037894931

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.