Evidence map›Paper›PMID 36313186›Full record

ArticleJHEP reports : innovation in hepatology2022

Clinical and genetic determinants of the fatty liver-coagulation balance interplay in individuals with metabolic dysfunction.

Luca Valenti, Armando Tripodi, Vincenzo La Mura, Serena Pelusi, Cristiana Bianco, Erica Scalambrino, Sara Margarita, Francesco Malvestiti, Luisa Ronzoni, Marigrazia Clerici and 5 more

Abstract read
In one paragraph

Article in JHEP reports : innovation in hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Impact of PNPLA3 I148M on Clinical Outcomes in Patients With MASLD.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Review
  5. Review
  6. Predictors of controlled attenuation parameter in metabolic dysfunction.United European gastroenterology journal · 2024
    Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
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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

15 authors.

Luca ValentiFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Precision Medicine Lab, Biological Resource Center, Department of Transfusion Medicine, Milan, Italy.
Armando TripodiFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Angelo Bianchi Bonomi Hemophilia and Thrombosis Center, Milan, Italy.
Vincenzo La MuraUniversità Degli Studi di Milano, Department of Pathophysiology and Transplantation, Milan, Italy.
Serena PelusiFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Precision Medicine Lab, Biological Resource Center, Department of Transfusion Medicine, Milan, Italy.
Cristiana BiancoFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Precision Medicine Lab, Biological Resource Center, Department of Transfusion Medicine, Milan, Italy.
Erica ScalambrinoFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Angelo Bianchi Bonomi Hemophilia and Thrombosis Center, Milan, Italy.
Sara MargaritaFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Precision Medicine Lab, Biological Resource Center, Department of Transfusion Medicine, Milan, Italy.
Francesco MalvestitiUniversità Degli Studi di Milano, Department of Pathophysiology and Transplantation, Milan, Italy.
Luisa RonzoniFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Precision Medicine Lab, Biological Resource Center, Department of Transfusion Medicine, Milan, Italy.
Marigrazia ClericiFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Angelo Bianchi Bonomi Hemophilia and Thrombosis Center, Milan, Italy.
Roberta D'AmbrosioFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Gastroenterology and Hepatology, Milan, Italy.
Mirella FraquelliFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Gastroenterology and Endoscopy, Milan, Italy.
Rossana CarpaniFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Precision Medicine Lab, Biological Resource Center, Department of Transfusion Medicine, Milan, Italy.
Daniele PratiFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Precision Medicine Lab, Biological Resource Center, Department of Transfusion Medicine, Milan, Italy.
Flora PeyvandiUniversità Degli Studi di Milano, Department of Pathophysiology and Transplantation, Milan, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background & Aims: The aim of this study was to examine the determinants of the interplay between liver damage and the coagulation balance in individuals at risk of non-alcoholic fatty liver disease (NAFLD). Methods: We considered 581 healthy participants with ≥3 metabolic alterations undergoing clinical and genomic evaluation, measurement of liver stiffness (LSM) and controlled attenuation parameter (CAP) by Fibroscan, Pro-C3, coagulation balance (von Willebrand factor [vWF], factor VIII/protein C ratio [F8/PC] as the main outcome, D-dimer as marker of coagulation/fibrinolysis activation). Results: Liver fibrosis indices (both Fibrosis-4 [FIB-4] and liver stiffness measurement [LSM]), but not liver fat (CAP), were independently associated with higher F8/PC ratio ( Conclusions: In individuals with metabolic dysfunction, liver damage severity and possibly the Lay summary: In individuals with metabolic alterations at risk of metabolic fatty liver disease, there is a tendency toward heightened blood coagulation (clotting), but the cause and the impact on the progression of liver disease remain unclear. Here we show that liver damage severity and metabolic alterations, but not hepatic fat, are mainly responsible for heightened coagulation in patients with metabolic fatty liver disease. By using genetic approaches, we showed that hepatic inflammation due to lipotoxicity may favour heightened coagulation, which in turn can trigger liver fibrosis, igniting a vicious cycle that leads to progressive liver disease.

Indexed as

ABO blood groupALT, alanine aminotransferaseAST, aspartate aminotransferaseCAP, continuous attenuation parameterCRP, C-reactive proteinF8, factor VIIIFIB-4, Fibrosis-4FNI, Fibrosis NASH indexFVL, factor V LeidenGGT, gamma glutamyl transferaseGLM, generalised linear modelHOMA-IR, Homeostatic Model Assessment for Insulin ResistanceLiver fibrosisLSM, liver stiffness measurementNAFLDNAFLD, non-alcoholic fatty liver diseaseNASH, non-alcoholic steatohepatitisPC, protein CPNPLA3Pro-C3, N-terminal pro-peptide of collagen-3PRS-5, polygenic risk cosre-5PRS-HFC, polygenic risk score - hepatic fat contentvon Willebrand factorvWF, von Willebrand factor

Identifiers

PMID36313186
PMCPMC9597122

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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.