Evidence map›Paper›PMID 29654817›Full record

ArticleJournal of hepatology2018

Dysregulation of serum bile acids and FGF19 in alcoholic hepatitis.

Katharina Brandl, Phillipp Hartmann, Lily J Jih, Donald P Pizzo, Josepmaria Argemi, Meritxell Ventura-Cots, Sally Coulter, Christopher Liddle, Lei Ling, Stephen J Rossi and 20 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of hepatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed
14.4field-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

130 citing papers in PubMed, 204 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Bile acid signaling in health and disease.Molecular biomedicine · 2026
    Review
  5. The Polysaccharides fromNutrients · 2026
    Article
  6. Review
  7. Review
  8. The Role of Gut Microbiota in Liver Regeneration After Partial Hepatectomy: New Evidence From Animal and Human Studies.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Cholestasis in Alcohol-Associated Liver Disease.The American journal of pathology · 2026
    Review
  17. Article
  18. Review
  19. Review
  20. Article

70 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

30 authors at 16 institutions in 8 countries.

Katharina BrandlSkaggs School of Pharmacy and Pharmaceutical Sciences, University of California San Diego, La Jolla, CA, USA.
Phillipp HartmannDepartment of Pediatrics, University of California San Diego, La Jolla, CA, USA; Department of Medicine, University of California San Diego, La Jolla, CA, USA.
Lily J JihDepartment of Pathology, University of California San Diego, La Jolla, CA, USA; Department of Pathology, VA San Diego Healthcare System, San Diego, CA, USA.
Donald P PizzoDepartment of Pathology, University of California San Diego, La Jolla, CA, USA.
Josepmaria ArgemiDivision of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh Liver Research Center, Pittsburgh, PA, USA.
Meritxell Ventura-CotsDivision of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh Liver Research Center, Pittsburgh, PA, USA.
Sally CoulterStorr Liver Centre, Westmead Institute for Medical Research and Sydney Medical School, University of Sydney, Australia.
Christopher LiddleStorr Liver Centre, Westmead Institute for Medical Research and Sydney Medical School, University of Sydney, Australia.
Lei LingNGM Bio, South San Francisco, CA, USA.
Stephen J RossiNGM Bio, South San Francisco, CA, USA.
Alex M DePaoliNGM Bio, South San Francisco, CA, USA.
Rohit LoombaDepartment of Medicine, University of California San Diego, La Jolla, CA, USA.
Wajahat Z MehalSection of Digestive Diseases, Yale University School of Medicine, New Haven, Connecticut, USA, and Section of Digestive Diseases, VA-CT Healthcare System, West Haven, CT, USA.
Derrick E FoutsJ. Craig Venter Institute, Rockville, MD, USA.
Michael R LuceyDivision of Gastroenterology and Hepatology, Department of Medicine, University of Wisconsin School of Medicine and Public Health, WI, USA.
Francisco Bosques-PadillaHospital Universitario, Departamento de Gastroenterología, Universidad Autonoma de Nuevo Leon, Monterrey, Mexico.
Philippe MathurinService des Maladies de L'appareil Digestif et Unité INSERM, Hôpital Huriez, Lille, France.
Alexander LouvetService des Maladies de L'appareil Digestif et Unité INSERM, Hôpital Huriez, Lille, France.
Guadalupe Garcia-TsaoSection of Digestive Diseases, Yale University School of Medicine, New Haven, Connecticut, USA, and Section of Digestive Diseases, VA-CT Healthcare System, West Haven, CT, USA.
Elizabeth C VernaDivision of Digestive and Liver Diseases, Department of Medicine, Columbia College of Physicians and Surgeons, Columbia University Medical Center, New York, NY, USA.
Juan G AbraldesDepartment of Medicine, University of Alberta, Edmonton, Alberta, Canada.
Robert S BrownDivision of Gastroenterology and Hepatology, Weill Cornell Medical College, New York, NY, USA.
Victor VargasLiver Unit, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain; Centro de Investigación en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Barcelona, Spain.
Jose AltamiranoLiver Unit, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
Juan CaballeríaCentro de Investigación en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Barcelona, Spain; Liver Unit, Hospital Clinic, Barcelona, Spain.
Debbie ShawcrossInstitute of Liver Studies, King's College London School of Medicine at King's College Hospital, King's College Hospital, London, UK.
Peter StärkelSt. Luc University Hospital, Université Catholique de Louvain, Brussels, Belgium.
Samuel B HoDepartment of Medicine, University of California San Diego, La Jolla, CA, USA; Department of Medicine, VA San Diego Healthcare System, San Diego, CA, USA.
Ramon BatallerDivision of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh Liver Research Center, Pittsburgh, PA, USA.
Bernd SchnablDepartment of Medicine, University of California San Diego, La Jolla, CA, USA; Department of Medicine, VA San Diego Healthcare System, San Diego, CA, USA. Electronic address: beschnabl@ucsd.edu.
University of California San Diego · USNGM Biopharmaceuticals (United States) · USUniversity of Pittsburgh Medical Center · USInserm · FRThe University of Sydney · AUUniversitat Autònoma de Barcelona · ESYale University · USColumbia University Irving Medical Center · USCornell University · USHospital Clínic de Barcelona · ESJ. Craig Venter Institute · USKing's College London · GBUCLouvain · BEUniversidad Autónoma de Nuevo León · MXUniversity of Alberta · CAUniversity of Wisconsin–Madison · US

Funding

Molecular Subtypes for Targeted Therapies in Alcoholic HepatitisU01AA021908 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BATALLER, RAMON · 2013 to 2017
$6.0M
The Role of the Intestinal Mycobiome in Alcoholic Liver DiseaseR01AA024726 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Bernd G. Schnabl · 2018 to 2026
$3.9M
Microbiome and intestinal innate immune response in alcoholic liver diseaseR01AA020703 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SCHNABL, BERND G. · 2011 to 2020
$3.6M
Microbiome as Therapeutic Target in Alcoholic HepatitisU01AA021856 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BRENNER, DAVID A., SCHNABL, BERND G. · 2013 to 2017
$2.1M
Targeting DAMPs in Alcoholic HepatitisU01AA021912 · NIAAA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MEHAL, WAJAHAT ZAFAR, SCHWABE, ROBERT F. · 2013 to 2017
$1.9M
The Role of the Intestinal Mycobiome in Alcoholic Liver DiseaseU01AA024726 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SCHNABL, BERND G. · 2017 to 2017
$353k
The Commensal Microflora Suppresses Liver FibrosisI01BX002213 · VA · VA SAN DIEGO HEALTHCARE SYSTEM · PI SCHNABL, BERND G. · 2015 to 2018
–
BLRD VA I01 BX002213NIAAA NIH HHS R01 AA020703NIAAA NIH HHS R01 AA024726NIAAA NIH HHS U01 AA021856NIAAA NIH HHS U01 AA021908NIAAA NIH HHS U01 AA021912NIAAA NIH HHS U01 AA024726
6 · The paper itself

Abstract

BACKGROUND &

aimsThe degree of cholestasis is an important disease driver in alcoholic hepatitis, a severe clinical condition that needs new biomarkers and targeted therapies. We aimed to identify the largely unknown mechanisms and biomarkers linked to cholestasis in alcoholic hepatitis.

methodsHerein, we analyzed a well characterized cohort of patients with alcoholic hepatitis and correlated clinical and histological parameters and outcomes with serum bile acids and fibroblast growth factor 19 (FGF19), a major regulator of bile acid synthesis.

resultsWe found that total and conjugated bile acids were significantly increased in patients with alcoholic hepatitis compared with controls. Serum FGF19 levels were strongly increased and gene expression of FGF19 was induced in biliary epithelial cells and ductular cells of patients with alcoholic hepatitis. De novo bile acid synthesis (CYP7A1 gene expression and C4 serum levels) was significantly decreased in patients with alcoholic hepatitis. Importantly, total and conjugated bile acids correlated positively with FGF19 and with disease severity (model for end-stage liver disease score). FGF19 correlated best with conjugated cholic acid, and model for end-stage liver disease score best with taurine-conjugated chenodeoxycholic acid. Univariate analysis demonstrated significant associations between FGF19 and bilirubin as well as gamma glutamyl transferase, and negative correlations between FGF19 and fibrosis stage as well as polymorphonuclear leukocyte infiltration, in all patients with alcoholic hepatitis.

conclusionSerum FGF19 and bile acids are significantly increased in patients with alcoholic hepatitis, while de novo bile acid synthesis is suppressed. Modulation of bile acid metabolism or signaling could represent a promising target for treatment of alcoholic hepatitis in humans. LAY SUMMARY: Understanding the underlying mechanisms that drive alcoholic hepatitis is important for the development of new biomarkers and targeted therapies. Herein, we describe a molecule that is increased in patients with alcoholic hepatitis. Modulating the molecular pathway of this molecule might lead to promising targets for the treatment of alcoholic hepatitis.

Indexed as

Bile Acids and SaltsCholestasisHepatitis, AlcoholicBiomarkersCorrelation of DataFemaleFibroblast Growth FactorsHumansMaleMiddle AgedNeutrophil InfiltrationNeutrophilsSeverity of Illness IndexSignal TransductionBile Acids and SaltsBiomarkersFGF19 protein, humanFibroblast Growth FactorsBile acidsFGF19Microbiome

Identifiers

PMID29654817
PMCPMC6054564
OpenAlexW2797379250

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.