Evidence map›Paper›PMID 31219169›Full record

ReviewAlcohol and alcoholism (Oxford, Oxfordshire)2019

Alcoholic Hepatitis: A Review.

Nooshin Hosseini, Julia Shor, Gyongyi Szabo

Open access · bronzeAbstract readReview
In one paragraph

Review in Alcohol and alcoholism (Oxford, Oxfordshire), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 1 pooled it
10.5field-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, 1 synthesis or guideline pooled it, 176 citations in OpenAlex.

  1. Epidemiology, risk factors, and clinical characteristics of amoebic liver abscess: a systematic review and meta-analysis from India.International microbiology : the official journal of the Spanish Society for Microbiology · 2025
    Pooled it
  2. Observational
  3. Review
  4. Article
  5. Observational
  6. Article
  7. Ultra-Micro Powder From Edible Plants (Food science & nutrition · 2026
    Article
  8. Article
  9. Article
  10. [Bioinformatics screening and analysis of key genes of ferroptosis and autophagy in alcoholic liver disease and their validation].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Assessment of Prognostic Factors of Acute Hepatitis Among Pediatric Patients: A Cross-Sectional Study.JGH open : an open access journal of gastroenterology and hepatology · 2025
    Article
  20. Article

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

3 authors at 1 institution in 1 country.

Nooshin HosseiniUniversity of Massachusetts, Gastroenterology, University of Massachusetts Medical School.
Julia ShorUniversity of Massachusetts, Gastroenterology, University of Massachusetts Medical School.
Gyongyi SzaboProfessor, Department of Medicine, University of Massachusetts, 364 Plantation Street, LRB-208, Worcester, MA, USA.
University of Massachusetts Chan Medical School · US

Funding

Novel Therapies for Alcoholic HepatitisU01AA021893 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI MCCLAIN, CRAIG J., MCCULLOUGH, ARTHUR JOSEPH · 2012 to 2017
$6.0M
NIAAA NIH HHS U01 AA021893
6 · The paper itself

Abstract

Alcoholic liver disease (ALD) represents a spectrum of injury, ranging from simple steatosis to alcoholic hepatitis to cirrhosis. Regular alcohol use results in fatty changes in the liver which can develop into inflammation, fibrosis and ultimately cirrhosis with continued, excessive drinking. Alcoholic hepatitis (AH) is an acute hepatic inflammation associated with significant morbidity and mortality that can occur in patients with steatosis or underlying cirrhosis. The pathogenesis of ALD is multifactorial and in addition to genetic factors, alcohol-induced hepatocyte damage, reactive oxygen species, gut-derived microbial components result in steatosis and inflammatory cell (macrophage and neutrophil leukocyte) recruitment and activation in the liver. Continued alcohol and pro-inflammatory cytokines induce stellate cell activation and result in progressive fibrosis. Other than cessation of alcohol use, medical therapy of AH is limited to prednisolone in a subset of patients. Given the high mortality of AH and the progressive nature of ALD, there is a major need for new therapeutic intervention for this underserved patient population.

Indexed as

Hepatitis, AlcoholicHumansInflammation MediatorsKupffer CellsReactive Oxygen SpeciesInflammation MediatorsReactive Oxygen SpeciesABIC scorealcoholic hepatitisalcoholic liver diseasealcoholic steatohepatitisglascow alcoholic hepatitis scorelille scoremaddrey scoreMELD scorepro-inflammatory cytokinesstellate cell activation

Identifiers

PMID31219169
PMCPMC6671387
OpenAlexW2950214167

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.