Evidence map›Paper›PMID 33073044›Full record

ReviewTranslational gastroenterology and hepatology2020

Pathogenesis and pathways: nonalcoholic fatty liver disease & alcoholic liver disease.

Kyle E Robinson, Vijay H Shah

Abstract readReview
In one paragraph

Review in Translational gastroenterology and hepatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. 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

2 authors.

Kyle E RobinsonDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA.
Vijay H ShahDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA.

Funding

TREAT-MayoU01AA021788 · NIAAA · MAYO CLINIC ROCHESTER · PI MALHI, HARMEET, SHAH, VIJAY H. · 2012 to 2022
$4.7M
Molecular Mechanisms of Liver Fibrosis (Diversity Supplement)R37AA021171 · NIAAA · MAYO CLINIC ROCHESTER · PI VIJAY H. SHAH · 2019 to 2026
$3.0M
Integrated Therapies for Alcohol use in Alcohol-associated Liver Disease (ITAALD) – Mayo ClinicU01AA026974 · NIAAA · MAYO CLINIC ROCHESTER · PI VICTOR M. KARPYAK, VIJAY H. SHAH · 2018 to 2026
$2.9M
Molecular Mechanisms of Liver FibrosisR01AA021171 · NIAAA · MAYO CLINIC ROCHESTER · PI SHAH, VIJAY H. · 2012 to 2018
$2.5M
Assessment of Alcoholic Hepatitis with Multiparametric Magnetic Resonance ElastographyUH3AA026887 · NIAAA · MAYO CLINIC ROCHESTER · PI SHAH, VIJAY H., YIN, MENG · 2020 to 2022
$1.1M
Noninvasive assessment of alcoholic hepatitis effects in promoting age-related cognitive decline with multiparametric magnetic resonance elastography (MRE) imagingUH2AA026887 · NIAAA · MAYO CLINIC ROCHESTER · PI SHAH, VIJAY H., YIN, MENG · 2018 to 2019
$653k
Randomized Placebo Controlled Pilot Trial to determine the efficacy of an IL22 agonist (F-652) in patients with Alcoholic HepatitisU01AA026886 · NIAAA · MAYO CLINIC ROCHESTER · PI SHAH, VIJAY H., SIMONETTO, DOUGLAS A. · 2018 to 2022
$375k
NIAAA NIH HHS R01 AA021171NIAAA NIH HHS R37 AA021171NIAAA NIH HHS U01 AA021788NIAAA NIH HHS U01 AA026886NIAAA NIH HHS U01 AA026974NIAAA NIH HHS UH2 AA026887NIAAA NIH HHS UH3 AA026887
6 · The paper itself

Abstract

Alcoholic liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD) account for the majority of hepatic morbidity and deaths due to cirrhosis in the United States. ALD is an umbrella term for a number of conditions linked to excessive alcohol consumption including simple steatosis, cirrhosis, acute alcoholic hepatitis (AH) with or without cirrhosis, and hepatocellular carcinoma (HCC) as a complication of cirrhosis. Although it presents with histological features resembling alcohol-induced liver injury, NAFLD occurs in patients with little or no history of alcohol consumption. NAFLD is a broad-spectrum term used to describe anything from fat accumulation in hepatocytes without inflammation or fibrosis (simple hepatic steatosis) to hepatic steatosis with a necroinflammatory component (steatohepatitis) with or without associated fibrosis. The pathogenesis is not fully understood for either disease. Development of severe liver disease is highly variable amongst chronic abusers of alcohol. Sex, age, genetics, host microbiome, and behavior are all factors linked to the development of ALD. These factors also contribute to NAFLD, but by contrast, insulin resistance is widely believed to be the main driver of nonalcoholic hepatic steatosis. The mechanism behind the transition from nonalcoholic steatosis to steatohepatitis remains a matter of debate with insulin resistance, oxidative injury, hepatic iron, gut hormones, antioxidant deficiency, and host microbiome all suspected to play part of the role.

Indexed as

Alcoholalcoholic hepatitis (AH)fibrosisliverportal hypertension

Identifiers

PMID33073044
PMCPMC7530314

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.