Evidence map›Paper›PMID 25356028›Full record

ReviewWorld journal of gastroenterology2014

Alcoholic disease: liver and beyond.

Alba Rocco, Debora Compare, Debora Angrisani, Marco Sanduzzi Zamparelli, Gerardo Nardone

Registry-linked trialOpen access · hybridAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05261620 (W.I.S.E.-Wine Implementation for Surgical Recovery Enhancement), which is not on this map. Cited by 116 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed, 4 pooled it
6.3field-weighted citation impact, top 3% 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.

NCT05261620 nacompletednot on this mapstarted 2022, after this paper: background citation

W.I.S.E.-Wine Implementation for Surgical Recovery Enhancement

TypeinterventionalSponsorIRCCS San RaffaeleRan2022 to 2025Enrolled132ConditionsQuality of LifeArmsred wine
3 · Its place in the literature

Who cites it

116 citing papers in PubMed, 4 syntheses or guidelines pooled it, 243 citations in OpenAlex.

  1. Pooled it
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  4. Pooled it
  5. Nutrients · 2019
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56 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 1 institution in 1 country.

Alba RoccoAlba Rocco, Debora Compare, Debora Angrisani, Marco Sanduzzi Zamparelli, Gerardo Nardone, Gastroenterology Unit, Department of Clinical Medicine and Surgery, University Federico II of Naples, 80131 Naples, Italy.
Debora CompareAlba Rocco, Debora Compare, Debora Angrisani, Marco Sanduzzi Zamparelli, Gerardo Nardone, Gastroenterology Unit, Department of Clinical Medicine and Surgery, University Federico II of Naples, 80131 Naples, Italy.
Debora AngrisaniAlba Rocco, Debora Compare, Debora Angrisani, Marco Sanduzzi Zamparelli, Gerardo Nardone, Gastroenterology Unit, Department of Clinical Medicine and Surgery, University Federico II of Naples, 80131 Naples, Italy.
Marco Sanduzzi ZamparelliAlba Rocco, Debora Compare, Debora Angrisani, Marco Sanduzzi Zamparelli, Gerardo Nardone, Gastroenterology Unit, Department of Clinical Medicine and Surgery, University Federico II of Naples, 80131 Naples, Italy.
Gerardo NardoneAlba Rocco, Debora Compare, Debora Angrisani, Marco Sanduzzi Zamparelli, Gerardo Nardone, Gastroenterology Unit, Department of Clinical Medicine and Surgery, University Federico II of Naples, 80131 Naples, Italy.
University of Naples Federico II · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The harmful use of alcohol is a worldwide problem. It has been estimated that alcohol abuse represents the world's third largest risk factor for disease and disability; it is a causal factor of 60 types of diseases and injuries and a concurrent cause of at least 200 others. Liver is the main organ responsible for metabolizing ethanol, thus it has been considered for long time the major victim of the harmful use of alcohol. Ethanol and its bioactive products, acetaldehyde-acetate, fatty acid ethanol esters, ethanol-protein adducts, have been regarded as hepatotoxins that directly and indirectly exert their toxic effect on the liver. A similar mechanism has been postulated for the alcohol-related pancreatic damage. Alcohol and its metabolites directly injure acinar cells and elicit stellate cells to produce and deposit extracellular matrix thus triggering the "necrosis-fibrosis" sequence that finally leads to atrophy and fibrosis, morphological hallmarks of alcoholic chronic pancreatitis. Even if less attention has been paid to the upper and lower gastrointestinal tract, ethanol produces harmful effects by inducing: (1) direct damaging of the mucosa of the esophagus and stomach; (2) modification of the sphincterial pressure and impairment of motility; and (3) alteration of gastric acid output. In the intestine, ethanol can damage the intestinal mucosa directly or indirectly by altering the resident microflora and impairing the mucosal immune system. Notably, disruption of the intestinal mucosal barrier of the small and large intestine contribute to liver damage. This review summarizes the most clinically relevant alcohol-related diseases of the digestive tract focusing on the pathogenic mechanisms by which ethanol damages liver, pancreas and gastrointestinal tract.

Indexed as

Alcohol DrinkingAlcoholismAnimalsDisease ProgressionEthanolGastrointestinal DiseasesGastrointestinal TractHumansLiverLiver Diseases, AlcoholicPancreasPancreatic DiseasesPrognosisRisk AssessmentRisk FactorsEthanolAlcohol and gastrointestinal tractAlcoholic liver diseaseAlcoholic pancreatitis

Identifiers

PMID25356028
PMCPMC4209531
OpenAlexW1999958782

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

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 Socratic graph.