Evidence map›Paper›PMID 26909228›Full record

ReviewWorld journal of gastrointestinal pathophysiology2016

Alcoholic pancreatitis: New insights into the pathogenesis and treatment.

Dahn L Clemens, Katrina J Schneider, Christopher K Arkfeld, Jaclyn R Grode, Mark A Wells, Shailender Singh

Open access · diamondAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in World journal of gastrointestinal pathophysiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 4% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Approach to the Patient With Pancreatogenic Diabetes.The Journal of clinical endocrinology and metabolism · 2026
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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

6 authors at 1 institution in 1 country.

Dahn L ClemensDahn L Clemens, Fred and Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198-8098, United States.
Katrina J SchneiderDahn L Clemens, Fred and Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198-8098, United States.
Christopher K ArkfeldDahn L Clemens, Fred and Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198-8098, United States.
Jaclyn R GrodeDahn L Clemens, Fred and Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198-8098, United States.
Mark A WellsDahn L Clemens, Fred and Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198-8098, United States.
Shailender SinghDahn L Clemens, Fred and Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198-8098, United States.
VA Nebraska Western Iowa Health Care System · US

Funding

UNMC Summer Undergraduate Alcohol Research ProgramR25AA020818 · NIAAA · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Kristina L Bailey · 2012 to 2026
$931k
NIAAA NIH HHS R25 AA020818
6 · The paper itself

Abstract

Acute pancreatitis is a necro-inflammatory disease of the exocrine pancreas that is characterized by inappropriate activation of zymogens, infiltration of the pancreas by inflammatory cells, and destruction of the pancreatic exocrine cells. Acute pancreatitis can progress to a severe life-threatening disease. Currently there is no pharmacotherapy to prevent or treat acute pancreatitis. One of the more common factors associated with acute pancreatitis is alcohol abuse. Although commonly associated with pancreatitis alcohol alone is unable to cause pancreatitis. Instead, it appears that alcohol and its metabolic by-products predispose the pancreas to damage from agents that normally do not cause pancreatitis, or to more severe disease from agents that normally cause mild pancreatic damage. Over the last 10 to 20 years, a tremendous amount of work has defined a number of alcohol-mediated biochemical changes in pancreatic cells. Among these changes are: Sustained levels of intracellular calcium, activation of the mitochondrial permeability transition pore, endoplasmic reticulum stress, impairment in autophagy, alteration in the activity of transcriptional activators, and colocalization of lysosomal and pancreatic digestive enzymes. Elucidation of these changes has led to a deeper understanding of the mechanisms by which ethanol predisposes acinar cells to damage. This greater understanding has revealed a number of promising targets for therapeutic intervention. It is hoped that further investigation of these targets will lead to the development of pharmacotherapy that is effective in treating and preventing the progression of acute pancreatitis.

Indexed as

Acute pancreatitisAlcoholAlcoholic pancreatitisEthanol metabolismFatty acid ethyl estersPancreatitis

Identifiers

PMID26909228
PMCPMC4753189
OpenAlexW2409878449

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.