Evidence map›Paper›PMID 18291265›Full record

ReviewSurgery2008

Bile and pancreatic juice exclusion activates acinar stress kinases and exacerbates gallstone pancreatitis.

Isaac Samuel

Open access · greenAbstract readReview
In one paragraph

Review in Surgery, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

10 citing papers in PubMed, 23 citations in OpenAlex.

  1. Research Progress onMediators of inflammation · 2026
    Review
  2. Article
  3. Biliary pancreatitis. Deadly threat to the elderly. Is it a real threat?International journal of health sciences · 2015
    Article
  4. Systemic inflammation with multiorgan dysfunction is the cause of death in murine ligation-induced acute pancreatitis.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2011
    Article
  5. Etiology and diagnosis of acute biliary pancreatitis.Nature reviews. Gastroenterology & hepatology · 2010
    Review
  6. Dominant negative p38 mitogen-activated protein kinase expression inhibits NF-kappaB activation in AR42J cells.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2010
    Article
  7. Acute pancreatitis: etiology and common pathogenesis.World journal of gastroenterology · 2009
    Review
  8. Article
  9. Article
  10. Enteral exclusion increases MAP kinase activation and cytokine production in a model of gallstone pancreatitis.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2008
    Article
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

1 author at 1 institution in 1 country.

Isaac SamuelDepartment of Surgery, University of Iowa Roy J. and Lucille A. Carver College of Medicine and Veterans Administration Medical Center, Iowa City, Iowa 52242, USA. Isaac-samuel@uiowa.edu
University of Iowa · US

Funding

Role of CCK Receptor in Acute Pancreatitis PathogenesisK08DK062805 · NIDDK · UNIVERSITY OF IOWA · PI SAMUEL, ISAAC · 2003 to 2007
$626k
NIDDK NIH HHS K08 DK062805NIDDK NIH HHS K08-DK062805
6 · The paper itself

Abstract

hypothesisBile and pancreatic juice exclusion from gut activates acinar stress kinases and exacerbates gallstone pancreatitis as evidenced by the ameliorating effects of replacement therapy in an experimental model of duct ligation-induced acute pancreatitis. In the early stages of gallstone pancreatitis, bile-pancreatic juice cannot enter the gut. Enteral exclusion worsens pancreatitis by causing feedback hyperstimulation of the exocrine pancreas that activates acinar cell stress kinases. Investigations using a unique surgical model, the Donor Rat Model, showed that duodenal replacement of bile-pancreatic juice in rats with duct ligation attenuates pancreatic stress kinase activation, reduces pancreatic cytokine production, and ameliorates pancreatic morphologic changes. These findings suggest that exclusion-induced acinar hyperstimulation, in the presence of duct obstruction, exacerbates acute pancreatitis via stress kinase activation. Although acinar hyperstimulation has often been implicated in the pathogenesis of acute pancreatitis, the lack of supporting evidence remains a conspicuous void. The proposed hypothesis draws on fresh evidence to present a new paradigm that reexamines the role of exocrine pancreatic hyperstimulation in gallstone pancreatitis pathogenesis.

Indexed as

Acute DiseaseAnimalsBileEnzyme ActivationGallstonesHumansPancreas, ExocrinePancreatic JuicePancreatitisProtein KinasesProtein Kinases

Identifiers

PMID18291265
PMCPMC2278165
OpenAlexW2088445767

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.