Evidence map›Paper›PMID 23622139›Full record

ReviewGastroenterology2013

Genetic risk factors for pancreatic disorders.

David C Whitcomb

Open access · greenAbstract readReview
In one paragraph

Review in Gastroenterology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
134citing papers in PubMed, 4 pooled it
26.7field-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

134 citing papers in PubMed, 4 syntheses or guidelines pooled it, 295 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. CFTR IVS8 Poly-T Variation Affects Severity of Acute Pancreatitis in Women.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2019
    Trial
  6. Mutations in the pancreatic secretory enzymesProceedings of the National Academy of Sciences of the United States of America · 2018
    Trial
  7. Trial
  8. Article
  9. Review
  10. Article
  11. Review
  12. Pancreatic exocrine insufficiency.EClinicalMedicine · 2026
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

74 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

1 author at 1 institution in 1 country.

David C WhitcombDivision of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. whitcomb@pitt.edu
University of Pittsburgh · US

Funding

North American Pancreatitis Study 2 (NAPS2)R01DK061451 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WHITCOMB, DAVID CLEMENT · 2002 to 2010
$4.9M
MOLECULAR GENETICS OF HEREDITARY PANCREATITISR01DK054709 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WHITCOMB, DAVID CLEMENT · 1999 to 2008
$2.0M
NAPS2 Continuation Genome Wide Association Study of PancreatitisR56DK061451 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WHITCOMB, DAVID CLEMENT · 2011 to 2011
$1.3M
NIDDK NIH HHS R01 DK054709NIDDK NIH HHS R01 DK061451NIDDK NIH HHS R56 DK061451
6 · The paper itself

Abstract

A combination of genetic, environmental, and metabolic factors contribute to the development and recurrence of acute and chronic pancreatitis; information on all of these is required to manage patients effectively. For example, variants that affect regulation of the protease, serine (PRSS)1-PRSS2, and claudin (CLDN)2 loci, rather than their coding sequences, interact with other genetic and environmental factors to affect disease development. New strategies are needed to use these data and determine their contribution to pathogenesis, because these variants differ from previously studied, rare variants in exons (coding regions) of genes such as PRSS1, SPINK1, cystic fibrosis transmembrane conductance regulator (CFTR), chymotrypsin (CTR)C, and calcium-sensing receptor (CASR). Learning how various genetic factors affect pancreatic cells and systems could lead to etiology-based therapies rather than treatment of symptoms.

Indexed as

Acute DiseaseDisease ProgressionGenetic Predisposition to DiseaseHumansPancreatic DiseasesPancreatitis, ChronicPhenotypePrognosisRisk FactorsTime Factors

Identifiers

PMID23622139
PMCPMC3684061
OpenAlexW1995243958

What OpenQuestion holds

Textmetadata
LicenceTDM
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.