Evidence map›Paper›PMID 32011822›Full record

SynthesisBJS open2020

Meta-analysis and field synopsis of genetic variants associated with the risk and severity of acute pancreatitis.

F F van den Berg, M A Kempeneers, H C van Santvoort, A H Zwinderman, Y Issa, M A Boermeester

Open access · goldAbstract readMeta-AnalysisSystematic Review
In one paragraph

Synthesis in BJS open, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

9 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Diagnosis and Management of Acute Pancreatitis.Diagnostics (Basel, Switzerland) · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
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 2 institutions in 1 country.

F F van den BergDepartment of Surgery, Amsterdam University Medical Centre, University of Amsterdam, Amsterdam, the Netherlands.
M A KempeneersDepartment of Surgery, Amsterdam University Medical Centre, University of Amsterdam, Amsterdam, the Netherlands.
H C van SantvoortDepartment of Surgery, St Antonius Hospital, Nieuwegein, the Netherlands.
A H ZwindermanDepartment of Clinical Epidemiology, Biostatistics and Bioinformatics, Amsterdam University Medical Centre, University of Amsterdam, Amsterdam, the Netherlands.
Y IssaDepartment of Surgery, Amsterdam University Medical Centre, University of Amsterdam, Amsterdam, the Netherlands.
M A BoermeesterDepartment of Surgery, Amsterdam University Medical Centre, University of Amsterdam, Amsterdam, the Netherlands.
University of Amsterdam · NLUniversity Medical Center Utrecht · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGenetic risk factors can provide insight into susceptibility for acute pancreatitis (AP) and disease progression towards (infected) necrotizing pancreatitis and persistent organ failure. The aim of the study was to undertake a systematic review of the genetic evidence for AP.

methodsOnline databases (MEDLINE, Embase, BIOSIS, Web of Science, Cochrane Library) were searched to 8 February 2018. Studies that reported on genetic associations with AP susceptibility, severity and/or complications were eligible for inclusion. Meta-analyses were performed of variants that were reported by at least two data sources. Venice criteria and Bayesian false-discovery probability were applied to assess credibility.

resultsNinety-six studies reporting on 181 variants in 79 genes were identified. In agreement with previous meta-analyses, credible associations were established for SPINK1 (odds ratio (OR) 2·87, 95 per cent c.i. 1·89 to 4·34), IL1B (OR 1·23, 1·06 to 1·42) and IL6 (OR 1·64, 1·15 to 2·32) and disease risk. In addition, two novel credible single-nucleotide polymorphisms were identified in Asian populations: ALDH2 (OR 0·48, 0·36 to 0·64) and IL18 (OR 1·47, 1·18 to 1·82). Associations of variants in TNF, GSTP1 and CXCL8 genes with disease severity were identified, but were of low credibility.

conclusionGenetic risk factors in genes related to trypsin activation and innate immunity appear to be associated with susceptibility to and severity of AP.

Indexed as

Polymorphism, Single NucleotideGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansInterleukin-1betaInterleukin-6PancreatitisRisk FactorsTrypsin Inhibitor, Kazal PancreaticIL1B protein, humanIL6 protein, humanInterleukin-1betaInterleukin-6SPINK1 protein, humanTrypsin Inhibitor, Kazal Pancreatic

Identifiers

PMID32011822
PMCPMC6996643
OpenAlexW2992515793

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.