Evidence map›Paper›PMID 23118780›Full record

ArticleClinical & developmental immunology2012

Ileal inflammation may trigger the development of GP2-specific pancreatic autoantibodies in patients with Crohn's disease.

Polychronis Pavlidis, Ourania Romanidou, Dirk Roggenbuck, Maria G Mytilinaiou, Faris Al-Sulttan, Christos Liaskos, Daniel S Smyk, Andreas L Koutsoumpas, Eirini I Rigopoulou, Karsten Conrad and 2 more

Open access · goldAbstract read
In one paragraph

Article in Clinical & developmental immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 3 pooled it
3.9field-weighted citation impact, top 6% 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

19 citing papers in PubMed, 3 syntheses or guidelines pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Pancreatic Exocrine Insufficiency Is Surprisingly Common.Integrative medicine (Encinitas, Calif.) · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Differential diagnosis of Crohn's disease using antibodies to glycoprotein 2 and Saccharomyces cerevisiae.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2019
    Article
  10. Pancreatic Involvement in Inflammatory Bowel Disease: A Review.Journal of clinical medicine research · 2018
    Review
  11. Article
  12. Article
  13. Observational
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
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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

12 authors at 7 institutions in 3 countries.

Polychronis PavlidisDivision of Transplantation Immunology and Mucosal Biology, King's College London School of Medicine at King's College Hospital, London SE5 9RJ, UK.
Ourania Romanidou
Dirk Roggenbuck
Maria G Mytilinaiou
Faris Al-Sulttan
Christos Liaskos
Daniel S Smyk
Andreas L Koutsoumpas
Eirini I Rigopoulou
Karsten Conrad
Alastair Forbes
Dimitrios P Bogdanos
Center for Research and Technology Thessaly · GRKing's College Hospital · GBUniversity College Hospital · GBGeneric Assays (Germany) · DETU Dresden · DEUniversity College London · GBUniversity of Thessaly · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Why zymogen glycoprotein 2 (GP2), the Crohn's disease (CD)-specific pancreatic autoantigen, is the major target of humoral autoimmunity in inflammatory bowel diseases (IBD) is uknown. Recent evidence demonstrates that GP2 is also present on the apical surface of microfold (M) intestinal cells. As the colon lacks GP2-rich M cells, we assumed that patients with colonic CD are seronegative for anti-GP2. Anti-GP2 antibodies were tested in 225 CDs, including 45 patients with colonic location (L2), 45 with terminal ileum (L1) and 135 with ileocolonic involvement; 225 patients with ulcerative colitis (UC) were also tested. Anti-GP2 reactivity was detected in 59 (26.2%) CDs and 15 (6.7%) UCs (P < 0.001). Only 5 CDs with L2 had anti-GP2 antibodies, compared to 54/180 (30.0%, P = 0.0128) of the CDs with L1 and L3. Anti-GP2 antibody positive CD patients had higher ASCA titres compared to seronegative cases. Amongst the 128 CD patients with previous surgical intervention, 45 (35.0%) were anti-GP2 antibody positive compared to 14/97 (14.0%) without surgical (P < 0.001). Our data support the assumption that ileal inflammation is required for the development of anti-GP2 antibodies in CD, and suggest that the intestine rather than the pancreatic juice is the antigenic source required for the initiation of anti-GP2 antibodies.

Indexed as

AdultAutoantibodiesAutoantigensColitis, UlcerativeCrohn DiseaseFemaleGPI-Linked ProteinsHumansIleitisImmunoglobulin GInflammationInflammatory Bowel DiseasesMaleMembrane GlycoproteinsMiddle AgedPancreasAutoantibodiesAutoantigensglycoprotein-2, pancreasGP2 protein, humanGPI-Linked ProteinsImmunoglobulin GMembrane Glycoproteins

Identifiers

PMID23118780
PMCPMC3483735
OpenAlexW2026271060

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.