Evidence map›Paper›PMID 18600384›Full record

ReviewJournal of gastroenterology2008

Recent advances in autoimmune pancreatitis: concept, diagnosis, and pathogenesis.

Kazuichi Okazaki, Kazushige Uchida, Toshiro Fukui

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of gastroenterology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 3 pooled it
13.1field-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

40 citing papers in PubMed, 3 syntheses or guidelines pooled it, 135 citations in OpenAlex.

  1. IgG4-related disorders of the gastrointestinal tract: Experience from a tertiary care centre with systematic review of Indian literature.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2024
    Pooled it
  2. [Guidelines on the diagnosis and management of primary sclerosing cholangitis (2021)].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2022
    Guideline
  3. Clinical practice guidelines for IgG4-related sclerosing cholangitis.Journal of hepato-biliary-pancreatic sciences · 2019
    Guideline
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. An overview of the diagnosis and management of immunoglobulin G4-related disease.CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne · 2016
    Review
  12. Review
  13. Etiology, pathology, management and prognosis of chronic pancreatitis in Chinese population: A retrospective study.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2015
    Article
  14. Article
  15. Review
  16. Article
  17. PRSS1_p.Leu81Met mutation results in autoimmune pancreatitis.World journal of gastroenterology · 2013
    Article
  18. Article
  19. Review
  20. IgG4 Cholangiopathy.International journal of hepatology · 2012
    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

3 authors at 1 institution in 1 country.

Kazuichi OkazakiThird Department of Internal Medicine, Division of Gastroenterology and Hepatology Kansai Medical University, Shinmachi, Hirakata, Osaka, 573-1197, Japan.
Kazushige Uchida
Toshiro Fukui
Kansai Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent advances support the concept of autoimmune pancreatitis (AIP) as a unique systemic disease, because it shows occasional extrapancreatic lesions such as sclerosing cholangitis, sclerosing sialoadenitis, and retroperitoneal fibrosis, pathological features similar to those of fibrosis, and abundant infiltration of IgG4-positive plasma cells, and it is steroid responsive. Based on these findings, several diagnostic criteria have been proposed. Although AIP is accepted worldwide as a unique clinical entity, its pathogenetic mechanism remains unclear. To clarify its pathogenesis, its genetic background, humoral immunity, candidate target antigens including self-antigens and molecular mimicry by microbes, and cellular immunity including regulatory T cells, the complement system, and experimental models are reviewed. On the basis of this review, we hypothesize that the pathogenesis of AIP involves a biphasic mechanism consisting of "induction" and "progression." In the early stage, the initial response to self-antigens [lactoferrin, carbonic anhydrase (CA)-II, CA-IV, pancreatic secretory trypsin inhibitor, and alpha-fodrin] and molecular mimicry (Helicobacter pylori) are induced by decreased naïve regulatory T cells (Tregs), and T-helper (Th) 1 cells release proinflammatory cytokines [interferon-gamma, interleukin (IL)-1beta, IL-2, and tumor necrosis factor alpha]. In the chronic stage, progression is supported by increased memory Tregs and Th2 immune responses. The classical complement system pathway may be activated by the IgG1 immune complex. As Tregs seem to play an important role in progression as well as in induction of the disease, further studies are necessary to clarify the pathogenesis of AIP.

Indexed as

Autoimmune DiseasesPancreatitisAnimalsHumans

Identifiers

PMID18600384
OpenAlexW2056930998

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.