Evidence map›Paper›PMID 30192315›Full record

ArticlePancreas2018

Distinct Inflammatory Changes of the Pancreas of Slowly Progressive Insulin-dependent (Type 1) Diabetes.

Kaoru Aida, Tomoyasu Fukui, Erika Jimbo, Soroku Yagihashi, Akira Shimada, Yoichi Oikawa, Yasumichi Mori, Takeshi Fujii, Yoriko Nishida, Rikako Koyama and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Pancreas, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 2 pooled it
1.3field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 2 syntheses or guidelines pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Association BetweenFrontiers in endocrinology · 2021
    Pooled it
  3. Article
  4. Article
  5. Latent autoimmune diabetes in youth.Frontiers in immunology · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Innate immunity in latent autoimmune diabetes in adults.Diabetes/metabolism research and reviews · 2022
    Review
  12. Article
  13. Article
  14. Slowly Progressive Type 1 Diabetes Mellitus: Current Knowledge And Future Perspectives.Diabetes, metabolic syndrome and obesity : targets and therapy · 2019
    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

11 authors at 5 institutions in 2 countries.

Kaoru Aida
Tomoyasu Fukui
Erika JimboDivision of Immunology and Molecular Medicine, Okinaka Memorial Institute for Medical Research, Tokyo.
Soroku YagihashiDepartment of Pathology and Molecular Medicine, Hirosaki University Graduate School of Medicine, Hirosaki.
Akira ShimadaDepartment of Endocrinology and Diabetes, Saitama Medical University, Saitama.
Yoichi OikawaDepartment of Endocrinology and Diabetes, Saitama Medical University, Saitama.
Yasumichi MoriEndocrinology and Metabolism and.
Takeshi FujiiPathology, Toranomon Hospital, Tokyo.
Yoriko NishidaDepartment of Nursing, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Yamanashi.
Rikako KoyamaDepartment of Gastroenterology, Toranomon Hospital, Tokyo, Japan.
Tetsuro Kobayashi
Saitama Medical University · JPToranomon Hospital · JPUniversity of Yamanashi · JPHirosaki University · JPInstitute for Medical Research · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe aim of this study was to identify the distinct pathological changes on the endocrine and exocrine pancreas of slowly progressive insulin-dependent diabetes mellitus (SPIDDM) or latent autoimmune diabetes in adults.

methodsThe pancreases from 12 islet autoantibody-positive SPIDDM patients and 19 age-matched subjects with no diabetes were examined histologically for islet inflammation/insulitis, expressions of cytokines, and enterovirus VP1 protein, exocrine pancreatic inflammation, pancreatic ductal changes, major histocompatibility complex class I hyperexpression, and amylin-positive amyloid in the islets.

resultsInsulitis dominant for CD8 T-cells and CD68 macrophages was observed in all SPIDDM cases irrespective of duration of diabetes and weight of residual beta cells. Major histocompatibility complex class I hyperexpression on residual beta cells was observed in SPIDDM. All SPIDDM exocrine pancreases showed extensive inflammation, dilated pancreatic ducts, and periductal fibrosis. As many as 75% (9/12) of pancreases had pancreatic intraepithelial neoplasia, which is assumed to be associated with ductal obstruction/narrowing and exocrine pancreatic inflammation, in SPIDDM. Amylin-positive amyloid deposition was not detected in SPIDDM.

conclusionsPersistent insulitis with preserved beta cells and major histocompatibility complex class I hyperexpression and exocrine pancreatic inflammation with pancreatic intraepithelial neoplasia are distinct histological features of SPIDDM pancreas.

Indexed as

AdultAgedAged, 80 and overAutoantibodiesCD8-Positive T-LymphocytesDiabetes Mellitus, Type 1FemaleHistocompatibility Antigens Class IHumansInsulin-Secreting CellsMacrophagesMaleMiddle AgedPancreasPancreatic DuctsPancreatitisAutoantibodiesHistocompatibility Antigens Class I

Identifiers

PMID30192315
PMCPMC6143218
OpenAlexW2889947901

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.