Evidence map›Paper›PMID 33088639›Full record

ReviewDiabetology international2020

Possible involvement of autoimmunity in fulminant type 1 diabetes.

Yoichi Oikawa, Akira Shimada

Open access · bronzeAbstract readReview
In one paragraph

Review in Diabetology international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
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  4. Review
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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

2 authors at 1 institution in 1 country.

Yoichi OikawaDepartment of Endocrinology and Diabetes, School of Medicine, Saitama Medical University, 38 Morohongo, Moroyamamachi, Iruma-gun, Saitama, 350-0495 Japan.
Akira ShimadaDepartment of Endocrinology and Diabetes, School of Medicine, Saitama Medical University, 38 Morohongo, Moroyamamachi, Iruma-gun, Saitama, 350-0495 Japan.
Saitama Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fulminant type 1 diabetes (FT1D) is characterized by a relatively low HbA1c level at the onset, despite the abrupt occurrence of marked hyperglycemia with ketosis or ketoacidosis. The initial symptoms/findings are flu-like, absence of islet-associated autoantibodies, and a drastic decrease in β-cells and α-cells, which strongly suggest the involvement of a viral infection. In fact, we successfully demonstrated that a FT1D-like phenotype can be reproduced in encephalomyocarditis virus-induced diabetes murine model. However, there is a discussion on the possible involvement of autoimmunity rather than viral infection as the underlying cause of FT1D. For example, HLA-DRB1*04:05, a susceptible antigen of type 1A diabetes, is reportedly associated with FT1D in Japan. Moreover, anti-glutamic acid decarboxylase antibody is reportedly detected in ~ 5% of the patients. Additionally, half of the patients with anti-programmed cell death-1 therapy-related type 1 diabetes fulfilled the criteria of the disease. These findings suggest that islet-associated autoimmunity can partially contribute to the development of FT1D. Furthermore, using nonobese diabetic mice with reduced regulatory T-cell (Treg) numbers, we found that a human FT1D-like phenotype can be induced by islet-associated autoimmunity through collaboration between innate immunity (macrophages and/or natural killer cells) and acquired immunity (predominantly cytotoxic CD8

Indexed as

Anti-glutamic acid decarboxylase antibodyCD28−/− nonobese diabetic mouseEncephalomyocarditis virusFulminant type 1 diabetesPolyinosinic-polycytidylic acidRegulatory T cell

Identifiers

PMID33088639
PMCPMC7538522
OpenAlexW3081821294

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.