Evidence map›Paper›PMID 28550517›Full record

ReviewDiabetologia2017

Early prediction of autoimmune (type 1) diabetes.

Simon E Regnell, Åke Lernmark

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Diabetologia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 2 pooled it
13.9field-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

102 citing papers in PubMed, 2 syntheses or guidelines pooled it, 195 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. ProtectiveiScience · 2026
    Article
  4. Review
  5. New and emerging therapies in type 1 diabetes mellitus.The Journal of clinical investigation · 2026
    Review
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42 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Simon E RegnellDepartment of Clinical Sciences, Lund University/CRC, Skåne University Hospital, Jan Waldenströms gata 35, SE-20502, Malmö, Sweden.
Åke LernmarkDepartment of Clinical Sciences, Lund University/CRC, Skåne University Hospital, Jan Waldenströms gata 35, SE-20502, Malmö, Sweden. ake.lernmark@med.lu.se.
Lund University · SESkåne University Hospital · SE

Funding

Data Coordinating Center (DCC)for the Consortium for Identification of EnvironmenUC4DK095300 · NIDDK · UNIVERSITY OF SOUTH FLORIDA · PI KRISCHER, JEFFREY P · 2011 to 2011
$56.0M
NIDDK NIH HHS UC4 DK095300NLM NIH HHS HHSN267200700014C
6 · The paper itself

Abstract

Underlying type 1 diabetes is a genetic aetiology dominated by the influence of specific HLA haplotypes involving primarily the class II DR-DQ region. In genetically predisposed children with the DR4-DQ8 haplotype, exogenous factors, yet to be identified, are thought to trigger an autoimmune reaction against insulin, signalled by insulin autoantibodies as the first autoantibody to appear. In children with the DR3-DQ2 haplotype, the triggering reaction is primarily against GAD signalled by GAD autoantibodies (GADA) as the first-appearing autoantibody. The incidence rate of insulin autoantibodies as the first-appearing autoantibody peaks during the first years of life and declines thereafter. The incidence rate of GADA as the first-appearing autoantibody peaks later but does not decline. The first autoantibody may variably be followed, in an apparently non-HLA-associated pathogenesis, by a second, third or fourth autoantibody. Although not all persons with a single type of autoantibody progress to diabetes, the presence of multiple autoantibodies seems invariably to be followed by loss of functional beta cell mass and eventually by dysglycaemia and symptoms. Infiltration of mononuclear cells in and around the islets appears to be a late phenomenon appearing in the multiple-autoantibody-positive with dysglycaemia. As our understanding of the aetiology and pathogenesis of type 1 diabetes advances, the improved capability for early prediction should guide new strategies for the prevention of type 1 diabetes.

Indexed as

AutoantibodiesChildDiabetes Mellitus, Type 1FemaleGlutamate DecarboxylaseHumansInsulin AntibodiesMaleAutoantibodiesGlutamate DecarboxylaseInsulin AntibodiesAutoimmunityBeta cells, diabetes mellitusGlutamic acid decarboxylase autoantibodiesHLAInsulin autoantibodiesInsulinoma-associated antingen-2 autoantibodiesInsulin secretionNext-generation sequencingReviewType 1 diabetesZnT8 autoantibodies

Identifiers

PMID28550517
PMCPMC5491594
OpenAlexW2620432821

What OpenQuestion 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 OpenQuestion graph.