Evidence map›Paper›PMID 36083343›Full record

Trial reportDiabetologia2022

Infections in the first year of life and development of beta cell autoimmunity and clinical type 1 diabetes in high-risk individuals: the TRIGR cohort.

Olga Kordonouri, David Cuthbertson, Malin Belteky, Bärbel Aschemeier-Fuchs, Neil H White, Elisabeth Cummings, Mikael Knip, Johnny Ludvigsson

Open access · hybridAbstract readClinical Trial
In one paragraph

Trial report in Diabetologia, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Skin bacteriota ameliorates androgenetic alopecia via harmonizing skin immuno inflammatory balance.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Type 1 diabetes - What's new in prevention and therapeutic strategies?Pediatric endocrinology, diabetes, and metabolism · 2023
    Article
  10. 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

8 authors at 7 institutions in 5 countries.

Olga KordonouriChildren's Hospital Auf Der Bult, Hannover Medical School, Hannover, Germany.ORCID 0000-0001-9563-3537
David CuthbertsonHealth Informatics Institute, University of South Florida, Tampa, FL, USA.ORCID 0000-0002-3785-9834
Malin BeltekyCrown Princess Victoria Children's Hospital and Division of Pediatrics, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.ORCID 0000-0002-4015-7075
Bärbel Aschemeier-FuchsChildren's Hospital Auf Der Bult, Hannover Medical School, Hannover, Germany.
Neil H WhiteDepartment of Pediatrics, Washington University in St Louis, St Louis, MO, USA.
Elisabeth CummingsDepartment of Pediatrics IWK Health/Dalhousie University, Halifax, NS, Canada.
Mikael KnipPediatric Research Center, New Children's Hospital, Helsinki University Hospital, Helsinki, Finland.ORCID 0000-0003-0474-0033
Johnny LudvigssonCrown Princess Victoria Children's Hospital and Division of Pediatrics, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden. Johnny.Ludvigsson@liu.se.ORCID 0000-0003-1695-5234
Medizinische Hochschule Hannover · DEDalhousie University · CALinköping University · SELinköping University Hospital · SEUniversity of Helsinki · FIUniversity of South Florida · USWashington University in St. Louis · US

Funding

Trial to Reduce IDDM in the Genetically at Risk StudyU01HD040364 · NICHD · UNIVERSITY OF HELSINKI · PI KNIP, MIKAEL · 2001 to 2015
$32.7M
Trial to Reduce IDDM in the Genetically at Risk: A Nutritional primary preventionU01HD042444 · NICHD · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BECKER, DOROTHY J · 2001 to 2015
$24.4M
Trial to Reduce IDDM in the Genetically at Risk (TRIGR) Data Management UnitU01HD051997 · NICHD · UNIVERSITY OF SOUTH FLORIDA · PI KRISCHER, JEFFREY P · 2006 to 2015
$7.1M
Trial to Reduce IDDM in the Genetically at Risk (TRIGR) Data Management UnitR01HD051997 · NICHD · UNIVERSITY OF SOUTH FLORIDA · PI KRISCHER, JEFFREY P · 2016 to 2018
$2.3M
NICHD NIH HHS R01 HD051997NICHD NIH HHS U01 HD040364NICHD NIH HHS U01 HD042444NICHD NIH HHS U01 HD051997
6 · The paper itself

Abstract

aims/hypothesisAccumulated data suggest that infections in early life contribute to the development of type 1 diabetes. Using data from the Trial to Reduce IDDM in the Genetically at Risk (TRIGR), we set out to assess whether children who later developed diabetes-related autoantibodies and/or clinical type 1 diabetes had different exposure to infections early in life compared with those who did not.

methodsA cohort of 2159 children with an affected first-degree relative and HLA-conferred susceptibility to type 1 diabetes were recruited between 2002 and 2007 and followed until 2017. Infections were registered prospectively. The relationship between infections in the first year of life and the development of autoantibodies or clinical type 1 diabetes was analysed using univariable and multivariable Cox regression models. As this study was exploratory, no adjustment was made for multiple comparisons.

resultsAdjusting for HLA, sex, breastfeeding duration and birth order, those who had seven or more infections during their first year of life were more likely to develop at least one positive type 1 diabetes-related autoantibody (p=0.028, HR 9.166 [95% CI 1.277, 65.81]) compared with those who had no infections. Those who had their first viral infection aged between 6 and 12 months were less likely to develop at least one positive type 1 diabetes-related antibody (p=0.043, HR 0.828 [95% CI 0.690, 0.994]) or multiple antibodies (p=0.0351, HR 0.664 [95% CI 0.453, 0.972]). Those who had ever had an unspecified bacterial infection were more likely to develop at least one positive type 1 diabetes-related autoantibody (p=0.013, HR 1.412 [95% CI 1.075, 1.854]), to develop multiple antibodies (p=0.037, HR 1.652 [95% CI 1.030, 2.649]) and to develop clinical type 1 diabetes (p=0.011, HR 2.066 [95% CI 1.182, 3.613]). CONCLUSIONS/

interpretationWe found weak support for the assumption that viral infections early in life may initiate the autoimmune process or later development of type 1 diabetes. In contrast, certain bacterial infections appeared to increase the risk of both multiple autoantibodies and clinical type 1 diabetes.

Indexed as

Diabetes Mellitus, Type 1Insulin-Secreting CellsIslets of LangerhansAutoantibodiesAutoimmunityChildCohort StudiesFemaleGenetic Predisposition to DiseaseHumansInfantMaleAutoantibodiesAutoimmunityChildrenEarly infectionsTRIGRType 1 diabetes

Identifiers

PMID36083343
PMCPMC9630400
OpenAlexW4295078808

What OpenQuestion holds

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LicenceCC BY
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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.