Evidence map›Paper›PMID 20062967›Full record

ArticleDiabetologia2010

Dimorphic histopathology of long-standing childhood-onset diabetes.

R Gianani, M Campbell-Thompson, S A Sarkar, C Wasserfall, A Pugliese, J M Solis, S C Kent, B J Hering, E West, A Steck and 5 more

Erratum issuedOpen access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
11.2field-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

95 citing papers in PubMed, 157 citations in OpenAlex.

  1. Trial
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  4. Review
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  8. Review
  9. Review
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  12. C-peptide and residual β-cell function in pediatric diabetes - state of the art.Pediatric endocrinology, diabetes, and metabolism · 2021
    Review
  13. Review
  14. ResidualJournal of diabetes research · 2021
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

35 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

15 authors at 6 institutions in 1 country.

R GiananiBarbara Davis Center for Childhood Diabetes, University of Colorado Denver, 1775 Aurora Court, Aurora, CO 80055, USA. roberto.gianani@ucdenver.edu
M Campbell-Thompson
S A Sarkar
C Wasserfall
A Pugliese
J M Solis
S C Kent
B J Hering
E West
A Steck
S Bonner-Weir
M A Atkinson
K Coppieters
M von Herrath
G S Eisenbarth
University of Colorado Denver · USUniversity of Florida · USLa Jolla Institute for Immunology · USHarvard University · USJoslin Diabetes Center · USUniversity of Minnesota · US

Funding

UCHSC DIABETES ENDOCRINOLOGY RESEARCH CENTERP30DK057516 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI HUTTON, JOHN C · 2000 to 2010
$14.0M
Multiple Autoantigens/Multiple Epitopes of Type 1DMR01DK032083 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI MICHELS, AARON W · 1986 to 2025
$6.9M
Indoleamine 2, 3 dioxygenasesignaling and function in Type 1 DiabetesK01DK080193 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI SARKAR, SUPARNA A · 2007 to 2009
$363k
MULTIPLE AUTOANTIGENS OF PRETYPE I DMR37DK032083 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI EISENBARTH, GEORGE S · 1992 to 1999
–
NIDDK NIH HHS DK080193NIDDK NIH HHS DK 32083NIDDK NIH HHS P30DK057516
6 · The paper itself

Abstract

aims/hypothesisChildhood diabetes is thought to usually result from autoimmune beta cell destruction (type 1A) with eventual total loss of beta cells. Analysis of C-peptide in children characterised at diabetes onset for autoantibodies shows heterogeneous preservation of insulin secretion in long-standing diabetes. The aim of this study was to characterise the pancreases of childhood-onset diabetes in order to define the pathological basis of this heterogeneity.

methodsWe evaluated 20 cadaveric organ donor pancreases of childhood-onset long-term patients for disease heterogeneity and obtained corresponding C-peptide measurements.

resultsPancreases from the majority of cadaveric donors contained only insulin-deficient islets (14 of 20). The remaining six patients (30%) had numerous insulin-positive cells within at least some islets, with two different histological patterns. Pattern A (which we would associate with type 1A diabetes) had lobular retention of areas with 'abnormal' beta cells producing the apoptosis inhibitor survivin and HLA class I. In pattern B, 100% of all islets contained normal-appearing but quantitatively reduced beta cells without survivin or HLA class I. CONCLUSIONS/

interpretationOur data demonstrate that C-peptide secretion in long-standing diabetic patients can be explained by two different patterns of beta cell survival,possibly reflecting different subsets of type 1 diabetes.

Indexed as

Sex CharacteristicsAdolescentAdultAge of OnsetAutoantibodiesChildChild, PreschoolC-PeptideDiabetes Mellitus, Type 1FemaleHistocompatibility TestingHLA-DR AntigensHumansHyperinsulinismInsulin-Secreting CellsMaleAutoantibodiesC-PeptideHLA-DR Antigens

Identifiers

PMID20062967
OpenAlexW2061159176

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.