Evidence map›Paper›PMID 8423232›Full record

ArticleThe Journal of clinical investigation1993

Quantitative assay using recombinant human islet glutamic acid decarboxylase (GAD65) shows that 64K autoantibody positivity at onset predicts diabetes type.

W A Hagopian, A E Karlsen, A Gottsäter, M Landin-Olsson, C E Grubin, G Sundkvist, J S Petersen, E Boel, T Dyrberg, A Lernmark

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00194896 (Rosiglitazone Intervention Study in Patients With Type 1.5 Diabetes), which is not on this map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
11.3field-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.

NCT00194896 nacompletednot on this mapstarted 2000, after this paper: background citation

Rosiglitazone Intervention Study in Patients With Type 1.5 Diabetes

TypeinterventionalSponsorUniversity of WashingtonRan2000 to 2008Enrolled64ConditionsType 2 Diabetes MellitusArmsrosiglitazone, glyburide
3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 200 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. The case for an autoimmune aetiology of type 1 diabetes.Clinical and experimental immunology · 2016
    Review
  10. Article
  11. Latent autoimmune diabetes of the adult: current knowledge and uncertainty.Diabetic medicine : a journal of the British Diabetic Association · 2015
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Autoimmune diabetes: more than just one flavor?Journal of endocrinological investigation · 2004
    Review
  19. Latent autoimmune diabetes in adults (LADA).Reviews in endocrine & metabolic disorders · 2003
    Review
  20. Article
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

10 authors at 5 institutions in 3 countries.

W A HagopianDepartment of Medicine, University of Washington, Seattle 98195.
A E Karlsen
A Gottsäter
M Landin-Olsson
C E Grubin
G Sundkvist
J S Petersen
E Boel
T Dyrberg
A Lernmark
Lund University · SENovo Nordisk (Denmark) · DKSeattle University · USUniversity of Washington · USDorn Research Institute · US

Funding

ISLET CELL MEMBRANE ANTIBODIES IN DIABTESR01DK026190 · NIDDK · UNIVERSITY OF WASHINGTON · PI HAMPE, CHRISTIANE S · 1986 to 2016
$4.9M
IMMUNE RESPONSE IN INSULIN-DEPENDENT DIABETESP01DK041801 · NIDDK · UNIVERSITY OF WASHINGTON · PI PIOUS, DONALD A · 1990 to 1994
–
ISOLATION OF ISLET CELL AUTOANTIGENSR01DK033873 · NIDDK · UNIVERSITY OF WASHINGTON · PI LERNMARK, AKE · 1986 to 1992
–
NIDDK NIH HHS DK-26190NIDDK NIH HHS DK-33873NIDDK NIH HHS DK-41801NIDDK NIH HHS R01 DK026190
6 · The paper itself

Abstract

At and before onset, most insulin-dependent diabetics (IDDM) have islet GAD65 autoantibodies (GAD65Ab). Since IDDM also occurs in older patients where non-insulin-dependent diabetes is common, we studied GAD65Ab at onset to classify diabetes type. Our quantitative immunoprecipitation assay uses recombinant human islet GAD65 stably expressed in hamster fibroblasts. Electrophoretic mobility was identical to native islet GAD65. Like native antigen, recombinant GAD65 migrated as two bands during electrophoresis, but converted to one under stronger reduction. Immunoprecipitation was linear with respect to antibody or antigen concentration. In 120 population-based diabetic patients of all ages grouped by treatment at onset and after 18 mo, GAD65Ab were present in 70% on insulin (n = 37), 10% on oral agent (n = 62, P < 0.0001), 69% changing from oral agent to insulin (n = 16, P < 0.001), and 1 of 33 controls. 65% with GAD65Ab, versus 8% without, changed from oral agent to insulin (P < 0.01). The GAD65Ab quantitative index was remarkably stable, and only 2 of 32 patients changed antibody status during follow-up. Concordance between GAD65Ab and islet cell antibodies was 93%. Quantitative correlation was approximate but significant. This highly sensitive, quantitative, high capacity assay for GAD65Ab reveals treatment requirements better than clinical criteria, perhaps guiding immunomodulatory therapy.

Indexed as

AdultAge FactorsAnimalsAutoantibodiesBiomarkersCell LineDiabetes MellitusDiabetes Mellitus, Type 1Follow-Up StudiesGlutamate DecarboxylaseHumansIslets of LangerhansPrognosisRecombinant ProteinsAutoantibodiesBiomarkersGlutamate Decarboxylaseislet cell antibodyRecombinant Proteins

Identifiers

PMID8423232
PMCPMC330036
OpenAlexW2151688741

What OpenQuestion holds

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Registered trials

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.