Evidence map›Paper›PMID 23379430›Full record

Trial reportClinical and experimental immunology2013

Characteristics of in-vitro phenotypes of glutamic acid decarboxylase 65 autoantibodies in high-titre individuals.

M Chéramy, C S Hampe, J Ludvigsson, R Casas

Open access · greenAbstract readClinical Trial, Phase II
In one paragraph

Trial report in Clinical and experimental immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Review
  5. Article
  6. Stiff-person Syndrome and GAD Antibody-spectrum Disorders: GABAergic Neuronal Excitability, Immunopathogenesis and Update on Antibody Therapies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
    Review
  7. Review
  8. Neuropsychiatric Disorders Due to Limbic Encephalitis: Immunologic Aspect.International journal of molecular sciences · 2020
    Review
  9. Review
  10. Multiplex family with GAD65-Abs neurologic syndromes.Neurology(R) neuroimmunology & neuroinflammation · 2018
    Article
  11. 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

4 authors at 2 institutions in 2 countries.

M ChéramyDivision of Pediatrics, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden. mikael.cheramy@liu.se
C S Hampe
J Ludvigsson
R Casas
Linköping University · SEUniversity of Washington · US

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Sakeneh Zraika · 1986 to 2026
$41.4M
ISLET CELL MEMBRANE ANTIBODIES IN DIABTESR01DK026190 · NIDDK · UNIVERSITY OF WASHINGTON · PI HAMPE, CHRISTIANE S · 1986 to 2016
$4.9M
NIDDK NIH HHS P30 DK017047NIDDK NIH HHS R01 DK026190
6 · The paper itself

Abstract

Previous studies have indicated phenotypical differences in glutamic acid decarboxylase 65 autoantibodies (GADA) found in type 1 diabetes (T1D) patients, individuals at risk of developing T1D and stiff-person syndrome (SPS) patients. In a Phase II trial using aluminium-formulated GAD(65) (GAD-alum) as an immunomodulator in T1D, several patients responded with high GADA titres after treatment, raising concerns as to whether GAD-alum could induce GADA with SPS-associated phenotypes. This study aimed to analyse GADA levels, immunoglobulin (Ig)G1-4 subclass frequencies, b78- and b96·11-defined epitope distribution and GAD(65) enzyme activity in sera from four cohorts with very high GADA titres: T1D patients (n = 7), GAD-alum-treated T1D patients (n = 9), T1D high-risk individuals (n = 6) and SPS patients (n = 12). SPS patients showed significantly higher GADA levels and inhibited the in-vitro GAD(65) enzyme activity more strongly compared to the other groups. A higher binding frequency to the b78-defined epitope was found in the SPS group compared to T1D and GAD-alum individuals, whereas no differences were detected for the b96·11-defined epitope. GADA IgG1-4 subclass levels did not differ between the groups, but SPS patients had higher IgG2 and lower IgG4 distribution more frequently. In conclusion, the in-vitro GADA phenotypes from SPS patients differed from the T1D- and high-risk groups, and GAD-alum treatment did not induce SPS-associated phenotypes. However, occasional overlap between the groups exists, and caution is indicated when drawing conclusions to health or disease status.

Indexed as

AdolescentAdultAgedAlum CompoundsAutoantibodiesDiabetes Mellitus, Type 1FemaleGlutamate DecarboxylaseHumansImmunoglobulin GMaleMiddle AgedPhenotypeStiff-Person SyndromeAlum Compoundsaluminum sulfateAutoantibodiesGlutamate Decarboxylaseglutamate decarboxylase 2Immunoglobulin G

Identifiers

PMID23379430
PMCPMC3569531
OpenAlexW1496641030

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.