Evidence map›Paper›PMID 29636076›Full record

ArticleOrphanet journal of rare diseases2018

GAD65 autoantibody characteristics in patients with co-occurring type 1 diabetes and epilepsy may help identify underlying epilepsy etiologies.

Suvi Liimatainen, Jerome Honnorat, Sean J Pittock, Andrew McKeon, Mario Manto, Jared R Radtke, T1D Exchange Biobank, Christiane S Hampe

Open access · goldAbstract read
In one paragraph

Article in Orphanet journal of rare diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  5. Article
  6. Article
  7. Review
  8. Article
  9. The JAK-STAT Signaling Pathway in Epilepsy.Current neuropharmacology · 2023
    Review
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  11. Article
  12. Article
  13. Review
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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 5 institutions in 4 countries.

Suvi LiimatainenDepartment of Neurology and Rehabilitation, Tampere University Hospital, Tampere, Finland.
Jerome HonnoratUniversity of Lyon - University Claude Bernard Lyon, Lyon, France.
Sean J PittockDepartment of Neurology, College of Medicine, Mayo Clinic, Rochester, MN, USA.
Andrew McKeonDepartment of Neurology, College of Medicine, Mayo Clinic, Rochester, MN, USA.
Mario MantoUnité d'Etude du Mouvement, Université Libre De Bruxelles, Brussels, Belgium.
Jared R RadtkeDepartment of Medicine, School of Medicine, University of Washington, 850 Republican, Seattle, WA, 98109, USA.
T1D Exchange Biobank
Christiane S HampeDepartment of Medicine, School of Medicine, University of Washington, 850 Republican, Seattle, WA, 98109, USA. champe@u.washington.edu.
Université Claude Bernard Lyon 1 · FRUniversité Libre de Bruxelles · BEUniversity of Washington · USMayo Clinic · USTampere University Hospital · FI

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Karin E Bornfeldt · 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

backgroundAutoantibodies against the smaller isoform of glutamate decarboxylase (GAD65Ab) reflect autoimmune etiologies in Type 1 diabetes (T1D) and several neurological disorders, including Stiff Person Syndrome (SPS). GAD65Ab are also reported in cases of epilepsy, indicating an autoimmune component. GAD65Ab in patients with co-occurring T1D, epilepsy or SPS may be part of either autoimmune pathogenesis. To dissect the etiologies associated with GAD65Ab, we analyzed GAD65Ab titer, epitope specificity and enzyme inhibition in GAD65Ab-positive patients diagnosed with epilepsy (n = 28), patients with epilepsy and T1D (n = 10), patients with SPS (n = 20), and patients with T1D (n = 42).

resultsGAD65Ab epitope pattern in epilepsy differed from T1D and SPS patients. Four of 10 patients with co-occurring T1D and epilepsy showed GAD65Ab profiles similar to T1D patients, while lacking GAD65Ab characteristics found in GAD65Ab-positive epilepsy patients. One of these patients responded well to anti-epileptic drugs (AEDs), while another patient did not require medication for seizure control. The third patient was refractory due to a diagnosis of meningioma. The response of the remaining patient to AEDs was unknown. GAD65Ab in the remaining six patients with T1D and epilepsy showed profiles similar to those in epilepsy patients.

conclusionsDifferent autoimmune responses associated with T1D, epilepsy and SPS are reflected by disease-specific GAD65Ab patterns. Moreover, the epileptic etiology in patients diagnosed with both T1D and epilepsy may present two different etiologies regarding their epileptic condition. In one group T1D co-occurs with non-autoimmune epilepsy. In the other group GAD65Ab are part of an autoimmune epileptic condition.

Indexed as

AdultAgedAged, 80 and overAutoantibodiesAutoimmunityDiabetes Mellitus, Type 1EpilepsyEpitopesFemaleGlutamate DecarboxylaseHumansMaleMiddle AgedProtein IsoformsStiff-Person SyndromeAutoantibodiesEpitopesGlutamate DecarboxylaseProtein IsoformsAutoimmune epilepsyEpitope mappingGAD65AbGAD65 enzyme activityType 1 diabetes

Identifiers

PMID29636076
PMCPMC5892043
OpenAlexW2804480894

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Registered trials

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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.