ArticleJCEM case reports2026
Triple islet autoantibody-positive type 1 diabetes in Japanese stiff-person syndrome despite a protective HLA haplotype.
Article in JCEM case reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 1 diabetes is a recognized complication of stiff-person syndrome (SPS), yet its immunogenetic determinants in non-European populations remain poorly characterized. A 39-year-old Japanese woman with a 14-year history of SPS presented with diabetic ketoacidosis and was found to have autoimmune type 1 diabetes with rapid beta-cell loss despite long-term immunosuppression. Anti-GAD65 titers were persistently ≥2000 U/mL by enzyme immunoassay, with anti-IA-2 at 8.2 U/mL and anti-ZnT8 at 53.1 U/mL. Urinary C-peptide declined from 4.16 μg/day (SI: 1.38 nmol/day) to <0.9 μg/day (SI: <0.3 nmol/day) over 13 months, indicating rapid progression to near-complete beta-cell failure. High-resolution human leukocyte antigen (HLA) typing revealed a susceptibility haplotype DRB1*04:05-DQA1*03:03-DQB1*04:01, a protective haplotype DRB1*15:02-DQA1*01:03-DQB1*06:01, and HLA-A*24:02; DRB1*03:01, the allele most strongly associated with SPS in European cohorts, was absent. This case demonstrates that SPS-associated autoimmunity can override protective HLA haplotypes, resulting in triple islet autoantibody-positive type 1 diabetes with an immunogenetic profile distinct from that reported in European cohorts.
Indexed as
Identifiers
What OpenQuestion holds
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.