ArticleCureus2026
Missed Autoimmune Diabetes: Latent Autoimmune Diabetes in Adults in the Setting of Autoimmune Clustering.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed.
- Pancreatogenic diabetes in immunoglobulin G4-related autoimmune pancreatitis managed with automated insulin delivery.JCEM case reports · 2026Article
- Late-onset autoimmune diabetes in 2 octogenarians: diagnostic misclassification and therapeutic heterogeneity.JCEM case reports · 2026Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Latent autoimmune diabetes in adults (LADA) is frequently misdiagnosed as type 2 diabetes mellitus (T2DM), particularly in older adults, owing to its adult onset, initial insulin independence, and indolent clinical course, resulting in the delayed initiation of insulin therapy. We present a woman in her sixties with Hashimoto's thyroiditis and a prior diagnosis of Sjögren syndrome who developed progressively worsening hyperglycemia and concurrent rheumatological symptoms, including chronic joint pain and stiffness, despite treatment with multiple noninsulin therapies. Her lean body habitus, absence of clinical insulin resistance, progressive glycemic deterioration, autoimmune background, and musculoskeletal manifestations prompted further evaluation, which revealed markedly elevated pancreatic autoantibodies, including glutamic acid decarboxylase (GAD-65), islet antigen-2 (IA-2), and zinc transporter 8 (ZnT8) antibodies, confirming the diagnosis of LADA with evolving β-cell failure. Transition to insulin-based therapy resulted in excellent glycemic control and was accompanied by substantial improvement in musculoskeletal symptoms, consistent with metabolic rather than inflammatory pathology. This case highlights the importance of recognizing LADA in patients with phenotypic discordance, autoimmune clustering, and systemic manifestations that improve with optimized glycemic control.
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Registered trials
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