ReviewEndocrinology, diabetes & metabolism2026
Type 1 Diabetes and Other Autoimmune Diseases-Epidemiology, Pathophysiology and Screening.
Review in Endocrinology, diabetes & metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Stress-driven remodeling of antigen presentation and chemokine signaling in pancreatic β-cells: implications for type 1 diabetes.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
introductionThe interplay between type 1 diabetes (T1D) and concomitant autoimmune diseases (AID) is both clinically and scientifically relevant. In this review, we delineate the epidemiological, pathophysiological and practical aspects underlying polyautoimmunity with a focus on T1D.
methodA comprehensive review of literature on T1D and associated AID was conducted, with the aim of drawing informed conclusions relevant to clinical practice. It draws on a targeted PubMed search conducted March-May 2025, emphasising recent peer-reviewed articles in English.
resultsEpidemiological data consistently indicate that individuals with T1D exhibit a significantly increased prevalence of additional AID. Familial aggregation of discordant AID and the concept of polyglandular autoimmune syndromes (PAS) or autoimmune polyendocrinopathy highlight that multiple AID can cluster and occur in a sequential and overlapping fashion, with T1D frequently acting as either an early or a subsequent manifestation. Thereby, genetic susceptibility, environmental triggers and epigenetic factors are pivotal in the initiation and progression of autoimmunity. Clinically, the coexistence of T1D with other AID poses significant challenges in disease management, often necessitating adjustments in therapeutic regimens and careful monitoring to mitigate complications. Early detection via stratified autoantibody testing is important for timely intervention and improved long-term outcomes.
conclusionsAccordingly, screening for T1D-associated autoantibodies in individuals with a personal or family history of AIDs, and vice versa, should be implemented in clinical practice.
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What Socratic 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 Socratic graph.