ArticleDiabetology & metabolic syndrome2025
Genetic evidence for causal links between type 1 diabetes and autoimmune liver diseases.
Article in Diabetology & metabolic syndrome, 2025. 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
5 authors.
Funding
Abstract
backgroundType 1 diabetes (T1D) and autoimmune liver diseases (AILDs), including autoimmune hepatitis (AIH), primary biliary cholangitis (PBC), and primary sclerosing cholangitis (PSC), are characterized by immune-mediated damage. Prior observational studies have reported associations between these conditions, but definitive causal relationships remain elusive. This study leverages genetic data to clarify the nature of these associations.
methodsWe conducted a bidirectional Mendelian randomization (MR) analysis using summary-level data from large-scale genome-wide association studies. The inverse variance weighted was the primary method, supplemented by diverse sensitivity analyses (MR-Egger, weighted median, weighted mode, cML-MA, BWMR, MR-PRESSO, and CAUSE) to rigorously assess causality and address potential pleiotropy. We assessed genetic correlation using linkage disequilibrium score regression and performed colocalization to evaluate shared causal variants.
resultsOur findings revealed a causal effect of genetically predicted T1D on an increased risk of AIH (OR = 1.32, 95% CI: 1.16-1.50, P = 2.72 × 10⁻⁵), robustly supported by sensitivity analyses and replicated in an independent cohort. Evidence for a potential bidirectional causal relationship emerged between T1D and PBC, where genetically predicted T1D increased PBC risk (OR = 1.10; 95% CI: 1.02-1.20; P = 0.014), and genetically predicted PBC also increased T1D risk (OR = 1.13; 95% CI: 1.09-1.17; P = 3.45 × 10⁻¹¹), albeit with potential pleiotropy. No evidence for a genetic causal relationship was observed between T1D and PSC (IVW, P = 0.695). Significant genetic correlations were present between T1D and all AILDs, but colocalization did not support shared causal variants.
conclusionsThis study provides genetic evidence for a causal effect of T1D on AIH and a likely bidirectional relationship between T1D and PBC. These findings refine our understanding of their comorbidity, suggesting the need for heightened clinical surveillance and warranting further mechanistic investigation to elucidate the biological pathways.
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.