ArticleCanadian journal of gastroenterology & hepatology2026
Association Between Inflammatory Bowel Disease and Venous Leg Ulcers: Insight From Mendelian Randomization Analyses.
Article in Canadian journal of gastroenterology & hepatology, 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
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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.
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Who cites it
1 citing paper in PubMed.
- Association Between Inflammatory Bowel Disease and Venous Leg Ulcers: Insight From Mendelian Randomization Analyses.Canadian journal of gastroenterology & hepatology · 2026Article
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Authors and funding
4 authors.
Funding
Abstract
backgroundThis study aimed to investigate the potential causal relationship between inflammatory bowel disease (IBD) and venous leg ulcers (VLU) using Mendelian randomization (MR). MATERIALS AND
methodsIndependent genetic variants for IBD and VLU were selected as instruments from previously published genome-wide association studies (GWAS) in people of primarily European descent. MR analyses were carried out utilizing inverse-variance weighted (IVW), weighted median, MR Egger, simple mode, and weighted mode.
resultsGenetically predicted IBD was not associated with VLU, according to the IVW analysis (OR 0.95, 95% CI 0.88-1.03, p = 0.23). MR Egger (OR 0.93, 95% CI 0.76-1.12, p = 0.44), weighted mode (OR 1.06, 95% CI 0.87-1.29, p = 0.55), simple mode (OR 1.03, 95% CI 0.79-1.34, p = 0.83), and weighted median (OR 0.99, 95% CI 0.89-1.10, p = 0.90) all produced results in line with IVW. According to the IVW technique, UC (OR 1.02, 95% CI 0.95-1.10, p = 0.62) and CD (OR 0.97, 95% CI 0.90-1.04, p = 0.36) did not appear to be associated with VLU in subtype analyses.
conclusionThe MR investigation found no genetic evidence to support a causal relationship between IBD and VLU. This finding clarifies that observed clinical associations are unlikely to be driven by shared genetics, and this genetic insight helps refine the clinical assessment of VLU in patients with IBD.
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