ArticleDigestive diseases and sciences2026
Evaluation of Obesity as an Independent Risk Factor for Colorectal Dysplasia Development in Inflammatory Bowel Disease: A Matched Case-Control Study.
Article in Digestive diseases and sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundChronic intestinal inflammation is a well-established driver of colorectal dysplasia in inflammatory bowel disease (IBD). However, the role of metabolic factors such as obesity remains poorly understood. We evaluated whether chronic obesity, measured using five-year longitudinal body mass index (BMI), is independently associated with colorectal dysplasia in patients with IBD.
methodsWe conducted a retrospective 1:1 matched case-control study at a tertiary academic center. Adult patients with ulcerative colitis (UC) or Crohn's disease (CD) who underwent surveillance colonoscopy between 2019 and 2025 were included. Cases had biopsy-confirmed colorectal dysplasia (indefinite, low grade, or high grade). Controls were dysplasia-free and matched by age (± 5 years), sex, and IBD subtype. Obesity was defined as a mean body mass index (BMI) ≥ 30 kg/m
resultsA total of 312 patients were included (156 dysplasia cases and 156 matched controls). Dysplasia cases had significantly longer IBD duration compared with controls (median 12.1 vs. 8.0 years, p < 0.01) and were more likely to have a history of prior colorectal dysplasia (16.0% vs. 3.8%, p < 0.01). In multivariable analysis, obesity was independently associated with colorectal dysplasia (adjusted odds ratio [aOR] 2.23, 95% CI 1.08-4.57). Longer disease duration (aOR 1.05 per year, 95% CI 1.02-1.08) and prior dysplasia (aOR 4.88, 95% CI 1.69-14.06) were also independently associated with dysplasia. In a secondary model adjusting for additional surveillance-related and structural colonic factors, obesity remained significantly associated with dysplasia (aOR 2.11, 95% CI 1.05-4.24).
conclusionsObesity is independently associated with colorectal dysplasia in patients with IBD, suggesting that metabolic factors contribute to neoplastic risk beyond traditional inflammation-driven pathways. Incorporation of metabolic risk into dysplasia risk stratification may improve CRC prevention strategies in IBD.
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