Evaluation of Obesity as an Independent Risk Factor for Colorectal Dysplasia Development in Inflammatory Bowel...

Chronic 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.

We 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/m² using all outpatient measurements over a five-year period prior to the index colonoscopy. Multivariable conditional logistic regression was used to evaluate the association between obesity and dysplasia, adjusting for established dysplasia risk factors and surveillance-related variables.

A 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).

Obesity 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.