686 Neither Obesity nor Hepatic Steatosis Are Associated With an Increased Prevalent or Incident Colonic Dysplasia in Patients With Inflammatory Bowel Disease and Concomitant Primary Sclerosing Cholangitis

Abstract

INTRODUCTION: A concomitant diagnosis of Primary Sclerosing Cholangitis (PSC) in patients with Inflammatory Bowel Disease (IBD) is associated with an increased risk of colonic dysplasia. Obesity and hepatic steatosis also have been associated with an increased risk of colonic dysplasia in non-IBD patients. Given the increasing prevalence of obesity in patients with IBD, we aimed to clarify if hepatic steatosis and obesity function as additional risk factors for PSC-associated colonic dysplasia. METHODS: This is a single-center, retrospective cohort study between 1/1/2013 through 12/1/2018. Adult patients with a clinical diagnosis of IBD and PSC that had undergone magnetic resonance cholangiopancreatography (MRCP) were included. Those with an alternative etiology of liver disease (e.g., chronic viral hepatitis, greater than moderate alcohol usage) were excluded. MRCP protocols had been modified to allow liver fat quantification by the MR-proton density fat fraction method. Hepatic steatosis was defined as >5.5% liver fat with obesity defined as body mass index (BMI) >30 kg/m2. Prevalent and incident colonic dysplasia were identified. The co-primary outcomes were the Odds Ratio (OR) for the association between hepatic steatosis or obesity and life-time prevalence of colonic dysplasia. Secondary outcomes included the analogous Hazards Ratio (HR) by a cox-proportional hazards model of colonic-dysplasia free-survival from the time of PSC diagnosis. RESULTS: 112 PSC-IBD patients (80% Ulcerative Colitis, median age at enrollment 48 years, median age at PSC diagnosis 39 years, median BMI 27 kg/m2) had a life-time prevalence of colonic dysplasia in 24 (21%), hepatic steatosis in 22 (20%) and obesity in 23 (21%). Neither hepatic steatosis (OR, 0.8; 95% CI, 0.2-2.6; P = 0.78) nor obesity (OR, 1.1; 95% CI, 0.4–2.9; P = 0.90) were risk factors for the life-time prevalence of colonic dysplasia. Similarly, neither hepatic steatosis (HR, 0.9; 95% CI, 0.3-2.3; P = 0.78) nor obesity (HR, 1.0; 95% CI, 0.9–1.0; P = 0.37), were risk factors for dysplasia-free survival. CONCLUSION: We found that hepatic steatosis and obesity were not associated with increased lifetime prevalence for colonic dysplasia in patients with IBD-PSC. This may imply a different pathway for carcinogenesis in IBD-PSC compared to non-IBD patients.