P1202 Metabolic-dysfunction associated liver disease in patient with Inflammatory Bowel Disease: Is obesity the major driver of disease progression?

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Abstract Background Prevalence of MASLD in patients with Inflammatory Bowel Disease (IBD) has been reported 24.4% in a recent metaanalysis and 21.6% in a previous cross-sectional study from our center. However, data on the progression of MASLD in IBD patients are scanty. We aimed to investigate the prevalence and the progression of MASLD, diagnosed by non-invasive tools, in a homogeneous cohort of patients with IBD followed in our referral center. Methods Consecutive IBD patients without known chronic liver disease were retrospectively enrolled and prospectively followed between 2020 and 2024. MASLD was defined as Controlled Attenuation Parameter (CAP) ≥275 dB/m according to EASL criteria. Significant fibrosis was defined as Liver Stiffness (LSM) ≥8 kPa by FibroScanÒ. Demographic, metabolic and biochemical data were collected at baseline and at the last follow-up visit. All patients were genotyped for PNPLA3 rs738409 C>G by Taqman assay. Univariate logistic regression analysis was performed to identify risk factors associated with the prevalence of MASLD and its progression. Results 230 patients (mean age was 46.1±13.4 years, 49.2% were males, 50.8% had Crohn’s disease, mean disease duration was 9.4±7.5 years) were recruited. 14.8% of them were obese (BMI > 30 kg/m2), 9.8% diabetic. 49.2% were PNPLA3 rs738409 CG/GG. 62 out of 230 patients had complete metabolic and biochemical assessment at follow-up. Mean follow-up time was 4 years. At baseline, according to EASL criteria, 31.1% (19/62) had MASLD. 19.1% (8/42) of patients without steatosis at baseline, developed steatosis at follow-up; while 42.1% of those having steatosis at baseline, did not show steatosis at follow-up. Two patients without fibrosis assessed by LSM at baseline developed significant fibrosis, while two patients with fibrosis at baseline experienced fibrosis regression. 13.5% developed obesity. Obesity was significantly associated with the prevalence of MASLD both at baseline (p=0.01) and on follow-up (p=0.01) and was a predictor of steatosis progression (p=0.01); no association was found in relation to sex, PNPLA3 polymorphism, disease characteristics and the use of biologics. Diabetes was not significantly associated with MASLD in our cohort, but the number of patients was low. Conclusion One third of IBD patients had MASLD and obesity was the main predictor of its prevalence and progression, highlighting the relevance of active surveillance of MASLD and appropriate nutritional and lifestyle counselling especially in obese IBD patients. The use of biologics to control inflammation seems to have no influence on MASLD progression but data need further confirm in larger cohorts.