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* = Presenting author

P212 Inflammatory bowel disease patients seem to develop non-alcoholic steatohepatitis (NASH) independently from an altered metabolic profile or active bowel disease

A. Sartini*, M. Bianchini, S. Gitto, M. Di Girolamo, A. Bertani, A. Merighi, E. Villa

Gastroenterology Unit, Azienda Ospedaliero-Universitaria di Modena, Policlinico, Modena, Italy


Non-Alcoholic Fatty Liver Disease (NAFLD) and steatohepatitis (NASH) could be detected in 8%–10% of inflammatory bowel disease (IBD) patients. The identification of NASH predictors in IBD could potentially offer better understanding of NAFLD pathogenesis and prevent NASH progression to cirrhosis and hepatocellular carcinoma in such population.


We conducted a retrospective study on 164 patients with NAFLD (isolated US steatosis or US steatosis and altered liver enzymes), 60 IBD patients and 104 subjects without IBD seen at our tertiary care centre between January 2012 and September 2015. We compared demographic characteristics of each group, performing univariate and multivariate analysis to identify factors associated to NASH diagnosis in IBD patients, and log-rank test to compare variables; p-level less than 0.05 was considered significant.


Half of IBD patients had Crohn’s disease (CD) and the majority were males (60%), whereas in non-IBD group, females were prevalent (75%). Only 13 IBD (21.7%) patients had active disease, according to CDAI > 150 and Mayo score > 5 for CD and ulcerative colitis, respectively, with 65% of patients in maintenance therapy with mesalamine only (5ASA) and 23,3% with anti-tumour necrosis factor-α antibodies (anti-TNFα). NASH was detected in 35 IBD patients (58.3%), 8 of whom had already undergone surgery for IBD. NAFLD IBD patients were younger than non-IBD at the time of diagnosis (p = 0.006), showed less metabolic syndrome prevalence (according to modified NCEP-ATPIII criteria) (36% vs 57.3%, p = 0.011), but seem to have more severe US steatosis compared with non-IBD (p = 0.0219). At univariate analysis, the presence of metabolic syndrome was the only predictor factor of NASH in patients without IBD (OR 2.76, 95% CI 1.174–6.531), whereas in the IBD group, the presence of elevated GGT (> 55 UI/ml) (OR 8.70, p = 0.002, 95% CI 2.20–34.53) and severe US steatosis (OR 5.25, p = 0.019, 95% CI 1.317–20.923) were predictors of NASH presence; at multivariate analysis, the only independent predictor factor of NASH presence in IBD group was the presence of elevated GGT (OR 7.84, p = 0.05, 95% CI 1.884–32.636).


IBD patients with NAFLD seem to be younger than the general population is, and they develop it independently from the presence of an altered metabolic profile/metabolic syndrome or of active gut disease; indeed, only the presence of elevated GGT seems to predict the presence of NASH in such group. This could be possibly due to the altered composition of gut microbiota, which characterises IBD itself and/or of a leak in the barrier function, leading in a breakdown of the gut/liver axis.