Background: Inflammatory Bowel Disease (IBD) is an inflammatory and chronic disease, as well as non-alcoholic fatty liver disease (NAFLD). Current literature has shown that IBD patients are at high risk for NAFLD. In those patients, the pathogenesis of NAFLD may be more complex and related to multifactor causes, such as gut dysbiosis, unhealthy nutritional behavior, body composition and systemic inflammation. There is an increase in NAFLD's incidence in the general population, otherwise, there are few studies evaluating NAFLD prevalence in IBD patients. So, this study aimed to evaluate prevalence of NAFLD and identify the clinical factors associated with the presence of NAFLD in patients with IBD.

Methods: This cross-sectional, descriptive, observational study included 71 IBD patients from an IBD public outpatient in São Paulo State, Brazil. Laboratory evaluation and clinical data were collected. The presence of NAFLD was evaluated by ultrasonography. The exclusion criteria were as follows: pre-existing liver disease, history of alcohol intake >20g/day for women and >30g/day for men, and glucocorticoids treatment >20mg/day. Statistical analysis: descriptive statistics and association tests.

Results: 71 patients were included, of which 34 (47.89%) were Crohn´s disease (CD) and 37 (52.11%) ulcerative colitis (UC). Median age was 45.32±13.59 years, 63.38% were female, 69.1% Caucasian, 7.04% smokers. The time from diagnosis was 12.55 ± 8.01 years. Regarding the characteristics of the diseases, 42.42% of patients with CD have ileocolonic involvement, 50% penetrating disease and 39.4% perianal involvement. In relation to patients with UC, most patients have pancolitis (72.22%). Mostly, the patients were in clinical (63.89%) and endoscopic (52.86%) remission. Regarding medical treatment, the most used drugs were biological therapy (79.41%) and azathioprine (52.94%) in CD, and mesalazine (45.95%), azathioprine (40.54%) and biological therapy (40.54%) in UC. The NAFLD group consists of 32 (45.07%) patients: 40.63% had mild steatosis; 40.63% moderate and 18.65% intense NAFLD. Development of NAFLD vs no NAFLD was associated with body mass index (29.49 ± 3.93 vs 24.32 ± 3.85, p < 0.0001), and laboratory biomarkers, such as C-reactive protein (1.99 ± 4.39 vs 0.87 ± 0.52, p = 0.0061), AST (29.72 ± 16.64 vs 23.46 ± 5.31, p = 0.0226), ALT (24.92 ± 14.22 vs 17.92 ± 6.57, p = 0.0099), albumin (4.1 ± 0.37 vs 4.36 ± 0.32, p = 0.0415), fasting glucose (95.5 ± 14.01 vs 84.36 ± 13.01, p = 0.0251) and blood insulin (18.41 ± 11.88 vs 6.4 ± 4.26, p = 0.0054). Also, the NAFLD group had higher prevalence of systemic arterial hypertension (31.25% vs 10.26%, p = 0.0369). When comparing patients with the presence or absence of NAFLD, there was no difference between the groups regarding time since diagnosis (p = 0.9684), previous surgery (p = 0.5908), Montreal classification, clinical activity assessed by CDAI (p = 0.2258), clinical activity assessed by the Mayo score (p = 0.4935), endoscopic activity (p = 0.0599), histological activity (p = 1.0), or medical treatment.

Conclusion: Development of NAFLD is a frequent occurrence in patients with IBD. NAFLD group had higher levels of body mass index, C-reactive protein, AST, ALT, fasting glucose and blood insulin, which are also associated with metabolic syndrome. Early diagnosis and appropriate nutritional orientation are necessary to prevent NAFLD related complications.

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