Metabolic Dysfunction-Associated Steatotic Liver Disease in Inflammatory Bowel Disease: From Gut-Liver Axis Dysfunction to Fibrosis and Clinical Risk Stratification

Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as an important component of the comorbid profile of patients with inflammatory bowel disease (IBD). Its occurrence in Crohn's disease and ulcerative colitis cannot be explained by excess body weight alone, because cardiometabolic risk, intestinal inflammatory activity, epithelial barrier dysfunction, microbial metabolites, nutritional status and body composition may act simultaneously. This narrative review critically integrates current evidence on the epidemiology, risk factors, gut-liver axis, dysbiosis, short-chain fatty acids, bile acid signaling, systemic inflammation, sarcopenia, fibrosis and non-invasive clinical risk stratification of MASLD in IBD. Contemporary meta-analyses indicate that steatotic liver disease affects approximately one-quarter to one-third of adults with IBD, although prevalence estimates vary substantially according to population characteristics and diagnostic methods. The most reproducible risk factors are age, excess adiposity, hypertension, dyslipidemia and disturbances of glucose metabolism, while disease duration, activity, repeated relapses and selected Crohn's disease phenotypes may modify individual risk. Mechanistically, the comorbidity is best viewed as a multi-hit process in which impaired intestinal barrier function, dysbiosis, altered short-chain fatty acid and bile acid metabolism, systemic inflammatory signaling, lipotoxicity and oxidative stress interact with the metabolic background of the patient. Fibrosis, rather than steatosis alone, is the principal prognostic endpoint. Clinical assessment should therefore move from simple detection of hepatic fat toward staged non-invasive fibrosis evaluation using liver tests, cardiometabolic profiling, FIB-4 and, when indicated, vibration-controlled transient elastography with controlled attenuation parameter. MASLD in IBD should be interpreted as a heterogeneous metabolic-inflammatory phenotype that requires integrated gastroenterological, hepatological, metabolic and nutritional assessment.