Inflammatory bowel disease (IBD) and metabolic dysfunction-associated steatotic liver disease (MASLD) frequently coexist, creating a clinical phenotype in which intestinal inflammation and cardiometabolic dysfunction intersect. This review re-examines the association from a fibrosis-oriented perspective rather than treating hepatic steatosis as an isolated extraintestinal finding. Current evidence indicates that hepatic risk in IBD is shaped by several overlapping domains: age and adiposity, dyslipidemia and glucose dysregulation, duration and activity of intestinal disease, altered intestinal permeability, microbiome-derived metabolites, bile-acid signaling, nutritional imbalance and changes in skeletal muscle mass. The gut-liver axis provides the central biological framework linking these processes, but no single pathway sufficiently explains the heterogeneity observed in clinical practice. Available cohort and meta-analytic data suggest that steatotic liver disease is common in IBD, whereas clinically relevant fibrosis is less frequent but prognostically more important. Accordingly, clinical evaluation should move beyond simple detection of steatosis and incorporate cardiometabolic profiling, liver biochemistry, first-line fibrosis scores and elastography when indicated. Particular attention is warranted in patients with Crohn's disease, persistent inflammatory activity, metabolic risk, or sarcopenic phenotypes. A fibrosis-oriented, multidisciplinary strategy may improve identification of patients at greatest long-term hepatic risk and provide a more clinically useful framework for this comorbidity.
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А. А. Антонів (2026) studied this question.
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