Statins, originally developed as lipid-lowering agents, have effects that extend well beyond cholesterol. By altering inflammatory signaling, vascular tone, fibrogenesis, and immune regulation, they engage pathways that shape a wide range of gastrointestinal diseases. Human data now suggest that these biological actions carry clinical weight. In metabolic dysfunction-associated steatotic liver disease and its progressive form, metabolic dysfunction-associated steatohepatitis, alcohol-associated liver disease, and chronic viral hepatitis (HBV and HCV), statin exposure is safe and associated with slower disease progression, fewer episodes of decompensation, and lower incidence of hepatocellular carcinoma. Randomized studies in cirrhosis show reductions in portal pressure, with cohort data linking use to fewer variceal bleeds, ascites, and hepatic encephalopathy. In inflammatory bowel disease, large registries and pilot trials indicate reduced flares, lower corticosteroid requirements, and decreased need for surgery, with early biomarker evidence supporting an anti-inflammatory effect. Smaller studies hint at benefits in other gastrointestinal contexts, though the evidence remains fragmented. Across these populations, true hepatotoxicity is rare; risk of myopathy is modest and largely confined to advanced cirrhosis or drug–drug interactions. Collectively, these findings support cautious repurposing of statins in gastroenterology and underline the need for definitive randomized trials to resolve class effects, optimize dose and duration, and identify reliable biomarkers of response.
Refaei et al. (Mon,) studied this question.