Serum iron profile alterations in metabolic dysfunction-associated fatty liver disease and their association with liver fibrosis: a case-control study

Abstract Background Metabolic dysfunction-associated fatty liver disease (MAFLD) is a common chronic liver disease associated with metabolic dysfunction. Disturbances in iron homeostasis have been implicated in its pathogenesis; however, differences in routine iron profile parameters and associations remain incompletely characterized. Aim To compare serum iron profile parameters between MAFLD patients and healthy controls and assess their discriminative performance and associations with liver fibrosis and metabolic dysfunction. Methods This prospective case-control study analyzed 60 age- and sex-matched individuals (30 MAFLD patients and 30 healthy controls) treated at Ain Shams University Hospitals. Clinical profiling and laboratory testing, including iron indices, were performed alongside abdominal ultrasonography and transient elastography. Results MAFLD cases demonstrated significantly higher serum ferritin and TIBC, with significantly lower serum iron and TSat. Iron profile abnormalities were not significantly associated with liver stiffness measurements in this cohort. ROC evaluation highlighted good discriminative performance across all iron biomarkers; TSat achieved the highest AUC, followed sequentially by serum iron and ferritin. Univariate regression analysis identified ferritin, serum iron, TSat, body mass index, HOMA-IR, and triglycerides as significant factors. In an exploratory multivariable logistic regression model, HOMA-IR and serum ferritin remained independently associated with MAFLD case status. Conclusion Routine iron profile parameters were significantly altered in patients with MAFLD, characterized by higher serum ferritin and TIBC and lower serum iron and TSat levels. Although TSat showed good discriminatory ability in distinguishing patients with MAFLD from healthy controls, these findings primarily reflect altered systemic iron homeostasis rather than definitive evidence of iron overload.