Ferritin and Liver Steatosis in Children: Interactions Between Metabolic Clustering and PNPLA3 Variants

Metabolic abnormalities are frequently associated with hepatic steatosis and low-grade inflammation, yet the contributions of iron metabolism and genetic susceptibility are not fully understood. We aimed to investigate the relationship between serum ferritin, hepatic steatosis, metabolic risk clustering, and the PNPLA3 rs738409 gene variant in children. A total of 68 children aged 6–14 years underwent anthropometric, biochemical, imaging, and genetic assessment. Hepatic steatosis was present in 72.1% of participants, with fibrosis greater than F1 in 42.6%. Serum ferritin showed a strong correlation with echographic liver steatosis severity (ρ = 0.804, p < 0.001) and a moderate correlation with the number of metabolic risk components (ρ = 0.482, p < 0.001). The highest metabolic burden occurred in children with low iron and elevated ferritin. While PNPLA3 status did not independently predict ferritin levels, carriers had a significantly higher prevalence of hypertension (50.0% vs. 25.0%, p = 0.038) and a non-significant trend toward low HDL-C (65.0% vs. 42.9%, p = 0.070). Ferritin was associated with metabolic clustering and ultrasound-defined hepatic steatosis, acting as a nonspecific marker of combined metabolic and hepatic alterations. PNPLA3 genotype was not independently related to ferritin or fibrosis in early pediatric disease. Given the cross-sectional design and the relatively small sample size, these findings should be interpreted as exploratory and further studies including larger populations and direct inflammatory markers should be conducted.