Ferritin as an Inflammatory Marker in Pediatric Metabolic Syndrome: Links to Obesity and Liver Ultrasound Alterations

Abstract

This study analyzed the relationship between obesity, metabolic syndrome (MetS) and its individual components, iron metabolism, and hepatic alterations in a pediatric group of patients. We mostly concentrated on the role of serum ferritin as a marker of inflammation. We conducted a retrospective study, in which we determined the presence of MetS and hepatic ultrasound changes in a cohort of 68 pediatric patients and examined the changes in serum iron and ferritin levels. MetS prevalence was significantly higher in obese children (64%) compared to those with average weight (11.1%). Abdominal circumference, triglycerides, and high-density lipoprotein cholesterol were the most relevant MetS criteria. Serum iron levels were significantly lower, while ferritin levels increased proportionally with MetS number of components. Liver ultrasound findings confirmed a strong association between hepatic steatosis and MetS, with advanced ultrasonographic scores correlating with increased ferritin and serum iron deficiency. These results reinforce the interplay between iron metabolism and inflammation in pediatric MetS. Given this study's unicentric design and limited ethnic diversity, further large-scale, longitudinal studies are needed to confirm these findings and improve early screening strategies for pediatric metabolic complications.

Keywords: hepatic steatosis; low-grade inflammation; metabolic syndrome; serum ferritin; serum iron.

Figure 1

Distribution of patients according to the presence of MetS and statistical correlates weight, deficiency serum iron, increased serum ferritin, and ultrasound changes.

Figure 2

The distribution of cases according to iron deficiency and increased ferritin and imaging evaluation.

Figure 3

Pathophysiological mechanism linking adipose tissue, chronic low-grade inflammation, and disorders in iron metabolism observed in children with obesity and MetS. Excess adipose tissue contributes to a pro-inflammatory state, characterized by elevated production of cytokines such as IL-6 and tumor necrosis factor-alpha (TNF-α), along with increased oxidative stress markers (reactive oxygen species—ROS) and C-reactive protein (CRP). These inflammatory mediators stimulate hepatic synthesis of hepcidin, a key regulator of systemic iron. It binds to ferroportin (FPN)—a cellular iron exporter expressed by enterocytes and hepatic macrophages—thereby reducing intestinal iron absorption and promoting iron sequestration in macrophages. As a consequence, we encounter low serum iron. In response to this functional iron deficiency and persistent inflammatory state, ferritin synthesis is upregulated as part of the acute-phase response. This explains the paradoxical finding of elevated serum ferritin despite low circulating iron levels in children with obesity and MetS. Created with https://www.biorender.com (accessed on 12 April 2025).