Erythroferrone as iron overload biomarker in thalassemic patients: a case control study

Background
Iron overload remains a leading cause of morbidity and mortality in β-thalassemia patients, despite the use of iron chelators. Erythroferrone (ERFE) and hepcidin are key regulators of iron homeostasis, with ERFE inhibiting hepcidin to enhance iron availability for erythropoiesis. Elevated ERFE levels in β-thalassemia, coupled with reduced hepcidin, may contribute to iron overload.


Aim
This study aimed to explore the relationship between serum ERFE and iron overload and evaluate its potential use as an iron overload biomarker, offering an alternative to ferritin, which can increase as an acute-phase reactant.


Patients and methods
This case–control study involved 47 adult β-thalassemia patients and 41 age and sex-matched healthy controls. The serum ERFE level was measured using the enzyme linked immunosorbent assay technique and correlated with serum ferritin, total iron binding capacity, serum iron, transferrin saturation, and complete blood count.


Results

Our research revealed that β-thalassemia patients had significantly higher serum ERFE levels than controls (
P
=0.018). However, we did not find any significant correlation between the serum ERFE level and Ferritin levels.



Conclusion
Our results suggest a potential role for ERFE in the pathophysiology of β-thalassemia. However, the lack of a significant correlation between serum ERFE levels and ferritin suggests that ERFE’s regulation and its relationship with iron homeostasis in β-thalassemia may be more complex than previously understood and require further research.