Erythroferrone and hepcidin levels in children with iron deficiency anemia

Iron deficiency anemia remains a significant public health issue in developing countries. The regulation of iron metabolism is primarily controlled by hepcidin, a key regulatory protein. During erythropoiesis, erythroferrone (ERFE), a hormone produced by erythroblasts in response to erythropoietin (EPO) synthesis, mediates the suppression of hepcidin. In this study, it was aimed to determine the correlation between erythroferrone (ERFE) and hepcidin levels in children with iron deficiency anemia.

The study found a strong and positive correlation between ferritin and hepcidin levels in iron-deficient children, but not between ERFE levels, suggesting that hepcidin is largely regulated by iron deposition levels. In addition, there was an increase in ferritin and hepcidin levels after iron treatment. The study found no significant difference in erythroferrone levels between the iron-deficient group and the control group. It is thought that this may be due to the short duration of iron treatment given to the patients with iron deficiency anemia included in the study.

This is a case-control study conducted at Kırşehir Ahi Evran University Training and Research Hospital Pediatrics Clinic between 1 and 31 September 2020. The study included 26 healthy children and 26 children with iron deficiency anemia. In order to evaluate iron status,whole blood count, serum iron, total iron binding capacity (TIBC), and ferritin levels were analyzed. The study measured the levels of hepcidin and erythroferrone in the serum of children diagnosed with iron deficiency before and after one month of iron treatment, as well as in a control group, using the ELISA method. Correlation between whole blood count, initial ferritin, hepcidin, ERFE and ferritin in the iron deficiency group was evaluated.

Compared with healthy controls, the iron-deficient group had significantly lower haemoglobin (p < 0.001), MCV (p = 0.001), MCH (p < 0.001), MCHC (p < 0.001), iron (p < 0.001), ferritin (p < 0.001) and hepcidin (p = 0.001). Ferritin and hepcidin levels increased while erythroferrone levels remained unchanged after iron deficiency treatment. There was no correlation between hepcidin and ferritin levels in treatment group. Conclusions: The study found a strong and positive correlation between ferritin and hepcidin levels in iron-deficient children, but not between ERFE levels, suggesting that hepcidin is largely regulated by iron deposition levels. In addition, there was an increase in ferritin and hepcidin levels after iron treatment. The study found no significant difference in erythroferrone levels between the iron-deficient group and the control group. It is thought that this may be due to the short duration of iron treatment given to the patients with iron deficiency anemia included in the study.