Hepcidin peptide hormone is a main controller of iron homeostasis, it becomes elevated in case of iron overload, however despite iron overload in b-Thalassemia major (b-TM) patients a contradictory decrease in Hepcidin occurs. The incompatible Hepcidin level is the main responsible factor causing the iron overload status in iron-loading anemias such as (b-TM) which contributes to organ dysfunction and to iron toxicity.

Aim of Study

To evaluate the conflicting effect of increased erythropoiesis in contrast to the effect of iron overloading on Hepcidin serum level and its correlation with iron status in (b-TM) patients.

Subjects and Methods

For all patients and controls Complete Blood Count (CBC), serum assays of Hepcidin, iron, ferritin, transferrin, HCV Abs, HBs Ag, CRP and serum level were performed.

Results

Hepcidin level was significantly lowered in (b-TM) patients compared to controls with high significant difference (p=0.00). There was no correlation between serum Hepcidin and ferritin level, neither was between Hepcidin and serum iron, transferrin, Hb level and reticulocyte count in the study group. Hepcidin/Ferritin ratio showed high significance difference (p<0.000) with mean value in the study group 0.056 vs. 4.75 in controls pointing to an incom-patible levels of Hepcidin to iron overload status. Hepcidin level was negative correlated with age (p<0.05).

Conclusion

Hepcidin was markedly decreased in the study group with no significant correlation between serum Hepcidin and ferritin level as a marker of iron overload in thalassemia major. Hepcidin deficiency is the main contributing factor of iron overload in b  thalassemia …