Hepcidin-mediated regulation of iron metabolism in myelodysplastic syndrome

Continuous red blood cell (RBC) transfusions are the main factor of hemosiderosis development, but many Myelodysplastic syndrome (MDS) patients develop iron overload at an early stage of the disease before the red blood cell (RBC) transfusions begin. Hepsidin is a hormone, produced by hepatocytes. It plays a leading role in iron hemostasis. MDS patients demonstrate elevated serum ferritin and hepcidin concentrations even before the RBC transfusions initiating. After 6 months of follow-up, serum ferritin concentration was increased up to 1278 µg / L without significant hepcidin concentration elevation. After 12 months, serum ferritin continued increasing up to 1898 µg / L with a significant hepcidin level decrease to 92±17 pg / ml. The patients group with a ferritin level above average after 12 months of treatment demonstrated significantly lower 5-year overall survival (OS) compared to the group with ferritin level after 12 months of treatment below 1598 µg / L: 5-year OS 9,1±8,7 %; median OS - 1,7 years, median observation time 2,9 years (1,2-5,8) in the first group versus 5-year OS 44,4±17,0 %; median OS - 4,5 years, median observation time 4,5 years (2,6-6) in the second one...