Serum Prohepcidin and Iron Homeostasis in Patients with Breast Cancer

Cancer-related anemia (CRA) has multifactorial etiology and complex pathogenesis. It is defined as normochromic, normocytic anemia with reticulocyto-penia and hypoferremia. Hepcidin is recognized as the central factor in causing CRA. Objective: To investigate the changes in the serum levels of prohepcidin (pHp) and markers of iron homeostasis for gathering more data on the pathogenesis of CRA.

The authors analyzed prospectively 46 newly diagnosed women with breast cancer, aged 29–72 years (average 47.5±9.0 SD), who had the same clinical stage, histology and hormonal status. They were diagnosed and treated in the Clinic of Oncology and Hematology - University Hospital for a 2-year period (2009–2010). Serum pHp levels and common markers of iron status including serum iron (sFe), transferrin saturation, soluble tranferrin receptor (sTfR), Zn-protoporphyrin (ZPP), ferritin as well as vitamin B₁₂ and folate were measured before treatment initiation and two months afterwards. Serum pHp was determined by a competitive immunotest. All statistical data was computed by the methods of variational and correlation analyses.

For the two-month follow up interval parameters of full blood count remained without statistically significant deviation. Although the analyzed parameters in the first and second blood samples remained within the reference intervals, the decrease of pHp and the changes of iron-containing substances and ZPP in red blood cells cannot be neglected. However the correlation coefficient (R) between decreased pHp, increased sFe (R=0.314), sTfR (R=0.258), ZPP (R=0.118) and decreased ferritin (R=0.099), were low instead of the expected higher relationship. The obtained results do not support the idea that iron increase and other changes of iron homeostasis in these patients is a direct result of regulatory decrease of pHp. The two-month interval is likely short enough to rule out a potential direct suppressive effect of the specific cytotoxic treatment, and therefore we do not discuss such potential influence on iron homeostasis.

Iron homeostasis dysregulation is one of CRA components. In its complex pathogenesis several other factors interfere e.g. such related to the disease; therapy related factors; altered erythropoietin production; activation of cytokines (IL-6 is the major promoter of hepcidin production).

No relevant conflicts of interest to declare.