Hepcidin plays a regulatory role in systemic iron homeostasis. GDF-15 has been found to be expressed from matured erythroblasts and very high levels of GDF-15 suppresses hepcidin secretion. In this study, we evaluated hepcidin and GDF-15 levels in polycythemia vera (PV) and essential thrombocythemia (ET).Methods:
The study included 29 patients and 21 healthy controls. The patient group included 13 patients with ET and 16 patients with PV. Serum hepcidin and GDF-15 levels were measured at the time of diagnosis, before the initiation of any therapy.Results:
Hepcidin levels did not differ significantly in patients with chronic myeloproliferative disease (CMPD) and healthy controls. However, GDF-15 levels were significantly increased in patients with CMPD (P = 0.038). No difference could be found between patients with PV and ET in terms of hepcidin and GDF-15 levels. Patients with JAK2-V617F mutation had increased GDF-15 levels when compared with patients without this mutation (P: 0.006).Conclusions:
The levels of GDF-15 were higher in CMPD, which are characterized by increased erythropoiesis, and this effect was more pronounced particularly in individuals with JAK2-V617F mutation. Hepcidin levels were not suppressed despite the increased erythroid activity and GDF-15 levels may be protective against the clinical complications of the disease such as thrombosis. This study revealed that, hepcidin levels were not suppressed despite increased erythroid activity and high GDF-15 levels in CMPD. We hypothesized that, this may be an attempt to prevent further amplification of erythropoietic activity by reducing iron utilization.