Abstract
Background/aim GDF15, hepcidin and mitoferrin-1 (mfrn-1) are proteins involved in systemic iron regulation. There are no studies in the literature demonstrating the serum mfrn-1 levels in polycythemia vera (PV) and essential thrombocythemia (ET) patients. The aim of this study was to investigate GDF15, hepcidin and mfrn-1 levels in PV and ET patients.Materials and methods Ten PV, 17 ET patients, and 27 healthy controls (HCs) were enrolled. GDF15, hepcidin and mfrn-1 values were measured with enzyme-linked immunosorbent assay (ELISA).Results GDF15 levels were higher in the myeloproliferative neoplasm (MPN) group (P = 0.002). Hepcidin levels were not different between MPN patients and HCs. The mfrn-1 levels were lower in MPN patients (P = 0.039). Hepcidin, GDF15, and mfrn-1 levels were not different between PV and ET patients. mfrn-1 levels were lower in ET patients than HCs (P = 0.038).Conclusion Increased erythropoiesis in MPNs may lead to high GDF15 levels in these patients. However, hepcidin was not suppressed despite the increased GDF15 levels and erythropoiesis in these patients. Decrease in mfrn-1 in MPNs can be the result of its increased turnover due to increased myelopoiesis. It can be hypothesized that similar hepcidin levels in patients and controls and low mfrn-1 levels in patients may be a defense mechanism against erythroid activity and thromboembolic complications.
Highlights
Myeloproliferative neoplasms (MPN) are clonal hematopoietic stem cell disorders [1]
Increased erythropoiesis in MPNs may lead to high GDF15 levels in these patients
Hepcidin was not suppressed despite the increased GDF15 levels and erythropoiesis in these patients
Summary
Myeloproliferative neoplasms (MPN) are clonal hematopoietic stem cell disorders [1]. In polycythemia vera (PV) and essential thrombocythemia (ET), there is an increase in all hematopoietic series, but essentially in erythroid and megakaryocytoid series [2]. JAK V617F mutation exists in PV, ET, and primary myelofibrosis patients [3]. The JAK2 gene is located on 9p24 [4,5]. Hepcidin is a small protein primarily released from the liver. It is the main regulator of iron absorption and transportation to the tissues. Plasma iron level and erythropoietic activity regulate the hepcidin level. The increase in the iron level increases the hepcidin production. High hepcidin level reduces dietary iron absorption and the use of iron within the cell; hepcidin prevents iron accumulation in tissues. In cases of inflammation and infection, as a host defense hepcidin production increases in order to prevent iron transportation to microorganisms [6]
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