Serum hepcidin and growth differentiation factor‐15 (<scp>GDF</scp>‐15) levels in polycythemia vera and essential thrombocythemia

Tarkun, Pınar; Mehtap, Özgür; Atesoglu, Elif Birtas; Gedük, Ayfer; Musul, Mahmut Mert; Hacıhanefioğlu, Abdullah

doi:10.1111/ejh.12150

Cited by 22 publications

(21 citation statements)

References 28 publications

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“…Our observation of a weak correlation between GDF-15 and hepcidin levels was consistent with published data [26,29], indicating that GDF-15 may not directly influence hepcidin levels [30,31].…”

Section: Discussionsupporting

confidence: 92%

Hepcidin/Ferritin Quotient Helps to Predict Spontaneous Recovery from Iron Loss following Blood Donation

Lotfi

Kroll

Plonné³

et al. 2015

Transfus Med Hemother

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Background: Iron supplementation is generally recommended for blood donors even though there are inter-individual differences in iron homeostasis. Methods: Ferritin levels of repeat donors were compared with first-time donors, retrospectively. Prospectively, we tested 27 male repeat donors for the following parameters at the day of blood donation as well as 1, 3, 7, 10, and 56 days thereafter: ferritin, hepcidin, transferrin, transferrin receptor, hemoglobin, erythropoietin, reticulocytes, hemoglobin in reticulocyte, twisted gastrulation protein homolog 1, and growth differentiation factor-15. Results: 56 days after blood donation, donors' average ferritin dropped to 55% (range 30-100%) compared to the initial value. Of all tested parameters hepcidin showed the highest and most significant changes beginning 1 day after donation and lasting for the whole period of 56 days. Along with ferritin, there was a high variation in hepcidin levels indicating inter-individual differences in hepcidin response to iron loss. Donors with a hepcidin/ferritin quotient < 0.3 regained 60% of their initial ferritin after 56 days, while those with a quotient ≥ 0.3 reached less than 50%. Conclusion: As hepcidin appears to integrate erythropoietic and iron-loading signals, clinical measurement of hepcidin (together with the hepcidin-ferritin ratio) may become a useful indicator of erythropoiesis and iron kinetics.

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Section: Discussionsupporting

confidence: 92%

Hepcidin/Ferritin Quotient Helps to Predict Spontaneous Recovery from Iron Loss following Blood Donation

Lotfi

Kroll

Plonné³

et al. 2015

Transfus Med Hemother

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“…[18] However, it is not clear which factors determine microcytosis in PMF. On MVA, one of the factors associated with microcytosis was low satTF.…”

Section: 0 Discussionmentioning

confidence: 99%

Clinical significance of microcytosis in patients with primary myelofibrosis

et al. 2014

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Microcytosis is a relatively frequent finding in primary myelofibrosis (PMF); however its prognostic significance is unknown. We identified factors associated with microcytosis in PMF and measured its impact on outcomes. Among 725 patients with PMF, 140 (19%) showed microcytosis. In multivariate analysis, factors associated with microcytosis were absence of prior therapy, low iron, low transferrin saturation (satTF), and splenomegaly. Among 375 untreated patients, low satTF and splenomegaly were associated with microcytosis. Overall, microcytosis was associated with a higher risk of transformation to leukemia (p=0.03), but not shorter leukemia-free survival. Microcytosis in PMF may be related to dysregulation of iron homeostasis.

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“…Recent translational studies found no significant contribution of GDF15 levels to hepcidin suppression in iron deficiency [46,47], anemia of chronic disease [47] or chronic myeloproliferative diseases [48]. Phlebotomy of wild-type and Gdf15 −/− mice showed similar suppression of hepatic hepcidin mRNA in both groups of mice [49 ■ ].…”

Section: ‘Erythroid Regulators’ Of Hepcidin Expressionmentioning

confidence: 99%

New insights into iron regulation and erythropoiesis

Kim

Nemeth

2015

Current Opinion in Hematology

145

115

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Purpose of review Iron homeostasis and erythropoiesis regulate each other to ensure optimal delivery of oxygen and iron to cells and tissues. Defining the mechanisms of this crosstalk is important for understanding the pathogenesis of common conditions associated with disordered iron metabolism and erythropoiesis. Recent findings Stress erythropoiesis causes suppression of hepcidin to increase iron availability for hemoglobin synthesis. The erythroid hormone erythroferrone (ERFE) was identified as the mediator of this process. ERFE and additional candidates (TWSG1 and GDF15) may also mediate hepcidin suppression in ineffective erythropoiesis. Several mechanisms by which iron regulates erythropoiesis were also recently identified. Iron deficiency suppresses erythropoietin production via the IRP1–HIF2α axis to prevent excessive iron usage by erythropoiesis during systemic iron restriction. Iron restriction also directly impairs erythroid maturation by inhibiting aconitase, and this can be reversed by the administration of the aconitase product isocitrate. Another novel target is GDF11, which is thought to autoinhibit erythroid maturation. GDF11 traps show promising pharmacologic activity in models of both ineffective erythropoiesis and iron-restricted anemia. Summary This review summarizes exciting advances in understanding the mechanisms of iron and erythropoietic regulation, and development of novel therapeutic tools for disorders resulting from dysregulation of iron metabolism or erythropoiesis.

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Serum hepcidin and growth differentiation factor‐15 (GDF‐15) levels in polycythemia vera and essential thrombocythemia

Cited by 22 publications

References 28 publications

Hepcidin/Ferritin Quotient Helps to Predict Spontaneous Recovery from Iron Loss following Blood Donation

Hepcidin/Ferritin Quotient Helps to Predict Spontaneous Recovery from Iron Loss following Blood Donation

Clinical significance of microcytosis in patients with primary myelofibrosis

New insights into iron regulation and erythropoiesis

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