{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,5]],"date-time":"2026-09-05T00:47:26Z","timestamp":1788569246408,"version":"build-2803163510"},"reference-count":29,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2013,6,28]],"date-time":"2013-06-28T00:00:00Z","timestamp":1372377600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["European J of Haematology"],"published-print":{"date-parts":[[2013,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objectives<\/jats:title><jats:p>Hepcidin plays a regulatory role in systemic iron homeostasis. <jats:styled-content style=\"fixed-case\">GDF<\/jats:styled-content>\u201015 has been found to be expressed from matured erythroblasts and very high levels of <jats:styled-content style=\"fixed-case\">GDF<\/jats:styled-content>\u201015 suppresses hepcidin secretion. In this study, we evaluated hepcidin and <jats:styled-content style=\"fixed-case\">GDF<\/jats:styled-content>\u201015 levels in polycythemia vera (<jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content>) and essential thrombocythemia (<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>The study included 29 patients and 21 healthy controls. The patient group included 13 patients with <jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content> and 16 patients with <jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content>. Serum hepcidin and <jats:styled-content style=\"fixed-case\">GDF<\/jats:styled-content>\u201015 levels were measured at the time of diagnosis, before the initiation of any therapy.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Hepcidin levels did not differ significantly in patients with chronic myeloproliferative disease (<jats:styled-content style=\"fixed-case\">CMPD<\/jats:styled-content>) and healthy controls. However, <jats:styled-content style=\"fixed-case\">GDF<\/jats:styled-content>\u201015 levels were significantly increased in patients with <jats:styled-content style=\"fixed-case\">CMPD<\/jats:styled-content> (<jats:italic>P<\/jats:italic>\u00a0=\u00a00.038). No difference could be found between patients with <jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content> in terms of hepcidin and <jats:styled-content style=\"fixed-case\">GDF<\/jats:styled-content>\u201015 levels. Patients with <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>2\u2010V617F mutation had increased <jats:styled-content style=\"fixed-case\">GDF<\/jats:styled-content>\u201015 levels when compared with patients without this mutation (<jats:italic>P<\/jats:italic>: 0.006).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>The levels of <jats:styled-content style=\"fixed-case\">GDF<\/jats:styled-content>\u201015 were higher in <jats:styled-content style=\"fixed-case\">CMPD<\/jats:styled-content>, which are characterized by increased erythropoiesis, and this effect was more pronounced particularly in individuals with <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>2\u2010V617F mutation. Hepcidin levels were not suppressed despite the increased erythroid activity and <jats:styled-content style=\"fixed-case\">GDF<\/jats:styled-content>\u201015 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 <jats:styled-content style=\"fixed-case\">GDF<\/jats:styled-content>\u201015 levels in <jats:styled-content style=\"fixed-case\">CMPD<\/jats:styled-content>. We hypothesized that, this may be an attempt to prevent further amplification of erythropoietic activity by reducing iron utilization.<\/jats:p><\/jats:sec>","DOI":"10.1111\/ejh.12150","type":"journal-article","created":{"date-parts":[[2013,6,3]],"date-time":"2013-06-03T13:49:47Z","timestamp":1370267387000},"page":"228-235","source":"Crossref","is-referenced-by-count":23,"title":["Serum hepcidin and growth differentiation factor\u201015 (<scp>GDF<\/scp>\u201015) levels in polycythemia vera and essential thrombocythemia"],"prefix":"10.1111","volume":"91","author":[{"given":"Pinar","family":"Tarkun","sequence":"first","affiliation":[{"name":"Department of Hematology Medical Faculty Kocaeli University Kocaeli Turkey"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ozgur","family":"Mehtap","sequence":"additional","affiliation":[{"name":"Department of Hematology Medical Faculty Kocaeli University Kocaeli Turkey"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elif B.","family":"Ateso\u011flu","sequence":"additional","affiliation":[{"name":"Department of Hematology Medical Faculty Kocaeli University Kocaeli Turkey"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ayfer","family":"Geduk","sequence":"additional","affiliation":[{"name":"Department of Hematology Medical Faculty Kocaeli University Kocaeli Turkey"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mahmut M.","family":"Musul","sequence":"additional","affiliation":[{"name":"Department of Medical Biochemistry Medical Faculty Kocaeli University Kocaeli Turkey"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abdullah","family":"Hacihanefioglu","sequence":"additional","affiliation":[{"name":"Department of Hematology Medical Faculty Kocaeli University Kocaeli 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