Megaloblastic anemia-related iron overload and erythroid regulators: a case report
Abstract Background In ineffective erythropoiesis, hepcidin synthesis is suppressed by erythroid regulators, namely erythroferrone and growth differentiation factor-15. For the first time, the hypothesis that iron overload in megaloblastic anemia may be related to ineffective erythropoiesis is explo...
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doaj-042113aecb8a4595b02ec9d0eb2e5f642021-09-26T11:49:20ZengBMCJournal of Medical Case Reports1752-19472021-09-011511510.1186/s13256-021-03065-0Megaloblastic anemia-related iron overload and erythroid regulators: a case reportNicolas Vallet0Jean-Baptiste Delaye1Martine Ropert2Amélie Foucault3Noémie Ravalet4Sophie Deriaz5Thomas Chalopin6Hélène Blasco7François Maillot8Olivier Hérault9Emmanuel Gyan10Department of Hematology and Cell Therapy, Tours University HospitalDepartment of Biochemistry and Molecular Biology, Tours University HospitalDepartment of Biochemistry, CHU RennesDepartment of Biological Hematology, Tours University HospitalDepartment of Biological Hematology, Tours University HospitalDepartment of Internal Medicine, Tours University HospitalDepartment of Hematology and Cell Therapy, Tours University HospitalDepartment of Biochemistry and Molecular Biology, Tours University HospitalDepartment of Internal Medicine, Tours University HospitalDepartment of Biological Hematology, Tours University HospitalDepartment of Hematology and Cell Therapy, Tours University HospitalAbstract Background In ineffective erythropoiesis, hepcidin synthesis is suppressed by erythroid regulators, namely erythroferrone and growth differentiation factor-15. For the first time, the hypothesis that iron overload in megaloblastic anemia may be related to ineffective erythropoiesis is explored by describing the kinetics of hepcidin, erythroferrone, and growth differentiation factor-15 levels in a patient diagnosed with megaloblastic anemia associated with iron overload. Case presentation An 81-year-old Caucasian male was admitted for fatigue. He had type-2 diabetes previously treated with metformin, ischemic cardiac insufficiency, and stage-3 chronic kidney disease. Vitiligo was observed on both hands. Biological tests revealed normocytic non-regenerative anemia associated with hemolysis, thrombocytopenia, and elevated sideremia, ferritin, and transferrin saturation levels. Megaloblastic anemia was confirmed with undetectable blood vitamin B12 and typical cytological findings like hyper-segmented neutrophils in blood and megaloblasts in bone marrow. The patient received vitamin B12 supplementation. At 3 months, biological parameters reached normal values. Hepcidin kinetics from diagnosis to 3 months inversely correlated with those of erythroferrone and growth differentiation factor-15. Conclusions This case suggests that iron-overload mechanisms of dyserythropoietic anemias may apply to megaloblastic anemias.https://doi.org/10.1186/s13256-021-03065-0Vitamin B12Iron overloadErythropoiesisErythroferroneGDF15Case report |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Nicolas Vallet Jean-Baptiste Delaye Martine Ropert Amélie Foucault Noémie Ravalet Sophie Deriaz Thomas Chalopin Hélène Blasco François Maillot Olivier Hérault Emmanuel Gyan |
spellingShingle |
Nicolas Vallet Jean-Baptiste Delaye Martine Ropert Amélie Foucault Noémie Ravalet Sophie Deriaz Thomas Chalopin Hélène Blasco François Maillot Olivier Hérault Emmanuel Gyan Megaloblastic anemia-related iron overload and erythroid regulators: a case report Journal of Medical Case Reports Vitamin B12 Iron overload Erythropoiesis Erythroferrone GDF15 Case report |
author_facet |
Nicolas Vallet Jean-Baptiste Delaye Martine Ropert Amélie Foucault Noémie Ravalet Sophie Deriaz Thomas Chalopin Hélène Blasco François Maillot Olivier Hérault Emmanuel Gyan |
author_sort |
Nicolas Vallet |
title |
Megaloblastic anemia-related iron overload and erythroid regulators: a case report |
title_short |
Megaloblastic anemia-related iron overload and erythroid regulators: a case report |
title_full |
Megaloblastic anemia-related iron overload and erythroid regulators: a case report |
title_fullStr |
Megaloblastic anemia-related iron overload and erythroid regulators: a case report |
title_full_unstemmed |
Megaloblastic anemia-related iron overload and erythroid regulators: a case report |
title_sort |
megaloblastic anemia-related iron overload and erythroid regulators: a case report |
publisher |
BMC |
series |
Journal of Medical Case Reports |
issn |
1752-1947 |
publishDate |
2021-09-01 |
description |
Abstract Background In ineffective erythropoiesis, hepcidin synthesis is suppressed by erythroid regulators, namely erythroferrone and growth differentiation factor-15. For the first time, the hypothesis that iron overload in megaloblastic anemia may be related to ineffective erythropoiesis is explored by describing the kinetics of hepcidin, erythroferrone, and growth differentiation factor-15 levels in a patient diagnosed with megaloblastic anemia associated with iron overload. Case presentation An 81-year-old Caucasian male was admitted for fatigue. He had type-2 diabetes previously treated with metformin, ischemic cardiac insufficiency, and stage-3 chronic kidney disease. Vitiligo was observed on both hands. Biological tests revealed normocytic non-regenerative anemia associated with hemolysis, thrombocytopenia, and elevated sideremia, ferritin, and transferrin saturation levels. Megaloblastic anemia was confirmed with undetectable blood vitamin B12 and typical cytological findings like hyper-segmented neutrophils in blood and megaloblasts in bone marrow. The patient received vitamin B12 supplementation. At 3 months, biological parameters reached normal values. Hepcidin kinetics from diagnosis to 3 months inversely correlated with those of erythroferrone and growth differentiation factor-15. Conclusions This case suggests that iron-overload mechanisms of dyserythropoietic anemias may apply to megaloblastic anemias. |
topic |
Vitamin B12 Iron overload Erythropoiesis Erythroferrone GDF15 Case report |
url |
https://doi.org/10.1186/s13256-021-03065-0 |
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