Abstract
BackgroundIn 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 presentationAn 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.ConclusionsThis case suggests that iron-overload mechanisms of dyserythropoietic anemias may apply to megaloblastic anemias.
Highlights
BackgroundIron overload related to hemolysis and ineffective erythropoiesis is a feature of megaloblastic anemia
In ineffective erythropoiesis, hepcidin synthesis is suppressed by erythroid regulators, namely eryth‐ roferrone and growth differentiation factor-15
Iron overload related to hemolysis and ineffective erythropoiesis is a feature of megaloblastic anemia
Summary
Iron overload related to hemolysis and ineffective erythropoiesis is a feature of megaloblastic anemia. Case presentation An 81-year-old Caucasian male was referred to emergency department for fatigue associated with profound anemia. He had type-2 diabetes previously treated with metformin, ischemic cardiac insufficiency, and stage-3 chronic kidney disease Vitamin B12 was undetectable, whereas vitamin B9 and C-reactive protein levels were normal (Table 1) He received one pack of red blood cells (RBC), was admitted to internal medicine department. Three-month (M3) biological control revealed that platelet count and hemoglobin, sideremia, and TSAT levels normalized (Table 1). The level of hepcidin was lower at the time of diagnosis than M3 but remained within reference levels, and its kinetics from diagnosis to M3 inversely correlated with those of EPO, ERFE, and GDF15 (Table 1). At 3 months: normalized vitamin B12 unsaturated transferrin saturated transferrin non transferrin bind iron ferroportin adapted erythropoiesis
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