Abstract
Background: Iron inhibits megakaryopoiesis so iron deficiency anemia (IDA) leads to microthrombosis. Iron therapy ameliorates thrombocytosis. In this study, we investigated whether young, active, and large platelets are released into peripheral blood during iron treatment. Mean platelet volume (MPV) was measured as an indicator for the presence of these platelets.
 Materials and Methods: A total of 80 patients (10 males and 70 females) with IDA were included in this retrospective study. IDA was defined as ferritin level <50 ng/mL with a transferrin saturation <20% or ferritin <15 ng/mL. Daily ferrous sulfate (270 mg iron II sulfate and 80 mg of elemental iron) was given orally to patients. We evaluated retrospectively the hematologic and biochemical parameters prior to and 1 month after iron treatment.
 Results: the mean ferritin level of the pretreatment group was 6.5 ± 4.0 ng/mL, MPV was
 7.9 ± 1.5 fL, hemoglobin (Hb) was 9.8 ± 1.5 g/dL and the mean cellular volume (MCV) was 71.2 ± 7.2 fL. The mean ferritin level of the posttreatment group was 40.3 ± 15.2 ng/mL, MPV was 8.6 ± 2.0 fL, Hb was 12.5 ± 6.6 g/dL, and MCV was 77.6 ± 5.4 fL. The levels of ferritin (P < 0.001), MPV (P < 0.001), MCV (P < 0.001), and Hb (P < 0.001) were significantly higher in the posttreatment group compared to the pretreatment group.
 Conclusion: There may be an increase in thrombotic events due to hypercoagulability related to microthrombosis during IDA. Even though thrombosis is corrected during iron treatment, the therapy increases the release of large and active thrombocytes into the peripheral blood.
 Keywords: Iron, iron deficiency anemia, mean platelet volume, thrombocytosis, thrombosis
Highlights
Iron is an essential trace element presents in a number of molecular systems and it is increasingly recognized as an important cofactor for a variety of cell systems.[1]
We investigated whether young, active, and large platelets are released into peripheral blood during iron treatment
There may be an increase in thrombotic events due to hypercoagulability related to microthrombosis during iron deficiency anemia (IDA)
Summary
Iron is an essential trace element presents in a number of molecular systems and it is increasingly recognized as an important cofactor for a variety of cell systems.[1] It is the basic element for the production of new red blood cells (RBC) If it is not used in erythropoiesis it is stored as ferritin or hemosiderin.[2] Serum ferritin levels are closely correlated with total body iron stores.[3] Iron deficiency anemia (IDA) occurs due to increased body requirements, insufficient iron supply (depending on dietary iron intake and duodenal absorption) and blood losses.[4] It has been estimated that 30% of the world population suffers from IDA and most of them live in the developing countries.[5] While iron deficiency leads to anemia its excess leads to both deposition of iron in the tissues as hemosiderosis and cellular damage by oxygen radicals as a result of the combination of free iron with peroxides radicals.[6] Excess iron in the body may be dependent on the HFE gene on chromosome 6 as well as it may occur with unnecessary or long-term treatment of iron.[7].
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