Abstract

Peripheral blood smears of 43 patients (26 males, median age 18 months, range: 6–180 months) with nutritional iron-deficiency anemia (IDA) were examined for the presence of trilineage hematological dysplasia. Twelve patients were reexamined for dysplastic findings after achieving a normal Hb and hematocrit level for age by the end of 2–3 months of iron treatment. A control group of 17 age-matched healthy children were also included. Neutrophils with loss of membrane entirety and protrusions were remarkable in 34/43 (79%) in the IDA group versus 1/12 (8%) after iron treatment and none of the control group. Microspherocytes were seen in 9/43 (21%) of IDA patients. Additionally, trilienage dysplasia was observed in the bone marrow samples available in 3 of the patients. It has been shown that iron-deficiency results in cellular DNA and RNA alterations, cell-cycle G1/S phase arrest, and apoptosis. Rac GTPases have been shown to control actin cytoskeleton, influencing cell polarity, microtubule dynamics, and the cytoskeletal organization of hematopoietic cells. Thus, the findings described above in neutrophils and red cells suggest a plausible link between iron and the Rac GTPase gene family. It may be a new avenue for iron waiting for proof.

Highlights

  • Iron-deficiency anemia (IDA) diagnosis was based on hemoglobin (Hb), mean corpuscular volume (MCV), red cell distribution width (RDW), serum iron (SI), serum iron binding capacity (SIBC), transferrin saturation (TS), and ferritin values that were compatible with IDA according to the age of the patient together with the presence of microcytic hypochromic red cells on the peripheral blood smear

  • This study presents the dysplastic hematological changes in peripheral blood and bone marrow (BM) of IDA patients

  • Myelodysplastic changes refer to abnormal morphology of the BM and/or peripheral blood and this feature is commonly seen in myelodysplastic syndrome (MDS)

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Summary

Introduction

Abnormalities of myeloid hemopoietic cells in IDA, such as neutrophil hypersegmentation and dysmorphic findings in red blood cells, might be termed as myelodysplasia. In our clinic we had an experience in a patient with severe IDA who was referred to our center with a possible diagnosis of MDS because of severe dysplasia and anemia. This index case and few previous reports on dysplastic findings, such as neutrophil hypersegmentation and thrombocytopenia in IDA patients, challenged us to examine dysplastic findings in IDA. On the basis of the dysplastic hematopoiesis, we observed trilineage dysplasia on peripheral blood and bone marrow (BM) smear examinations in IDA patients

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