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Dysplasia and disorder of cell membrane entirety in iron-deficiency anemia
Sevgi Yetgin1, Deniz Aslan, Sule Unal
1Faculty of Medicine, Department of Pediatrics, Division of Pediatric Hematology, Hacettepe University, Ankara, Turkey. yetgins@superonline.com
Insights
Iron deficiency anemia causes neutrophil and red blood cell dysplasia, potentially linked to Rac GTPase genes. Treatment with iron reverses these cellular changes.
Area of Science:
- Hematology
- Cell Biology
- Nutritional Science
Background:
- Nutritional iron-deficiency anemia (IDA) is a common condition affecting children.
- Cellular alterations and apoptosis have been linked to iron deficiency.
- The role of Rac GTPases in hematopoietic cell cytoskeleton organization is established.
Purpose of the Study:
- To investigate trilineage hematological dysplasia in children with IDA.
- To examine the reversibility of these dysplastic changes after iron treatment.
- To explore a potential link between iron deficiency and Rac GTPase activity.
Main Methods:
- Peripheral blood smears from 43 children with IDA were analyzed for dysplasia.
- Twelve patients were re-evaluated after 2-3 months of iron therapy.
- A control group of 17 healthy children was included for comparison.
Main Results:
- Neutrophil membrane abnormalities were observed in 79% of IDA patients, significantly reduced after treatment.
- Microspherocytes were present in 21% of IDA patients.
- Trilineage dysplasia was noted in bone marrow samples from 3 patients.
Conclusions:
- Iron deficiency anemia is associated with significant neutrophil and red blood cell dysplasia.
- Iron supplementation effectively reverses these hematological abnormalities.
- Findings suggest a potential link between iron status and the Rac GTPase gene family in hematopoietic cells.
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.
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