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INVESTIGATION OF IRON METABOLISM FOR REGULATING MEGAKARYOPOIESIS AND PLATELET COUNT ACCORDING TO THE MECHANISMS OF ANEMIA
Author(s): ,
Suekyeung Kim
Affiliations:
Kyung Hee University Hospital,Seoul,Korea, Republic Of
,
Sun Young Cho
Affiliations:
Kyung Hee University Hospital,Seoul,Korea, Republic Of
Tae Sung Park
Affiliations:
Kyung Hee University Hospital,Seoul,Korea, Republic Of
(Abstract release date: 05/18/17) EHA Library. Cho S. 05/18/17; 182622; PB1908
Sun Young Cho
Sun Young Cho
Contributions
Abstract

Abstract: PB1908

Type: Publication Only

Background
Iron deficiency anemia (IDA) is characterized by depletion of total body iron stores. By contrast, chronic inflammation makes iron unavailable for hematopoiesis through a cytokine-mediated cascade, resulting in anemia of chronic disease (AOC). However, the laboratory data regarding the regulatory role of iron metabolism on platelet count has not been fully discussed yet.

Aims
In this study, we investigated the relationship between iron status and platelet production according to different anemic mechanisms representing different iron metabolisms.

Methods
The study included total of 759 blood specimens from 537 different patients. The complete blood count with various CBC index were measured using Advia 2120 (Siemens, USA). Biochemical indexes including iron level were estimated using Toshiba chemical analyzer (Toshiba, Japan).

Results
We found a significant relationship between platelet count and serum iron level in AOC group (p<0.27), whereas there was no correlation in IDA group. In AOC group, platelet count was significantly correlated to serum iron level only in AOC group with decreased serum iron level (p<0.0001), unlike AOC group with normal serum iron level.

Conclusion
Reactive thrombocytosis in inflammatory states occurs by cytokine cascades involving interleukin-6 and thrombopoietin in AOC. Moreover, iron deficiency in AOC involves upregulated hepcidin production induced by increased inflammatory cytokines. It can cause increased iron sequestration in macrophage and decreased iron absorption for bone marrow. The condition of decreased megakaryocytic iron supply makes megakaryocytes with higher ploidy which can release more platelets than lower ploidy. These two features may enhance thrombocytosis in patients of AOC with decreased iron level. In the future, the further study should be performed to elucidate underlying mechanism involving the tight regulation between iron metabolism and megakaryopoiesis in anemic patients.

Session topic: 28. Iron metabolism, deficiency and overload

Keyword(s): Platelet count, Megakaryopoiesis, Iron Metabolism, Anemia

Abstract: PB1908

Type: Publication Only

Background
Iron deficiency anemia (IDA) is characterized by depletion of total body iron stores. By contrast, chronic inflammation makes iron unavailable for hematopoiesis through a cytokine-mediated cascade, resulting in anemia of chronic disease (AOC). However, the laboratory data regarding the regulatory role of iron metabolism on platelet count has not been fully discussed yet.

Aims
In this study, we investigated the relationship between iron status and platelet production according to different anemic mechanisms representing different iron metabolisms.

Methods
The study included total of 759 blood specimens from 537 different patients. The complete blood count with various CBC index were measured using Advia 2120 (Siemens, USA). Biochemical indexes including iron level were estimated using Toshiba chemical analyzer (Toshiba, Japan).

Results
We found a significant relationship between platelet count and serum iron level in AOC group (p<0.27), whereas there was no correlation in IDA group. In AOC group, platelet count was significantly correlated to serum iron level only in AOC group with decreased serum iron level (p<0.0001), unlike AOC group with normal serum iron level.

Conclusion
Reactive thrombocytosis in inflammatory states occurs by cytokine cascades involving interleukin-6 and thrombopoietin in AOC. Moreover, iron deficiency in AOC involves upregulated hepcidin production induced by increased inflammatory cytokines. It can cause increased iron sequestration in macrophage and decreased iron absorption for bone marrow. The condition of decreased megakaryocytic iron supply makes megakaryocytes with higher ploidy which can release more platelets than lower ploidy. These two features may enhance thrombocytosis in patients of AOC with decreased iron level. In the future, the further study should be performed to elucidate underlying mechanism involving the tight regulation between iron metabolism and megakaryopoiesis in anemic patients.

Session topic: 28. Iron metabolism, deficiency and overload

Keyword(s): Platelet count, Megakaryopoiesis, Iron Metabolism, Anemia

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