Diminished Platelet Aggregation in Patients with Iron Deficiency Anemia

Çalışkan, Ümran; Öner, Ahmet Faik; Kabakuş, Nimet; Koç, Hasan

doi:10.1177/107602969900500304

Cited by 27 publications

(26 citation statements)

References 11 publications

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“…However, other studies do not confirm these findings. It has been demonstrated by several authors that maximum aggregation rates of platelet induced by various concentrations of ADP and collagen are significantly lower in children with IDA and it can be reversed by iron therapy [1,2,11]. In this study, MATs were significantly longer in iron-deficient children, although ADP and collagen-induced maximum aggregation rates were not different from those in control group.…”

Section: Discussioncontrasting

confidence: 48%

“…There are a few studies investigating platelet aggregation in children with IDA with conflicting results [1,2,11,12]. Tekin et al [12] reported that platelet aggregation responses to collagen and ADP are significantly higher in iron-deficient children than in controls.…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that iron deficiency anemia (IDA) may cause platelet aggregation dysfunction and this can be reversed by iron therapy [1][2][3]. Although it is thought that iron-containing enzymes of the platelets might have a role, the main cause of this abnormality is not clear.…”

Section: Introductionmentioning

confidence: 99%

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Platelet function alterations and their relation to P-selectin (CD62P) expression in children with iron deficiency anemia

Yıldırım¹,

Orhan²,

Büyükavcı³

2011

Blood Coagulation &Amp; Fibrinolysis

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Iron deficiency anemia (IDA) may cause platelet aggregation dysfunction and this can be reversed by iron therapy. On the other hand, it has been reported that the platelet fractions carrying the platelet activation markers, CD62P and CD63, are increased in thalassemic patients and there is a significant correlation between the increased levels of soluble P-selectin and free iron in sickle cell disease. This study was performed to investigate the alterations of platelet functions and whether iron deficiency results in diminished expression of activation marker (P-selectin; CD62P) leading to platelet aggregation dysfunction in children with IDA. Hemoglobin, erythrocyte indices (mean erythrocyte volume and red blood cell distribution width), serum levels of iron, transferrin and ferritin, platelet aggregation tests (with ADP, collagen, and ristocetin), PFA-100 closure time, and CD62P expression were evaluated in fasting blood samples of 22 children with IDA and 20 children without anemia. CD62P expression was detected by flow cytometry in normal and 5 μmol/l ADP-activated platelets. Mean closure times were longer in the patient group than control. In platelet aggregation tests, mean values of maximum aggregation times by ristocetin, ADP, and collagen were also more prolonged in patient group. Ristocetin-induced maximum aggregation rates (amplitude) were significantly higher in patients. However, ADP and collagen induction did not produce the same effect. CD62P expressions were significantly higher on activated platelets of the patient group, although they were similar in both groups before activation by ADP. These findings suggest that platelet aggregation and adhesion have been delayed in children with IDA; however, platelet function abnormalities are not associated with CD62P expression on platelet surface.

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Section: Discussioncontrasting

confidence: 48%

Section: Discussionmentioning

confidence: 99%

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Platelet function alterations and their relation to P-selectin (CD62P) expression in children with iron deficiency anemia

Yıldırım¹,

Orhan²,

Büyükavcı³

2011

Blood Coagulation &Amp; Fibrinolysis

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“…In fact, patients with iron deficiency anemia who have no thrombocytosis can also be complicated by disturbance of retinochoroidal circulation. In addition, the functions of platelets such as aggregation activity can be altered in patients with iron deficiency anemia (13)(14)(15)(16). In the present case, almost normal prothrombin time (12.6 seconds) and activated partial thromboplastin time (26.2 seconds) were demonstrated at the time of diagnosis, suggesting that deregulation of the coagulation-fibrinolysis system was not mainly involved in the disturbance of retinochoroidal circulation.…”

Section: Discussionmentioning

confidence: 48%

Iron Deficiency Anemia with Marked Thrombocytosis Complicated by Central Retinal Vein Occlusion

et al. 2005

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We report a case of severe iron deficiency anemia with marked thrombocytosis that was complicated by central retinal vein occlusion. Platelet count was over one million per microliter and an increased number of megakaryocytes was observed in the bone marrow at the time of diagnosis of iron deficiency anemia, features that resemble those of essential thrombocythemia. However, the platelet count rapidly declined with the administration of ferrous fumarate. Accordingly, central retinal vein occlusion was improved and has not recurred. In this case, significant thrombocytosis caused by iron deficiency anemia may have been involved in the development of central retinal vein occlusion.

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“…All defective platelet aggregation responses were reversed by iron supplementation therapy and therefore it was advised that care should be taken when using antiaggregant agents in IDA. Çalışkan et al [12] evaluated platelet functions using impedance and optic method in 42 children with IDA during and after iron therapy. Decrease in collagen-induced platelet aggregation by the 2 methods and ADP-induced platelet aggregation by the whole-blood method were normalized after therapy.…”

Section: Discussionmentioning

confidence: 99%

Effect of Iron Therapy on Platelet Function among Iron-Deficient Women with Unexplained Menorrhagia

Akay

Akin²,

Mutlu³

et al. 2007

Pathophysiol Haemos Thromb

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This study was performed to evaluate the effect of iron therapy on platelet function among women with unexplained menorrhagia in order to better understand possible interactions between iron deficiency anemia and platelet behavior and menorrhagia. Platelet aggregation and adenosine triphosphate (ATP) release induced by 5.0 mM adenosine diphosphate (ADP), 0.5 mM arachidonic acid (AA), 1.0 mg/ml ristocetin and 2 μg/ml collagen were studied by whole-blood platelet lumi-aggregometer in 50 menorrhagic women before and after oral iron therapy and in 22 women of the control group. There was a significant increase in AA- induced platelet aggregation (p < 0.05) and a decrease in ristocetin-induced platelet aggregation (p < 0.01) after treatment. Pre- and posttreatment platelet aggregation responses to ADP and collagen were not significantly different (p > 0.05). Pre- and posttreatment platelet secretion responses to all agonists disclosed no significant difference (p > 0.05). There was no significant difference between the study group after treatment and the control group in respect to platelet aggregation and ATP secretion values induced by all agonists (p > 0.05). We conclude that iron deficiency anemia in women causes AA-induced platelet dysfunction, which may give rise to increased menstrual blood loss and can be reversed by iron repletion.

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Diminished Platelet Aggregation in Patients with Iron Deficiency Anemia

Cited by 27 publications

References 11 publications

Platelet function alterations and their relation to P-selectin (CD62P) expression in children with iron deficiency anemia

Platelet function alterations and their relation to P-selectin (CD62P) expression in children with iron deficiency anemia

Iron Deficiency Anemia with Marked Thrombocytosis Complicated by Central Retinal Vein Occlusion

Effect of Iron Therapy on Platelet Function among Iron-Deficient Women with Unexplained Menorrhagia

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