Thromb Haemost 2008; 100(05): 864-870
DOI: 10.1160/TH08-03-0157
Platelets and Blood Cells
Schattauer GmbH

Increased platelet adhesion under flow conditions is induced by both thalassemic platelets and red blood cells

Neta Goldschmidt*
1   Department of Haematology and Coagulation Unit, Hadassah Hebrew University Medical Center, Jerusalem, Israel
,
Galia Spectre*
1   Department of Haematology and Coagulation Unit, Hadassah Hebrew University Medical Center, Jerusalem, Israel
,
Alexander Brill
1   Department of Haematology and Coagulation Unit, Hadassah Hebrew University Medical Center, Jerusalem, Israel
,
Orly Zelig
1   Department of Haematology and Coagulation Unit, Hadassah Hebrew University Medical Center, Jerusalem, Israel
,
Ada Goldfarb
1   Department of Haematology and Coagulation Unit, Hadassah Hebrew University Medical Center, Jerusalem, Israel
,
Eliezer Rachmilewitz
2   Department of Haematology, Edit Wolfson Medical Center, Holon, Israel
,
David Varon
1   Department of Haematology and Coagulation Unit, Hadassah Hebrew University Medical Center, Jerusalem, Israel
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Publikationsverlauf

Received 11. März 2008

Accepted after major revision 10. August 2008

Publikationsdatum:
22. November 2017 (online)

Summary

Thromboembolic complications are not uncommon in thalassemia. Previous studies suggest increased platelet aggregation and a potential role of pathological changes in the red blood cell (RBC) lipid membrane, induced by oxidative stress. In the present study,platelet adhesion and the effect of thalassemic RBC on platelet adhesion under flow conditions were evaluated, using the Cone and Plate (let)Analyzer(CPA).Twenty-two β-thalasse-mia patients and 22 blood type-matched healthy controls were studied. An increased platelet adhesion (% surface coverage, SC),was observed in patients as compared to controls (p<0.05). When platelet count and haematocrit were normalized by auto-logous reconstitution, a significant increase in platelet aggregation (average size,AS) was observed (p<0.05). Increased platelet adhesion (SC and AS), was demonstrated in six patients with a history of thrombosis as compared to 16 patients without any history of thrombosis (p≤0.007) and in 17 splenectomized patients as compared to five non-splenectomized patients (p=0.003). In reconstitution studies, thalassemic RBC mixed with normal platelet-rich plasma significantly increased platelet adhesion compared to normal RBC (SC p<0.03, AS p<0.02). Thalassemic platelets reconstituted with normal RBC, had increased aggregation (AS, p<0.004) in comparison with normal platelets.The results indicate that increased platelet adhesion in β-thalassemia is induced by both platelets and RBC. Increased platelet adhesion correlated with clinical thrombotic events and thus may suggest a mechanism of thrombosis in thalassemic patients.The potential application of the CPA in identifying thalassemic patients with high risk for thrombosis should be studied prospectively in a larger cohort of patients.

* These authors contributed equally to the paper.


 
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