4th Palermo Conference on INNOVATIVE THERAPIES FOR LYMPHOID MALIGNANCIES
Published online 8 October 2009
Haematologica, Vol 94, Issue 11, 1513-1519 doi:10.3324/haematol.2009.008938
Copyright © 2009 by Ferrata Storti Foundation
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Sickle Cell Disease

Circulating erythrocyte-derived microparticles are associated with coagulation activation in sickle cell disease

Eduard J. van Beers1,2, Marianne C.L. Schaap3, René J. Berckmans3, Rienk Nieuwland3, Augueste Sturk3, Frederiek F. van Doormaal4, Joost C.M. Meijers4,5, Bart J. Biemond1 on behalf of the CURAMA study group*

1 Department of Hematology, Academic Medical Center, University of Amsterdam, Amsterdam
2 Department of Internal Medicine, Slotervaart Hospital, Amsterdam
3 Department of Clinical Chemistry, Academic Medical Center, University of Amsterdam, Amsterdam
4 Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam
5 Department of Experimental Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

Correspondence: Bart J. Biemond, Department of Haematology, F4-224, Academic Medical Center PO box 22660, 1100 DD Amsterdam, The Netherlands. E-mail:b.j.biemond{at}amc.uva.nl

Background: Sickle cell disease is characterized by a hypercoagulable state as a result of multiple factors, including chronic hemolysis and circulating cell-derived microparticles. There is still no consensus on the cellular origin of such microparticles and the exact mechanism by which they may enhance coagulation activation in sickle cell disease.

Design and Methods: In the present study, we analyzed the origin of circulating microparticles and their procoagulant phenotype during painful crises and steady state in 25 consecutive patients with sickle cell disease.

Results: The majority of microparticles originated from platelets (GPIIIa,CD61) and erythrocytes (glycophorin A,CD235), and their numbers did not differ significantly between crisis and steady state. Erythrocyte-derived microparticles strongly correlated with plasma levels of markers of hemolysis, i.e. hemoglobin (r=–0.58, p<0.001) and lactate dehydrogenase (r=0.59, p<0.001), von Willebrand factor as a marker of platelet/endothelial activation (r=0.44, p<0.001), and D-dimer and prothrombin fragment F1+2 (r=0.52, p<0.001 and r=0.59, p<0.001, respectively) as markers of fibrinolysis and coagulation activation. Thrombin generation depended on the total number of microparticles (r=0.63, p<0.001). Anti-human factor XI inhibited thrombin generation by about 50% (p<0.001), whereas anti-human factor VII was ineffective (p>0.05). The extent of factor XI inhibition was associated with erythrocyte-derived microparticles (r=0.50, p=0.023).

Conclusions: We conclude that the procoagulant state in sickle cell disease is partially explained by the factor XI-dependent procoagulant properties of circulating erythrocyte-derived microparticles.

Key words: microparticles, sickle cell disease, coagulation activation, hemolysis.


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K. I. Ataga
Hypercoagulability and thrombotic complications in hemolytic anemias
Haematologica, November 1, 2009; 94(11): 1481 - 1484.
[Full Text] [PDF]