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Volume 37, Issue 9, Pages 1054-1059 (September 2009)


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Elevated endothelial progenitor cells during painful sickle cell crisis

Rachel T. van Beema, Erfan Nurbcd, Jaap Jan Zwagingaae, Precious P. Landburgdf, Eduard J. van Beersbcd, Ashley J. Duitsdf, Dees P. Brandjesbd, Ingrid Lommersea, Hetty C. de Boerg, C. Ellen van der Schoota, John-John B. Schnogd, Bart J. BiemondcdCorresponding Author Informationemail address, CURAMA Study Group

Received 5 March 2009; received in revised form 6 May 2009; accepted 9 June 2009. published online 18 June 2009.

Objective

Circulating endothelial progenitor cells (EPCs) counts were determined in patients with sickle cell disease (SCD) to elucidate their role in SCD-related ischemia-induced angiogenesis and reendothelialization.

Materials and Methods

Circulating EPC counts (KDR+/CD34+/Cd45dim cells) and their relation to serum levels of EPC mobilizing growth factors erythropoietin, vascular endothelial growth factor, and interleukin-8 were investigated in SCD patients during asymptomatic state (n=66) and painful crisis (n=36) and compared to healthy controls (n=13).

Results

EPC counts were comparable between controls (0; range, 0–1.1 cells/mL) and patients (0; range, 0–0 cells/mL) in asymptomatic state, but were significantly higher during painful crisis (41.7; range, 0–186 cells/mL; p<0.05). Also in a paired analysis of 12 patients who were included both during asymptomatic state and painful crisis, EPC counts increased significantly during painful crisis (from 0 [range, 0–0] to 26 [range, 0–149 cell/mL; p<0.05). EPC counts were not related to any of the measured growth factors.

Conclusion

The higher EPC counts during painful crisis might indicate a role for EPC mobilization in reendothelialization. As a relationship of EPCs with the established mobilizing growth factors, measured in this study was not observed, the mechanism of EPC mobilization in SCD remains to be elucidated.

a Department of Experimental Immunohematology, Sanquin Research and Landsteiner Laboratory, Amsterdam, The Netherlands

b Department of Internal Medicine, Slotervaart Hospital, Amsterdam, The Netherlands

c Department of Haematology, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands

d The CURAMA Study Group, The Netherlands

e Department of Immunohematology and Blood Transfusion, Leiden University Medical Centre, Leiden, The Netherlands

f Immunology Laboratory Department, Red Cross Blood Bank Foundation, Curaçao, The Netherlands Antilles

g Department of Nephrology, Leiden University Medical Centre, Leiden, The Netherlands

Corresponding Author InformationOffprint requests to: Bart J. Biemond, M.D., Ph.D., Department of Haematology, F4-224, Academic Medical Center, P.O. Box 22660, 1100 DD Amsterdam, The Netherlands

 Rachel T. van Beem and Erfan Nur contributed equally to this study.

PII: S0301-472X(09)00213-6

doi:10.1016/j.exphem.2009.06.003


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