title: Clinical significance of circulating blood and endothelial cell microparticles in sickle-cell disease.
abstract: Increased thrombocyte activation leads to a higher likelihood of coagulation in sickle-cell disease. On the other hand, chronic inflammation and endothelial cell activation promote vaso-occlusion. The effect of circulating microparticles derived from erythrocytes, monocytes, thrombocytes, and endothelial cells on the vaso-occlusive process is unclear. This study aims to analyze the relationship between sickle-cell disease and miscellaneous organ complications by defining the circulating microparticles during the steady-state and painful crisis periods in 45 patients with sickle-cell disease. Microparticle analysis was conducted using an eight-parameter flow cytometric method, using CD61 PERCP, CD142PE, CD106 FITC, CD14 APC-H7, CD235a FITC, and Annexin-V APC monoclonal antibodies. Microparticle levels of sickle-cell patients were found to be significantly higher during both painful crisis and steady-state situations compared with the control group (for all, p < 0.001). Among these microparticles, levels of erythrocyte microparticles (eMPs) were significantly higher during crisis than in the steady-state period (eMP steady state vs. painful crisis: 7.59 ± 12.24 vs. 7.59 ± 12.24, respectively; p < 0.01). Microparticles, including eMPs, were not affected by hydroxyurea treatment. Their level did not reflect the high frequency of crisis (>3 times/year). Thrombocyte microparticle levels were found to be higher in patients with nephropathia than in those without (48.05 ± 40.23 vs. 7.67 ± 6.75, respectively; p < 0.049). Circulating microparticles seem to be involved in the pathogenesis of sickle-cell disease. eMPs may help with the management of crisis. Thrombocyte microparticles might predict renal damage induced by vaso-occlusion.
authors.affiliation: Department of Hematology, University of Baskent, Ankara, Turkey, drmkasar@hotmail.com.
authors.forename: Mutlu
authors.initials: M
authors.lastname: Kasar
authors.forename: Can
authors.initials: C
authors.lastname: Boğa
authors.forename: Mahmut
authors.initials: M
authors.lastname: Yeral
authors.forename: Suheyl
authors.initials: S
authors.lastname: Asma
authors.forename: Ilknur
authors.initials: I
authors.lastname: Kozanoglu
authors.forename: Hakan
authors.initials: H
authors.lastname: Ozdogu
mesh_terms: D000293:Adolescent; D000328:Adult; D000755:Anemia, Sickle Cell / Q000097:blood* / Q000188:drug therapy / Q000473:pathology; D000943:Antigens, Differentiation / Q000097:blood*; D000986:Antisickling Agents / Q000008:administration & dosage; D001792:Blood Platelets / Q000378:metabolism / Q000473:pathology; D055252:Cell-Derived Microparticles / Q000378:metabolism* / Q000473:pathology; D003430:Cross-Sectional Studies; D042783:Endothelial Cells / Q000378:metabolism* / Q000473:pathology; D004912:Erythrocytes / Q000378:metabolism / Q000473:pathology; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D006918:Hydroxyurea / Q000008:administration & dosage; D008297:Male; D008875:Middle Aged; D015539:Platelet Activation / Q000187:drug effects; D011446:Prospective Studies
chemical_list: D000943:Antigens, Differentiation; D000986:Antisickling Agents; D006918:Hydroxyurea