03435nas a2200421   4500008004100000022004200041245009200083210006900175250001000244260000800254300001200262490000700274520208500281653001902366653001002385653005302395653001902448653002902467653001102496653006002507653006002567653004402627653003102671653001102702653000902713653001602722653004002738653002402778653002802802653003202830653003902862100001502901700001102916700001402927700001002941700001402951856004802965       1999                        eng d  a0268-3369 (Print) 0268-3369 (Linking)00aA prospective study of G-CSF effects on hemostasis in allogeneic blood stem cell donors0 aprospective study of GCSF effects on hemostasis in allogeneic bl  a36329  cMay  a991 - 60 v233 aGranulocyte colony-stimulating factor (G-CSF) is used in healthy donors of peripheral blood stem cells (PBSC) for allogeneic transplantation. However, some data have recently suggested that G-CSF may induce a hypercoagulable state, prompting us to study prospectively 22 PBSC donors before and after G-CSF 5 microg/kg twice daily. We sought evidence for changes in the following parameters: platelet count, von Willebrand factor antigen (vWF:Ag) and activity (vWF activity), beta-thromboglobulin (beta-TG), platelet factor 4 (PF-4), platelet activation markers (GMP-140 and PAC-1), activated partial thromboplastin time (aPTT), prothrombin time (PT), coagulant factor VIII (FVIII:C), thrombin-antithrombin complex (TAT), prothrombin fragment 1+2 (F1+2), thrombomodulin (TM) and tissue plasminogen activator antigen (tPA:Ag) prior to G-CSF and immediately before leukapheresis. ADP-induced platelet aggregation studies were also performed. G-CSF administration produced only mild discomfort. We found a significant increase in vWF:Ag (from 0.99 +/- 0.32 U/ml to 1.83 +/- 0.69 U/ml; P < 0.001), in vWF activity (from 1.04 +/- 0.34 U/ml to 1.78 +/- 0.50 U/ml; P < 0.001) and in FVIII:C (from 1.12 +/- 0.37 U/ml to 1.73 +/- 0.57 U/ml; P < 0.001) after G-CSF. Of note, four donors with low baseline vWF had a two- to three-fold increase after receiving G-CSF. G-CSF had no impact on the platelet count, beta-TG, PF-4, GMP-140 or PAC-1. The final% of platelet aggregation decreased from 73 +/- 22% to 37 +/- 26% after G-CSF (P < 0.001). We found a significant decrease in aPTT after G-CSF (29.9 +/- 3.1 s to 28.3 +/- 3.3 s; P = 0.004), but the PT was unaffected. In addition, we also observed a significant increase in TAT, F1+2 and TM, but not in tPA:Ag. Our data suggest that G-CSF may possibly induce a hypercoagulable state by increasing levels of FVIII:C and thrombin generation. In contrast to this information, we found reduced platelet aggregation after G-CSF administration. The clinical implications of these findings remain unclear and larger studies are definitely required.10a*Tissue Donors10aAdult10aBlood Coagulation Disorders / chemically induced10aCohort Studies10aFactor VIII / metabolism10aFemale10aFilgrastim / administration & dosage / *adverse effects10aHematopoietic Stem Cell Mobilization / *adverse effects10aHematopoietic Stem Cell Transplantation10aHemostasis / *drug effects10aHumans10aMale10aMiddle Aged10aPlatelet Aggregation / drug effects10aProspective Studies10aThrombin / biosynthesis10aTransplantation, Homologous10avon Willebrand Factor / metabolism1 aLeBlanc, R1 aRoy, J1 aDemers, C1 aVu, L1 aCantin, G  uhttps://www.notifylibrary.org/reference/878