Summary:Granulocyte 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 g/kg twice daily. We sought evidence for changes in the following parameters: platelet count, von Willebrand factor antigen (vWF:Ag) and activity (vWF activity), -thromboglobulin (-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 Ͻ 0.001), in vWF activity (from 1.04 ؎ 0.34 U/ml to 1.78 ؎ 0.50 U/ml; P Ͻ 0.001) and in FVIII:C (from 1.12 ؎ 0.37 U/ml to 1.73 ؎ 0.57 U/ml; P Ͻ 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, -TG, PF-4, GMP-140 or PAC-1. The final% of platelet aggregation decreased from 73 ؎ 22% to 37 ؎ 26% after G-CSF (P Ͻ 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.
Background
The purpose of our studies was to determine if fecal blood loss can provide a quantitative measure of bleeding at platelet counts of 20 000/μL or less in patients with hypoproliferative thrombocytopenia and to document the effects of different prophylactic platelet transfusion triggers on fecal blood loss.
Methods and Materials
Patients had an aliquot of their autologous red blood cells (RBCs) labeled with 51Cr. Following reinjection of their radiolabeled RBCs, all feces and a daily blood sample were collected to determine fecal blood loss per day. Three different studies were performed in patients with thrombocytopenia: The first was in patients with thrombocytopenia with aplastic anemia who were not receiving platelet transfusions, and the other two trials involved thrombocytopenic patients with cancer who were receiving prophylactic platelet transfusions at platelet transfusion triggers of 5000/μL, 10 000/μL, or 20 000/μL.
Results
In patients with thrombocytopenia not receiving platelet transfusions, fecal blood loss does not increase substantially until platelet counts are 5000/μL or less. When platelet transfusions are given prophylactically to patients with cancer with chemotherapy‐induced thrombocytopenia at platelet counts of 5000/μL or less, fecal blood loss and red cell transfusion requirements are the same as those for patients transfused prophylactically at higher transfusion triggers of 10 000 platelets/μL or 20 000 platelets/μL. However, the total number of platelet transfusions needed increases significantly, and the duration of the patient's thrombocytopenia tends to be longer at the higher platelet transfusion thresholds.
Conclusion
A prophylactic platelet transfusion threshold of 5000/μL or greater is sufficient to maintain hemostasis in patients with thrombocytopenia.
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