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rHuG‐CSF Increases the Platelet‐Neutrophil Complex Formation and Neutrophil Adhesion Molecule Expression in Volunteer Granulocyte and Stem Cell Apheresis Donors
Author(s) -
Karadogan Cavidan,
Karadogan Ihsan,
Bilgin Aynur Ugur,
Undar Levent
Publication year - 2006
Publication title -
therapeutic apheresis and dialysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.415
H-Index - 53
eISSN - 1744-9987
pISSN - 1744-9979
DOI - 10.1111/j.1744-9987.2006.00361.x
Subject(s) - medicine , apheresis , granulocyte , platelet , cell adhesion molecule , granulocyte colony stimulating factor , adhesion , neutrophil extracellular traps , immunology , platelet activation , volunteer , soluble cell adhesion molecules , cell adhesion , inflammation , chemistry , organic chemistry , agronomy , biology , chemotherapy
Several reports have shown that granulocyte colony‐stimulating factor (G‐CSF) administration induces a transient, mild hypercoagulable state, which might predispose certain donors to thrombotic complications. In the present study, changes in the expression of neutrophil adhesion molecules (CD11b/CD18, CD62L) and platelet‐neutrophil complex formation following rHuG‐CSF administration were investigated in normal granulocyte and stem cell donors. For granulocyte apheresis ( N = 10), rHuG‐CSF (5 µg/kg) was given subcutaneously every 12 h three times and apheresis was carried out two hours after the last dose. For stem cell apheresis ( N = 8), rHuG‐CSF (10 µg/kg/day) was given subcutaneously for 5 days and apheresis was carried out when peripheral CD34+ cell counts exceeded 20 cell/µL. Expression of neutrophil adhesion molecules (CD11b/CD18, CD62L) and platelet‐neutrophil complex formation following rHuG‐CSF administration were investigated in donors by a flow cytometric method. A significant increase in neutrophil counts ( P < 0.001), and decreases in platelet counts ( P < 0.01) and hemoglobin levels ( P < 0.01) occurred following G‐CSF administration. The expression of CD11b/CD18 significantly increased ( P < 0.001) over pretreatment values with G‐CSF administration and returned to baseline 1 week after stopping the drug. In contrast, CD62L expression was decreased ( P < 0.01) with G‐CSF and returned to normal after cessation of the drug. rHuG‐CSF caused more than a two‐fold increase (from 0.3 to 7.0 × 10 9 /L) in circulating platelet‐neutrophil complexes ( P < 0.01), which returned to normal after 1 week. Although clinical significance of these laboratory changes is not clear, the occurrence of neutrophil activation and increased platelet‐neutrophil complex formation might predispose certain donors or patients to thrombotic complications following G‐CSF administration.