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Blood, Vol. 93 No. 8 (April 15), 1999:
pp. 2506-2514
Neutrophil Activation and Hemostatic Changes in Healthy Donors
Receiving Granulocyte Colony-Stimulating Factor
A. Falanga,
M. Marchetti,
V. Evangelista,
S. Manarini,
E. Oldani,
S. Giovanelli,
M. Galbusera,
C. Cerletti, and
T. Barbui
From the Hematology Division, Ospedali Riuniti, Bergamo, Italy; the
Istituto di Ricerche Farmacologiche Mario Negri Consorzio Mario Negri
Sud, S. Maria Imbaro, Italy; and NegriBergamo Laboratories, Bergamo,
Italy.
Granulocyte colony-stimulating factor (G-CSF) enhances neutrophil
functions in vitro and in vivo. It is known that neutrophil-derived products can alter the hemostatic balance. To understand whether polymorphonuclear leukocyte (PMN) activation, measured as PMN degranulation and phenotypical change, may be associated to hemostatic alterations in vivo, we have studied the effect of recombinant human
G-CSF (rHuG-CSF) administration on leukocyte parameters and hemostatic
variables in healthy donors of hematopoietic progenitor cells (HPCs).
Twenty-six consecutive healthy donors receiving 10 µg/kg/d rHuG-CSF
subcutaneously for 5 to 7 days to mobilize HPCs for allogeneic
transplants were included in the study. All of them responded to
rHuG-CSF with a significant white blood cell count increase. Blood
samples were drawn before therapy on days 2 and 5 and 1 week after
stopping rHuG-CSF treatment. The following parameters were evaluated:
(1) PMN activation parameters, ie, surface CD11b/CD18 antigen
expression, plasma elastase antigen levels and cellular elastase
activity; (2) plasma markers of endothelium activation, ie,
thrombomodulin (TM) and von Willebrand factor (vWF) antigens; (3)
plasma markers of blood coagulation activation, ie, F1+2, TAT
complex, D-dimer; and (4) mononuclear cell (MNC) procoagulant activity
(PCA) expression. The results show that, after starting rHuG-CSF, an in
vivo PMN activation occurred, as demonstrated by the significant
increment of surface CD11b/CD18 and plasma elastase antigen levels.
Moreover, PMN cellular elastase activity, which was significantly
increased at 1 day of treatment, returned to baseline at day 5 to 6, in
correspondence with the elastase antigen peak in the circulation. This
change was accompanied by a parallel significant increase in plasma
levels of the two endothelial and the three coagulation
markers. The PCA generated in vitro by unstimulated MNC
isolated from rHuG-CSF-treated subjects was not different from that of
control cells from untreated subjects. However, endotoxin-stimulated
MNC isolated from on-treatment individuals produced significantly more
PCA compared with both baseline and control samples. All of the
parameters were decreased or normal 1 week after stopping treatment.
These data show that rHuG-CSF induces PMN activation and transiently
affects some hemostatic variables in healthy HPC donor subjects. The
clinical significance of these findings remains to be established.
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