SERUM LEVELS OF GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR AND GRANULOCYTE-COLONY-STIMULATING FACTOR IN TREATED PATIENTS WITH CHRONICMYELOGENOUS LEUKEMIA IN CHRONIC PHASE

Citation
E. Balleari et al., SERUM LEVELS OF GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR AND GRANULOCYTE-COLONY-STIMULATING FACTOR IN TREATED PATIENTS WITH CHRONICMYELOGENOUS LEUKEMIA IN CHRONIC PHASE, Haematologica, 79(1), 1994, pp. 7-12
Citations number
32
Categorie Soggetti
Hematology
Journal title
ISSN journal
03906078
Volume
79
Issue
1
Year of publication
1994
Pages
7 - 12
Database
ISI
SICI code
0390-6078(1994)79:1<7:SLOGCF>2.0.ZU;2-Q
Abstract
Background. Despite the fact that granulocyte-macrophage colony-stimul ating factor (GMCSF) and granulocyte colony-stimulating factor (G-CSF) are increasingly used in clinical practice, little is known of their endogenous production, especially in myeloproliferative disorders such as chronic myelogenous leukemia (CML). Methods. In order to define se rum levels of GM-CSF and G-CSF in subjects affected by CML, the sera o f 17 patients with CML in chronic phase treated either with hydroxyure a or interferon-alpha were tested by specific enzyme immunoassays. Fif teen age- and sex-matched healthy volunteers were used as normal contr ols. Results. Eight out of the 17 patients (44%) with CML showed detec table (> 3 pg/mL) serum levels of GM-CSF (range 3.9-55 pg/mL). Detecta ble levels (> 50 pg/mL) of G-CSF were observed in 9 of these patients (52%) (range 150-2,830 pg/mL). On the contrary, among the normal contr ols only one had detectable GM-CSF concentrations, and none had detect able G-CSF concentrations. The highest concentrations of both GM-CSF a nd G-CSF were seen in patients with the highest white blood cell count s, although a linear correlation between the levels of these growth fa ctors and the number of circulating leukocytes was not demonstrated. C onclusions. Our data indicate that significant amounts of both endogen ous GM-CSF and G-CSF are detectable in the serum of a substantial perc entage of patients with CML in chronic phase. The pathophysiological m eaning of this finding remains to be determined.