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NTIS 바로가기Cytokines, cellular & molecular therapy, v.6 no.3, 2000년, pp.149 - 154
Fukuda, Akira (First Department of Internal Medicine, Oska Medical College, Japan) , Kobayashi, Hiroyuki (First Department of Internal Medicine, Oska Medical College, Japan) , Teramura, Kazuhisa (First Department of Internal Medicine, Oska Medical College, Japan) , Yoshimoto, Satomine (First Department of Internal Medicine, Oska Medical College, Japan) , Ohsawa, Nakaaki (Aino Institute for Aging Research, Osaka, Japan)
Granulocytopenia is commonly observed in interferon- f (IFN- f ) therapy. Granulocyte colony-stimulating factor (G-CSF) has been identified as a primary cytokine that regulates neutrophil production, but the kinetics of G-CSF in IFN- f -induced granulocytopenia remains unclear. We investigated the effects of IFN- f on serum G-CSF levels and peripheral neutrophil counts (NC) in 15 chronic hepatitis C patients treated with standard-dose (10 MU) recombinant IFN- f for 24 weeks by using a chemlluminescent enzyme immunoassay for G-CSF. The time course of change after a single IFN- f injection showed that mean serum G-CSF levels and NC increased significantly compared with pretreatment values ( p < 0.05 ), and were statistically correlated ( r = 0.914 , p = 0.0015 ). On repeating IFN- f administration, this change gradually became unclear, and granulocytopenia occurred, accompanied by a significant increase in serum G-CSF ( p < 0.01 ). Both values reached a plateau within 2 weeks after starting treatment, and recovered rapidly after the cessation of therapy. Although continuous administration of IFN- f caused a time-dependent granulocytopenia, our results suggest that a single injection of IFN- f would be a potent inducer of G-CSF and NC in vivo as a short-term effect and that there would be negative-feedback regulation between them during long-term IFN- f therapy.
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