Mirimostim (macrophage colony-stimulating factor; M-CSF) improves chemotherapy-induced impaired natural killer cell activity, Th1/Th2 balance, and granulocyte function.
The purpose of this study was to clarify the effects of mirimostim (macrophage colony-stimulating factor; M-CSF) on immunological functions after chemotherapy. The percentage of natural killer (NK) cells in peripheral blood mononuclear cells (PBMCs), NK cell activity, T-helper cell 1/T-helper cell 2 (Th1/Th2) ratio, and superoxide anion production by granulocytes (granulocyte function) were measured as immunological parameters before and after chemotherapy in 44 patients with primary ovarian cancer who received at least three consecutive courses of postoperative chemotherapy. Patients were observed during the first course of chemotherapy, and 39 patients who presented grade III or IV neutropenia were entered into this study and randomly allocated to an M-CSF-administered group (group 1; 19 patients) and a non-M-CSF-administered group (group 2; 20 patients) for the second course. For the third course, a crossover trial was conducted. In the observation period, chemotherapy significantly impaired the immunological parameters. In particular, those parameters were significantly decreased at day 14 compared to the level before chemotherapy. The values of the parameters of group 1 were significantly higher than those of group 2. In the course of chemotherapy during which M-CSF was administered, 19 of the 39 patients presented grade IV neutropenia, and received granulocyte colony-stimulating factor (G-CSF) between days 7 and 14. We compared the changes of those immunological parameters in the M-CSF alone group and the M-CSF + G-CSF group, and found that the concomitant use of G-CSF did not further improve the parameters. These results indicate that chemotherapy markedly impaired the immunological functions, and that the administration of M-CSF significantly improved the impaired immunological functions.
Hidaka
Takao
T
Department of Obstetrics and Gynecology, Toyama Medical and Pharmaceutical University, Sugitani, Toyoma-shi, Toyama 930-0194, Japan. s30saito@ms.toyama-mpu.ac.jp
Akada
Shinobu
S
Teranishi
Akiko
A
Morikawa
Hajime
H
Sato
Shinji
S
Yoshida
Yuji
Y
Yajima
Akira
A
Yaegashi
Nobuo
N
Okamura
Kunihiro
K
Saito
Shigeru
S
D000293:Adolescent; D000328:Adult; D000368:Aged; D018592:Cross-Over Studies; D004359:Drug Therapy, Combination; D005260:Female; D005334:Fever / Q000139:chemically induced / Q000276:immunology / Q000517:prevention & control; D016179:Granulocyte Colony-Stimulating Factor / Q000627:therapeutic use; D006098:Granulocytes / Q000502:physiology*; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology*; D007958:Leukocyte Count; D016173:Macrophage Colony-Stimulating Factor / Q000627:therapeutic use*; D008875:Middle Aged; D009367:Neoplasm Staging; D009503:Neutropenia / Q000139:chemically induced / Q000276:immunology / Q000517:prevention & control; D010051:Ovarian Neoplasms / Q000188:drug therapy* / Q000276:immunology; D013481:Superoxides / Q000378:metabolism; D018417:Th1 Cells / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*
D013481:Superoxides; D016179:Granulocyte Colony-Stimulating Factor; D016173:Macrophage Colony-Stimulating Factor