Background: At the myeloid progenitor cell level, G-CSF stimulates the growth of neutrophil granulocyte precursors. To prove its clinical usefullness, we planned to administer rhG-CSF to prevent or overcome myclosuppression after chemotherapy.
Methods: rhG-CSF was started 1 day after chemotherapy in preventive trial and at nadir of myelosuppression in therapeutic trial(75μg/day subcutaneously for 10 days).
Results: All the enrolled 36 patients were evaluable, which consisted of 11 with stomach cancer, 7 with malignant lymphoma, 6 with lung cancer, 4 with osteosarcoma, 2 with breast cancer, ovarian cencer, glioblastoma multiforme, and 1 with
choriocarcinoma, neuroblastoma, respectively. The male to female was 1 : 1, with median age of 50(13~73). The commonly used chemotherapeutic agents were VP-16, cisplatin, adriamycin. Twenty five patients were treated with rhG-CSF to prevent
chemotherapy
induced neutropenia: 14 of these patients received rhG-CSF with observation period(controlled trial group), 11 patients without(uncontrolled trial group). rhG-CSF was administered to 11 patients for treatment of chemotherapy induced severe
neutropenia
and infection(rescue therapy group). The mean nadir of WBC counts during the observation period and treatment period were 928.6±385.5/㎣ and 2810.7±1937.7/㎣, respectively(p=0.004) in conrolled trial group, and 1760.0±1004.0/㎣ in uncontrolled
trial
group. In controlled trial group, the mean duration of WBC count less than 4,000/㎣ were 9.9±5.5days in the observation period and 2.3±1.6 days in the treatment period(p<0.001), 4.5±2.6 days in uncontrolled trial group. The recovery time of
WBC
from
nadir to >3,000/㎣ was 5.4±4.2 days in rescue therapy group. In controlled trial group, the incidence of infection was decreased in rhG-CSF treated period. The G-CSF related toxicities were mild bone pain, fever, general weakness, and myalgia.
Conclusion: This study proved the effects of rhG-CSF to prevent or overcome the chemotherapy induced myclosuppression in cancer patients.
|