Sugawara Y, Fisher S J, Zasadny K R, Kison P V, Baker L H, Wahl R L
Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor 48109-0028, USA.
J Clin Oncol. 1998 Jan;16(1):173-80. doi: 10.1200/JCO.1998.16.1.173.
To evaluate the effect of granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) on bone marrow glucose metabolism in rodents and in patients, as assessed by 2-[fluorine-18]-fluoro-2-deoxy-D-glucose (FDG) uptake measured directly or by positron-emission tomography (PET) scanning.
Groups of three rats received either daily saline, G-CSF, or GM-CSF injections for 7 days. After treatment, FDG was injected and F-18 activities in tissues measured 1 hour later. Twenty-two breast cancer patients treated with multiagent chemotherapy were sequentially studied with PET. Eleven patients received G-CSF therapy as an adjunct to chemotherapy, while 11 received chemotherapy only. The standardized uptake value-lean (SUL) of bone marrow FDG uptake was measured and compared.
In rats, bone marrow F-18 activity was significantly higher in both CSF groups than in the saline group (G-CSF, 0.44 +/- 0.08; GM-CSF, 0.33 +/- 0.02; saline, 0.18 +/- 0.02% injected dose [ID]/g x kg; P < .05), but the other normal tissues had comparable biodistributions to controls. In breast cancer patients, the FDG uptake of bone marrow did not change with chemotherapy alone; however, marrow uptake was increased after treatment with G-CSF. The dose of G-CSF and duration of treatment were correlated with the extent of increase in FDG uptake. The SUL of bone marrow was as follows: baseline, 1.56 +/- 0.23; after one cycle, 3.13 +/- 1.40 (P < .01); after two cycles, 2.22 +/- 0.85 (P < .05); and after three cycles, 2.14 +/- 0.79 (P < .05), respectively. Although the FDG uptake of bone marrow declined after G-CSF treatment was completed, it was higher than the baseline level for up to 4 weeks postcompletion of G-CSF and the elevated marrow FDG uptake was sustained longer than the period of blood neutrophil count elevation.
Substantial increases in bone marrow FDG uptake are rapidly induced by CSF treatments and should not be misinterpreted as diffuse bone marrow metastases.
通过直接测量2-[氟-18]-氟-2-脱氧-D-葡萄糖（FDG）摄取或正电子发射断层扫描（PET）来评估粒细胞集落刺激因子（G-CSF）和粒细胞巨噬细胞集落刺激因子（GM-CSF）对啮齿动物和患者骨髓葡萄糖代谢的影响。
将三只大鼠分为一组，连续7天每日分别注射生理盐水、G-CSF或GM-CSF。治疗后，注射FDG，并在1小时后测量组织中的F-18活性。对22例接受多药化疗的乳腺癌患者进行PET序贯研究。11例患者接受G-CSF作为化疗辅助治疗，11例仅接受化疗。测量并比较骨髓FDG摄取的标准化摄取值-去脂（SUL）。
在大鼠中，两个集落刺激因子组的骨髓F-18活性均显著高于生理盐水组（G-CSF组为0.44±0.08；GM-CSF组为0.33±0.02；生理盐水组为0.18±0.02%注射剂量[ID]/g×kg；P<.05），但其他正常组织的生物分布与对照组相当。在乳腺癌患者中，单独化疗时骨髓FDG摄取无变化；然而，G-CSF治疗后骨髓摄取增加。G-CSF剂量和治疗持续时间与FDG摄取增加程度相关。骨髓的SUL如下：基线时为1.56±0.23；一个周期后为3.13±1.40（P<.01）；两个周期后为2.22±0.85（P<.05）；三个周期后为2.14±0.79（P<.05）。虽然G-CSF治疗完成后骨髓FDG摄取下降，但在G-CSF完成后长达4周内仍高于基线水平，且骨髓FDG摄取升高持续的时间长于血中性粒细胞计数升高的时间。
集落刺激因子治疗可迅速引起骨髓FDG摄取显著增加，不应将其误解为弥漫性骨髓转移。
