Acute effects of stereotactic radiosurgery on the kinetics of glucose metabolism in metastatic brain tumors: FDG PET study

Citation
T. Yamamoto et al., Acute effects of stereotactic radiosurgery on the kinetics of glucose metabolism in metastatic brain tumors: FDG PET study, ANN NUCL M, 15(2), 2001, pp. 103-109
Citations number
22
Categorie Soggetti
Radiology ,Nuclear Medicine & Imaging
Journal title
ANNALS OF NUCLEAR MEDICINE
ISSN journal
09147187 → ACNP
Volume
15
Issue
2
Year of publication
2001
Pages
103 - 109
Database
ISI
SICI code
0914-7187(200104)15:2<103:AEOSRO>2.0.ZU;2-F
Abstract
Hyperacute changes in the expression of glycolysis-associate gene products as well as FDG uptake in tumor cells after high-dose irradiation reflect re sponse of the cells to noxious intervention and may be a potential indicato r of the outcome of treatment. To understand acute effects on the kinetics of glucose metabolism of tumors in vivo after high-dose irradiation, we ana lyzed dynamic FDG PET data in patients with metastatic brain tumors receivi ng stereotactic radiosurgery. Materials and Methods: We studied 5 patients with metastatic brain tumors by means of dynamic FDG PET be fore and 4 hour s after stereotactic radiosurgery. Rate constants of glucose metabolism (K- 1* - k(3)*) were determined in a total of 13 tumors by a non-linear least s quares fitting method for dynamic PET and arterial blood sampling data. Rat e constants after radiosurgery were compared with those before radiosurgery . Changes in the rate constants induced by the therapy were also correlated with changes in tumor size evaluated by CT and/or MRI 6 months later. Resu lts: Four hours after radiosurgery, the phosphorylation rate indicated by k (3)* was significantly higher (0.080 +/- 0.058) than that before radiosurge ry (0.049 +/- 0.023) (p < 0.05, paired t test), but there was no significan t change in the membrane transport rates indicated by K-1* and k(2)*. Altho ugh increases in the net influx rate constant K* (= K-1*k(3)*/(K-2* + k(3)* )) were correlated with increases in k(3)*, K* after radiosurgery (0.027.0. 011) was not significantly different from that before the therapy (0.024 +/ - 0.012). The reduction in the tumor size was correlated with k(3)* after r adiosurgery. Conclusion: Acceleration of the phosphorylation process was de monstrated ill vivo in metastatic brain tumors as early as 4 hours after st ereotactic radiosurgery, as shown experimentally in vitro in a previous rep ort. The phenomenon may be a sensitive indicator of cell damage.