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Issues in the in vivo measurement of glucose metabolism of human central nervous system tumors
Author(s) -
di Chiro Giovanni,
Brooks Rodney A.,
Patronas Nicholas J.,
Bairamian Dikran,
Kornblith Paul L.,
Smith Barry H.,
Mansi Luigi,
Barker John
Publication year - 1984
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410150727
Subject(s) - in vivo , backflow , positron emission tomography , fluorodeoxyglucose , nuclear medicine , central nervous system , glioma , deoxyglucose , chemistry , hexokinase , glycolysis , medicine , metabolism , endocrinology , biology , biochemistry , cancer research , mechanical engineering , microbiology and biotechnology , engineering , inlet
Over 150 cases of central nervous system tumors have been studied with positron emission tomography using fluorine‐18‐labeled fluorodeoxyglucose ( 18 FDG) as a tracer. From this material 100 consecutive cases of cerebral glioma have been reviewed and analyzed. The results show a strong correlation of tumor grade with glycolytic rate, with visual “hot spots” present in all high‐grade neoplasms and in only four low‐grade tumors. The quantitative accuracy is limited by three basic factors. First, the measurement of tissue uptake, as compared with the parent technique, autoradiography, is more difficult because detection must be done outside the body. Effects such as scattered radiation and self‐attenuation introduce errors unless properly corrected. A more serious problem when measuring small structures, such as a rim‐shaped high‐grade glioma, is the limited spatial resolution. The most advanced scanner, the Neuro‐PET, has a resolution of 6 to 7 mm. Second, corrections are needed for backflow, including free tracer at the time of the scan that will return to the blood and “trapped” tracer that will backflow because of the presence of phosphatase. These corrections are calculated from the blood activity using nominal rate constants for 18 FDG. Out study found no significant alteration in rate constants between normal and tumoral tissue. Finally, a lumped constant is needed to correct for kinetic differences between 18 FDG and glucose. If there is a change in the mechanism of either membrane transport or the hexokinase reaction, the lumped constant may change. However, measurements of actual glucose utilization in tissue culture lines from six patients support the 18 FDG results.