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Uptake of ¹⁸F-Fluorocholine, ¹⁸F-Fluoroethyl-L-Tyrosine, and ¹⁸F-FDG in Acute Cerebral Radiation Injury in the Rat: Implications for Separation of Radiation Necrosis from Tumor Recurrence

¹ PET Center, Division of Nuclear Medicine, University Hospital Zurich, Zurich, Switzerland
² Center for Radiopharmaceutical Science of ETH, PSI, and USZ, Paul Scherrer Institute, Villigen, und University Hospital Zurich, Zurich, Switzerland
³ Section of Diagnostic Imaging and Radio-Oncology, Veterinary Hospital, University Zurich, Zurich, Switzerland
⁴ Institute of Diagnostic Radiology, University Hospital Zurich, Zurich, Switzerland
⁵ Division of Radiation Medicine, Paul Scherrer Institute, Villigen, Switzerland
⁶ Institute of Neuropathology, Department of Pathology, University Hospital Zurich, Zurich, Switzerland
⁷ Department of Neurology, University Hospital Zurich, Zurich, Switzerland

Differentiation between posttherapy radiation necrosis and recurrent tumor in humans with brain tumor is still a difficult diagnostic task. The new PET tracers ¹⁸F-fluoro-ethyl-L-tyrosine (FET) and ¹⁸F-fluorocholine (N,N-dimethyl-N-¹⁸F-fluoromethyl-2-hydroxyethylammonium [FCH]) have shown promise for improving diagnostic accuracy. This study assessed uptake of these tracers in experimental radiation injury. Methods: In a first model, circumscribed lesions were induced in the cortex of 35 rats using proton irradiation of 150 or 250 Gy. After radiation injury developed, uptake of ¹⁸F-FET, ¹⁸F-FCH, and ¹⁸F-FDG was measured using autoradiography and correlated with histology and disruption of the blood-brain barrier as determined with Evans blue. In a second model, uptake of the tracers was assessed in acute cryolesions, which are characterized by the absence of inflammatory cells. Results: Mean ¹⁸F-FET, ¹⁸F-FCH, and ¹⁸F-FDG standardized uptake values in the most active part of the radiation lesion and the contralateral normal cortex (in parentheses) were 2.27 ± 0.46 (1.42 ± 0.23), 2.52 ± 0.42 (0.61 ± 0.12), and 6.21 ± 1.19 (4.35 ± 0.47). The degree of uptake of ¹⁸F-FCH and ¹⁸F-FDG correlated with the density of macrophages. In cryolesions, ¹⁸F-FET uptake was similar to that in radiation lesions, and ¹⁸F-FCH uptake was significantly reduced. Conclusion: Comparison of tracer accumulation in cryolesions and radiation injuries demonstrates that ¹⁸F-FET uptake is most likely due to a disruption of the blood-brain barrier alone, whereas ¹⁸F-FCH is additionally trapped by macrophages. Uptake of both tracers in the radiation injuries is generally lower than the published uptake in tumors, suggesting that ¹⁸F-FET and ¹⁸F-FCH are promising tracers for separating radiation necrosis from tumor recurrence. However, the comparability of our data with the literature is limited by factors such as different species and acquisition protocols and modalities. Thus, more studies are needed to settle this issue. Nevertheless, ¹⁸F-FCH and ¹⁸F-FET seem superior to ¹⁸F-FDG for this purpose.

Key Words: radiation necrosis • ¹⁸F-fluorocholine • ¹⁸F-fluoroethyl-L-tyrosine • ¹⁸F-FDG • autoradiography

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