Regional Brain Glucose Metabolism and Its Prognostic Value in Pretreatment Extranodal Natural Killer/T-Cell Lymphoma Patients

Objective: To explore regional brain glucose metabolic abnormalities of pretreatment stage I/II extranodal natural killer/T-cell lymphoma (ENKTL) patients using positron emission tomography with 2-deoxy-2-[fluorine-18]fluoro-D-glucose integrated with computed tomography (F-18-FDG PET/CT) and assess its prognostic value. Methods: Sixty pretreatment stage I/II ENKTL patients were enrolled in this retrospective study and divided into survival (n = 45) and death (n = 15) groups according to their status at the end of follow-up. A control group consisted of 60 healthy subjects. Regional cerebral glucose metabolism was evaluated on a voxel-by-voxel basis using statistical parametric mapping (SPM8) under a certain significance level (P < 0. 001) and voxel threshold (K = 100 voxels). Results: Decreased metabolism was noted in patients, involving the bilateral prefrontal and orbitofrontal cortex, partial parietal and occipital cortex, cingulate gyms and cerebellum; the sensorimotor cortex was largely spared. Increased metabolism was observed in the bilateral putamen, amygdala, and parahippocampal gyms. Compared with the survival group, the death group had higher metabolism in the bilateral amygdala, putamen, left thalamus, uncus, and parahippocampal gyms. Only B symptoms were associated with the increased metabolism of basal ganglia and thalamus (BGT). Patients with high metabolic tumor volume, total lesion glycolysis (TLG) and BGT metabolism had a poor prognosis. TLG and maximum standardized uptake value (SUVmax) LBGT/SUVmaxRight cerebellum were associated with Eastern Cooperative Oncology Group (ECOG) and prognostic index of natural killer lymphoma and Epstein-Barr virus-DNA (PINKE) scores. In multivariate analysis, only ECOG was an independent prognostic factor of both progression-free survival (PFS) and overall survival (OS). PINKE was an independent prognostic factor of OS. Conclusion: Pretreatment stage I/II ENKTL patients exhibited abnormal regional cerebral glucose metabolism. Higher pretreatment glucose metabolism in BGT could predict a relatively poor prognosis but did not surpass the predictive values of ECOG and PINKE in stage I/II ENKTL patients.