Decreases Cerebral FDG Uptake in Association with High WBC Values and Low RBC Values

Abstract

PURPOSE: In most cases the SUV values in the tele-encephalon range in values around 10 to 12. In patients with Hematologic Malignancy we observed a high frequency of patients with low SUV values in the brain. Casual observation suggested that the phenomenon was associated with symptoms of infection. The goal is to find a biological correlate of low cerebral SUV values. METHOD AND MATERIALS: The data consist of a 50 PET/CT studies in 12 patients. Their median age was 49 and 9 were male. They were selected because one of their studies the cerebral SUV values seemed low and all the relevant data were available. In this study we looked at the peripheral WBC count and RBC count, and the Cerebral SUV values. RESULTS: The average WBC count was 5.34 k, the RBC was 3.3 million. SUV values were measured in frontal, central motor, visual cortex and the basal nuclei. The average SUV values were 5.14, 5.67, 7.51 and 5.63 respectively. The values in the different regions correlated strongly (>90%). In contradistinction the WBC and RBC values were not related (P=0.96), suggesting that the phenomenon was not a global marrow one. However, there was a significant correlation between the WBC and brain SUV values and the RBC and brain SUV values. For the WBC the relation was negative: SUV= -0.13 WBC + 6.00, with the regression coefficient F=4.30 (p<0.05). For the RBC, the relation was positive: SUV= 1.27 WBC + 0.98 with the regression coefficient F=8.36, (P<0.006). In individual patients an increase of the WBC value over 10 universally resulted in a significant drop of cerebral SUV. CONCLUSION: In a population of patients, treated and untreated low cerebral SUV values were associated with high WBC values. The finding did not seem associated with intrinsic bone marrow disease, since the effect was opposite to the effect of increase in RBC values. RBC affect is probably associated to oxygen transport and metabolism. We surmise that the finding is associated to clinical or subclinical infection or inflammation, but cannot conclude that the effect is direct or a co-association with an underlying mechanism. CLINICAL RELEVANCE/APPLICATION: Low cerebral FDG uptake is usually explained by degenerative brain disease (e.g. Alzheimer's) or anesthesia. Here it is shown caused by systemic disease with secondary repercussion on the brain.