Effect of corticosteroids on <tex>$^{18}F-FDG$</tex> uptake in tumor lesions after chemotherapyEffect of corticosteroids on <tex>$^{18}F-FDG$</tex> uptake in tumor lesions after chemotherapy
Faculty of Medicine and Health Sciences
Publication type
New York,
Human medicine
Source (journal)
The Journal of nuclear medicine. - New York
48(2007):3, p. 390-397
Target language
English (eng)
To be a reliable predictor of response, 18F-FDG uptake should reflect changes in the amount of viable tumor cells. However, 18F-FDG also accumulates in inflammatory cells. Shortly after treatment, the influx of inflammatory cells in the tumor can therefore interfere with early response evaluation. The aim of this study was to investigate whether this inflammation is suppressed by the administration of corticosteroids and, in turn, can improve the correlation of 18F-FDG uptake with tumor cell kill. Methods: Severe combined immunodeficiency mice were inoculated subcutaneously with Daudi cells. When the tumor measured 15 mm, mice were divided in 2 groups treated with 1 single dose of cyclophosphamide, 125 mg/kg (group A) or cyclophosphamide followed by hydrocortisone (0.2 mg/d) for 5 d (group B). The change in 18F-FDG uptake was evaluated with small-animal PET (5 mice/group) on D+6, D+9, D+13, and D+16 (days after treatment). At each time point, 4 mice per group were sacrificed for quantification of the different tumor cell fractions by flow cytometry and histopathology. Changes in 18F-FDG uptake were correlated with inflammation and viable tumor cells. Results: Cyclophosphamide administration resulted in a steady reduction in viable cell fraction until D+9 (reduction from baseline, −64%). The viable cell fraction increased again on D+13. A transient influx of inflammatory cells was seen from D+6 to D+13 (peak on D+9, 24% of total cell fraction). After hydrocortisone administration, a similar reduction in the viable cell fraction was seen. The inflammatory response was less pronounced but developed with earlier kinetics (peak on D+6 [15% of total cell fraction], almost resolved on D+9) and consisted primarily of granulocytes instead of mononuclear cells in the absence of corticosteroids. In both groups, a significant reduction in 18F-FDG uptake was seen until D+6. On D+9, a transient increase in 18F-FDG uptake was seen in group A, whereas a further decrease was observed in group B. Conclusion: After corticosteroid administration, the contribution of inflammatory cells to the 18F-FDG uptake was less important than that in mice treated with chemotherapy alone. The earlier, but weaker, inflammatory response after corticosteroid administration consists primarily of granulocytes instead of mononuclear cells.