Objective: In poorly differentiated thyroid cancer originating from thyroid follicular cells, the ability to concentrate iodine is lost. This makes recurrence undetectable by (131)I whole-body scan. In this situation, other radiopharmaceuticals, such as (18)F-fluorodeoxyglucose ((18)F-FDG) and technetium-99m-methoxyisobutylisonitrile ((99m)Tc-MIBI), are used to evaluate recurrence or metastasis. Some reports suggest that (18)F-FDG uptake is increased by thyroid-stimulating hormone (TSH) stimulation. This study aimed to determine the influence of TSH on (18)F-FDG and (99m)Tc-MIBI uptake in human poorly differentiated thyroid cancer cells in vitro.
Materials and methods: The cells were stimulated with 1000 muU/ml of recombinant human thyroid-stimulating hormone (rhTSH) for 1 day, 3 days, and 5 days. Each cell was incubated with 0.5 MBq/ml-1 MBq/ml of (18)F-FDG or 0.5 MBq/ml-1 MBq/ml of (99m)Tc-MIBI for 1 h at 37 degrees C. The uptake of each radiopharmaceutical in the cells was quantified as a percent of whole radioactivity per total viable cell number. The quantification of glucose transporter 1, 2, 3 and 4 mRNA expression was measured using RT-PCR.
Results: TSH stimulation increased (18)F-FDG uptake in a time-dependent manner. Following 5 days of rhTSH stimulation, (18)F-FDG uptake was approximately 2.2 times that of the control. The increase in (18)F-FDG uptake following rhTSH stimulation was correlated to the increase in GLUT4 mRNA level. The GLUT1 mRNA level was unchanged. An increased uptake of (99m)Tc-MIBI was observed with a pattern similar to that of (18)F-FDG. The (99m)Tc-MIBI uptake was approximately 1.5 times that of the control 5 days later.
Conclusions: These results suggest that TSH stimulates (18)F-FDG and (99m)Tc-MIBI uptake in poorly differentiated papillary thyroid cancer, and therefore (18)F-FDG-PET or (99m)Tc-MIBI scans under TSH stimulation may be more accurate than under suppression.