Milan Grkovski1, Karem Gharzeddine2, Peter Sawan2, Heiko Schöder2,3, Laure Michaud2, Wolfgang A Weber2,3,4, John L Humm5. 1. Department of Medical Physics, Memorial Sloan Kettering Cancer Center, New York, New York grkovskm@mkscc.org. 2. Department of Radiology, Memorial Sloan Kettering Cancer Center, New York, New York. 3. Molecular Imaging and Therapy Service, Memorial Sloan Kettering Cancer Center, New York, New York; and. 4. University Hospital Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany. 5. Department of Medical Physics, Memorial Sloan Kettering Cancer Center, New York, New York.
Abstract
The aim of this study was to investigate the value of pharmacokinetic modeling for quantifying 11C-choline uptake in patients with recurrent prostate cancer. Methods: In total, 194 patients with clinically suspected recurrence of prostate cancer underwent 11C-choline dynamic PET over the pelvic region (0-8 min), followed by a 6-min static acquisition at about 25 min after injection. Regions of interest were drawn over sites of disease identified by a radiologist with experience in nuclear medicine. 11C-choline uptake and pharmacokinetics were evaluated by SUV, graphical analysis (Patlak plot; K i P), and 1- and 2-compartment pharmacokinetic models (K 1, K 1/k 2, k 3, k 4, and the macro parameter K i C). Twenty-four local recurrences, 65 metastatic lymph nodes, 19 osseous metastases, and 60 inflammatory lymph nodes were included in the analysis, which was subsequently repeated for regions of interest placed over the gluteus maximus muscle and adipose tissue as a control. Results: SUVmean and K i P were 3.60 ± 2.16 and 0.28 ± 0.22 min-1 in lesions, compared with 2.11 ± 1.33 and 0.15 ± 0.10 min-1 in muscle and 0.26 ± 0.07 and 0.02 ± 0.01 min-1 in adipose tissue. According to the Akaike information criterion, the 2-compartment irreversible model was most appropriate in 85% of lesions and resulted in a K 1 of 0.79 ± 0.98 min-1 (range, 0.11-7.17 min-1), a K 1/k 2 of 2.92 ± 3.52 (range, 0.31-20.00), a k 3 of 0.36 ± 0.30 min-1 (range, 0.00-1.00 min-1) and a K i C of 0.28 ± 0.22 min-1 (range, 0.00-1.33 min-1). The Spearman ρ between SUV and K i P, between SUV and K i C, and between K i P and K i C was 0.94, 0.91, and 0.97, respectively, and that between SUV and K 1, between SUV and K 1/k 2, and between SUV and k 3 was 0.70, 0.44, and 0.33, respectively. Malignant lymph nodes exhibited a higher SUV, K i P, and K i C than benign lymph nodes. Conclusion: Although 11C-choline pharmacokinetic modeling has potential to uncouple the contributions of different processes leading to intracellular entrapment of 11C-choline, the high correlation between SUV and both K i P and K i C supports the use of simpler SUV methods to evaluate changes in 11C-choline uptake and metabolism for treatment monitoring.
The aim of this study was to investigate the value of pharmacokinetic modeling for quantifying 11C-choline uptake in patients with recurrent prostate cancer. Methods: In total, 194 patients with clinically suspected recurrence of prostate cancer underwent 11C-choline dynamic PET over the pelvic region (0-8 min), followed by a 6-min static acquisition at about 25 min after injection. Regions of interest were drawn over sites of disease identified by a radiologist with experience in nuclear medicine. 11C-choline uptake and pharmacokinetics were evaluated by SUV, graphical analysis (Patlak plot; K i P), and 1- and 2-compartment pharmacokinetic models (K 1, K 1/k 2, k 3, k 4, and the macro parameter K i C). Twenty-four local recurrences, 65 metastatic lymph nodes, 19 osseous metastases, and 60 inflammatory lymph nodes were included in the analysis, which was subsequently repeated for regions of interest placed over the gluteus maximus muscle and adipose tissue as a control. Results: SUVmean and K i P were 3.60 ± 2.16 and 0.28 ± 0.22 min-1 in lesions, compared with 2.11 ± 1.33 and 0.15 ± 0.10 min-1 in muscle and 0.26 ± 0.07 and 0.02 ± 0.01 min-1 in adipose tissue. According to the Akaike information criterion, the 2-compartment irreversible model was most appropriate in 85% of lesions and resulted in a K 1 of 0.79 ± 0.98 min-1 (range, 0.11-7.17 min-1), a K 1/k 2 of 2.92 ± 3.52 (range, 0.31-20.00), a k 3 of 0.36 ± 0.30 min-1 (range, 0.00-1.00 min-1) and a K i C of 0.28 ± 0.22 min-1 (range, 0.00-1.33 min-1). The Spearman ρ between SUV and K i P, between SUV and K i C, and between K i P and K i C was 0.94, 0.91, and 0.97, respectively, and that between SUV and K 1, between SUV and K 1/k 2, and between SUV and k 3 was 0.70, 0.44, and 0.33, respectively. Malignant lymph nodes exhibited a higher SUV, K i P, and K i C than benign lymph nodes. Conclusion: Although 11C-choline pharmacokinetic modeling has potential to uncouple the contributions of different processes leading to intracellular entrapment of 11C-choline, the high correlation between SUV and both K i P and K i C supports the use of simpler SUV methods to evaluate changes in 11C-choline uptake and metabolism for treatment monitoring.
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