Donika Plyku1,2,3,4, Robert F Hobbs3,5, Di Wu1,2, Carlos Garcia2, George Sgouros6,7, Douglas Van Nostrand8,9,10. 1. Division, Nuclear Medicine Research, MedStar Health Research Institute, Hyattsville, MD, USA. 2. Division of Nuclear Medicine, MedStar Washington Hospital Center, Washington, DC, USA. 3. Radiological Physics Division Department of Radiology and Radiological Sciences, Johns Hopkins University, School of Medicine, 1550 Orleans St., CRBII 4M.61, Baltimore, MD, 21231, USA. 4. Nuclear Medicine Research, Georgetown University School of Medicine, MedStar Health Research Institute and Washington Hospital Center, 110 Irving Street, N.W., Suite GA60F, Washington, DC, 20010, USA. 5. Department of Radiation Oncology and Department of Radiology and Radiological Sciences, Johns Hopkins University, School of Medicine, 1550 Orleans St., CRBII 4M.62, Baltimore, MD, 21231, USA. 6. Radiological Physics Division Department of Radiology and Radiological Sciences, Johns Hopkins University, School of Medicine, 1550 Orleans St., CRBII 4M.61, Baltimore, MD, 21231, USA. gsgouros@gmail.com. 7. Department of Radiation Oncology and Department of Radiology and Radiological Sciences, Johns Hopkins University, School of Medicine, 1550 Orleans St., CRBII 4M.62, Baltimore, MD, 21231, USA. gsgouros@gmail.com. 8. Division, Nuclear Medicine Research, MedStar Health Research Institute, Hyattsville, MD, USA. douglas.van.nostrand@medstar.net. 9. Division of Nuclear Medicine, MedStar Washington Hospital Center, Washington, DC, USA. douglas.van.nostrand@medstar.net. 10. Nuclear Medicine Research, Georgetown University School of Medicine, MedStar Health Research Institute and Washington Hospital Center, 110 Irving Street, N.W., Suite GA60F, Washington, DC, 20010, USA. douglas.van.nostrand@medstar.net.
Abstract
PURPOSE: The objective of this study is to evaluate the lesion absorbed dose (AD), biological effective dose (BED), and equivalent uniform dose (EUD) to clinical-response relationship in lesional dosimetry for 131I therapy. METHODS: Nineteen lesions in four patients with metastatic differentiated thyroid cancer (DTC) were evaluated. The patients underwent PET/CT imaging at 2 h, 24 h, 48 h, 72 h, and 96 h post administration of ~ 33-65 MBq (0.89-1.76 mCi) of 124I before undergoing 131I therapy. The 124I PET/CT images were used to perform dosimetry calculations for 131I therapy. Lesion dose-rate values were calculated using the time-activity data and integrated over the measured time points to obtain AD and BED. The Geant4 toolkit was used to run Monte Carlo on spheres the same size as the lesions to estimate EUD. The lesion AD, BED, and EUD values were correlated with response data (i.e. change in lesion size pre- and post-therapy): complete response (CR, i.e. disappearance of the lesion), partial response (PR, i.e. any decrease in lesion length), stable disease (SD, i.e., no change in length), and progressive disease (PD, i.e., any increase in length). RESULTS: The lesion responses were CR and PR (58%, 11/19 lesions), SD (21%, 4/19), and PD (21%, 4/19). For CR and PR lesions, the ADs, BEDs and EUDs were > 75 Gy for 82% (9/11) and < 75 Gy for 18% (2/11). The ADs and BEDs were < 75 Gy for SD and PD lesions. CONCLUSION: By performing retrospective dosimetry calculations for 131I therapy based on 124I PET/CT imaging, we evaluated the correlation of three dosimetric quantities to lesional response. When lesion AD, BED, and EUD values were > 75 Gy, 47% (9/19) of the lesions had a CR or PR. The AD, BED, and EUD values for SD and PD lesions were < 75 Gy. The data presented herein suggest that the greater the lesion AD, BED, and/or EUD, the higher the probability of a therapeutic response to 131I therapy.
PURPOSE: The objective of this study is to evaluate the lesion absorbed dose (AD), biological effective dose (BED), and equivalent uniform dose (EUD) to clinical-response relationship in lesional dosimetry for 131I therapy. METHODS: Nineteen lesions in four patients with metastatic differentiated thyroid cancer (DTC) were evaluated. The patients underwent PET/CT imaging at 2 h, 24 h, 48 h, 72 h, and 96 h post administration of ~ 33-65 MBq (0.89-1.76 mCi) of 124I before undergoing 131I therapy. The 124I PET/CT images were used to perform dosimetry calculations for 131I therapy. Lesion dose-rate values were calculated using the time-activity data and integrated over the measured time points to obtain AD and BED. The Geant4 toolkit was used to run Monte Carlo on spheres the same size as the lesions to estimate EUD. The lesion AD, BED, and EUD values were correlated with response data (i.e. change in lesion size pre- and post-therapy): complete response (CR, i.e. disappearance of the lesion), partial response (PR, i.e. any decrease in lesion length), stable disease (SD, i.e., no change in length), and progressive disease (PD, i.e., any increase in length). RESULTS: The lesion responses were CR and PR (58%, 11/19 lesions), SD (21%, 4/19), and PD (21%, 4/19). For CR and PR lesions, the ADs, BEDs and EUDs were > 75 Gy for 82% (9/11) and < 75 Gy for 18% (2/11). The ADs and BEDs were < 75 Gy for SD and PD lesions. CONCLUSION: By performing retrospective dosimetry calculations for 131I therapy based on 124I PET/CT imaging, we evaluated the correlation of three dosimetric quantities to lesional response. When lesion AD, BED, and EUD values were > 75 Gy, 47% (9/19) of the lesions had a CR or PR. The AD, BED, and EUD values for SD and PD lesions were < 75 Gy. The data presented herein suggest that the greater the lesion AD, BED, and/or EUD, the higher the probability of a therapeutic response to 131I therapy.
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