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Article

Intra-Individual Comparisons of [18F]fluorodeoxyglucose and Prostate-Specific Membrane Antigen Positron Emission Tomography in Prostate Cancer Patients Across Different Disease States: New Insights into Disease Heterogeneity

by
Stephen McGeorge
1,2,3,
David A. Pattison
3,4,
Nattakorn Dhiantravan
4,
Paul A. Thomas
3,4,
John W. Yaxley
1,3,5 and
Matthew J. Roberts
1,2,3,6,*
1
Department of Urology, Royal Brisbane and Women’s Hospital, Butterfield St., Brisbane 4029, Australia
2
Department of Urology, Redcliffe Hospital, Anzac Avenue, Redcliffe 4020, Australia
3
Faculty of Medicine, The University of Queensland, 20 Weightman St., Brisbane 4006, Australia
4
Department of Nuclear Medicine & Specialised PET Services, Royal Brisbane and Women’s Hospital, Butterfield St., Herston 4029, Australia
5
Wesley Urology Clinic, Wesley Hospital, 451 Coronation Dr., Brisbane 4066, Australia
6
Faculty of Medicine, University of Queensland Centre for Clinical Research, Building 71/918 RBWH, Butterfield St., Brisbane 4029, Australia
*
Author to whom correspondence should be addressed.
Submission received: 14 October 2024 / Revised: 22 November 2024 / Accepted: 19 December 2024 / Published: 27 December 2024

Abstract

:
Background/Objectives: Prostate-specific membrane antigen (PSMA) PET/CT is more accurate than CT and bone scans for staging intermediate and high-risk prostate cancer (PCa). Fluorodeoxyglucose (FDG) PET has improved disease characterisation in metastatic castrate-resistant PCa (mCRPCa) and indicates patients with a particularly poor prognosis. The aim of this study was to assess the benefits of both PSMA and FDG PET in PCa staging by the direct intra-individual comparison of PSMA and FDG uptake patterns. Methods: Patients who underwent both PSMA and FDG PET/CT from 2015 to 2020 at our institution were identified and included if they had a histological or clinical diagnosis of PCa. Medical records were reviewed for demographic information and clinical details (including PSA, previous treatment, and disease status). Imaging interpretation was based on reporting by experienced nuclear medicine physicians. Results: Sixteen patients were identified. In 11 men with localised or hormone-sensitive PCa, PSMA-avid and FDG-avid disease was seen in 64% (n = 7) and 9% (n = 1) of patients, respectively. FDG-avid disease was present in 60% of patients with mCRPCa (n = 3/5), all of whom showed PSMA uptake. Of note, one patient showed higher initial FDG uptake that progressed in size and uptake on PSMA PET over 12 months. Conclusions: FDG PET might be useful in the assessment of patients with high clinical suspicion of metastases (e.g., high PSA, symptoms) with negative PSMA PET, particularly in castrate-resistant PCa.

1. Introduction

Prostate cancer (PCa) is the most common non-cutaneous malignancy in men and a significant cause of morbidity and mortality [1,2]. An increasing incidence of de novo metastatic PCa has been observed following the release of the United States Preventive Services Taskforce guidelines, as has a shift towards the earlier use of systemic treatments in the disease course [3,4,5,6,7,8]. Therefore, accurate staging and patient selection for systemic treatments is a key issue in current PCa management.
Staging of PCa has traditionally been performed with conventional imaging (CT and bone scans), but prostate-specific membrane antigen (PSMA) positron-emission tomography (PET) has emerged as a superior modality [9,10,11,12]. The prospective ProPSMA trial by Hofman et al. reported PSMA PET/CT to be 27% (95% CI 23–31) more accurate than conventional imaging (92% [88–95] vs. 65% [60–69]; p < 0·0001) for the initial staging of intermediate and high-risk PCa [10]. However, an intrinsic limitation of PSMA-targeted imaging and therapy is that 5–10% of primary tumours do not express PSMA, and they are therefore negative on PSMA PET [12,13,14,15,16,17,18].
The application of fluorodeoxyglucose (FDG) PET has traditionally been limited by poor sensitivity in PCa staging, being most commonly used for staging of known neuroendocrine variant diseases [19,20]. However, FDG PET/CT use in patient selection for radioligand therapy in metastatic castrate-resistant PCa (mCRPCa) is improving our understanding of PCa tumour heterogeneity [21,22]. Lack of PSMA expression has been reported in dedifferentiated advanced PCa, ductal pattern malignancy, and neuroendocrine transformation [17,23,24]. Conversely, these more aggressive histological types can have increased glycolysis and are therefore more readily detectable by FDG PET [25]. As such, FDG PET can provide complementary information to PSMA PET in the assessment of advanced PCa [26]. The addition of FDG PET after PSMA PET can increase the detection of lymph node (LN) or distant metastases in mCRPCa [27]. It can also provide prognostic information, with shorter overall survival reported for men with ≥1 FDG-positive PSMA-negative lesions compared to other patterns of disease on imaging [24,28].
The value of FDG PET in the PSMA PET era, particularly in PSMA-negative patients, is unclear. There are very few reports with intra-individual comparison of FDG and PSMA PET/CT for staging in prostate cancer, aside from patient selection for radioligand therapy (RLT). The aim of this study was to assess the use and potential benefits of using both PSMA and FDG PET for PCa staging using direct intra-individual comparisons of disease patterns with each.

2. Materials and Methods

All patients who underwent both PSMA and FDG PET/CT between 1 January 2015 and 31 December 2020 at the Royal Brisbane and Women’s Hospital, a major tertiary referral hospital, were identified from the Department of Nuclear Medicine and Specialised PET Services. Patients were included if they had a histological or clinical diagnosis of PCa, with PSMA and FDG PET/CT performed within a six-month interval. The study was approved by the institutional ethics committee (approval number LNR/2020/QRBW/67789).
Patients underwent PET imaging using a Biograph mCT scanner (Siemens Medical Solutions, Erlangen, Germany) from vertex to thighs according to standardised protocols. Low-dose structural CT was acquired during tidal respiration for attenuation correction and lesion localisation. Radiotracers were manufactured in Queensland—The Radiopharmaceutical Centre of Excellence (Q-TRaCE). Patients received 18F-FDG via intravenous cannula with a mean dose of 319 MBq (213–382) and mean uptake time of 74 min (58–129). The first nine patients received 68Ga-PSMA-11 radiotracer with a mean dose of 146 MBq (129–156) and a mean uptake time of 64 min (48–86). Our institution transitioned to using 18F-PSMA-1007 radiotracer, with the subsequent seven patients receiving a mean dose of 248 MBq (222–261) and a mean uptake time of 137 min (124–166). Images were reported by two experienced nuclear medicine physicians, each reading approximately 1000 PET scans annually, including 200 PSMA PET/CT scans. For this series, each PSMA and FDG PET were retrospectively reviewed by a third consultant, with lesions classified according to the maximum standardised uptake value (SUVmax) and considered non-avid if this was <3.
Clinical information was obtained from patient records, including demographic information, medical history, PSA, diagnosis, biopsy/prostate histology, and prior PCa treatments. PSA was taken at the time of PSMA PET. Imaging details were collected, including indication, timing, locations of uptake on PET, and SUVmax where available. Data management and descriptive statistical analysis were performed in Excel.

3. Results

3.1. Demographic Information

Twenty patients underwent both PSMA and FDG PET/CT at our institution over the 5-year period, of whom seventeen patients had PCa. One patient was excluded due to a 261-day interval between PSMA and FDG PET/CT. Patient characteristics are summarised in Table 1.
The most common indication (n = 9, 56.3%) was for multiple malignancies, defined as use of PSMA and FDG PET for staging of separate clinically or pathologically diagnosed non-PCa malignancy, arising synchronously or metachronously with PCa (Table 2). Six patients (37.5%) had FDG PET used as a means to characterise sites of disease which were considered atypical for PCa metastases, such as a solitary adrenal gland mass (n = 1), complex liver lesions (n = 2), and mesenteric, mediastinal, or supraclavicular lymphadenopathy (n = 3). One patient underwent FDG PET due to persistent clinical suspicion of metastatic disease after an equivocal PSMA PET/CT (6.3%). PSMA and FDG avidity by lesion is summarised in Table 3 and Table 4 (SUVmax indicators <3: −, 3–4.9: +, 5–9.9: ++, 10–14.9: +++, >15: ++++).

3.2. Non-Metastatic (Localised, Biochemical, or Local Recurrence)

Among six patients with non-metastatic PCa according to both PSMA and FDG PET/CT, three patients showed PSMA avidity within either the prostate (n = 2; Gleason 4 + 5 with PSA 15 ng/mL and Gleason 4 + 4 with PSA 9.6 ng/mL) or prostate bed (n = 1; radical prostatectomy (RP) and external beam radiotherapy (EBRT) > 15 years prior), all of whom did not display reciprocal FDG avidity. Three patients had no local uptake on either PSMA or FDG, of whom two were post-RP (for Gleason 3 + 4 disease) and the other patient had untreated localised Gleason 3 + 4 disease with PSA 8.6 ng/mL.
Most cases had confirmed or suspected additional malignancies based on their FDG appearance and histology (where obtained). PSMA avidity was observed in primary renal, lung, and rectal cancer, and also in a primary lung cancer with metastases. One patient with a complex liver lesion was deemed likely to be experiencing an indolent process, given the clinical features and inconclusive biopsy.

3.3. Metastatic Hormone-Sensitive Prostate Cancer

Sixty percent of patients (n = 3/5) in the metastatic hormone-sensitive PCa (mHSPCa) group demonstrated PSMA avidity within the prostate. Of the two without local PSMA avidity, one (patient 10) had undergone RP and post-operative radiotherapy, now receiving treatment for mHSPCa with androgen-deprivation therapy (ADT), whilst the other (patient 9) had Gleason 4 + 5 PCa diagnosed 12 years prior, treated by surgical castration, with a current PSA of 0.035. Three patients had Gleason ≥ 8 histology. One patient did not undergo biopsy as diagnosis was made with clinical findings. Most patients (n = 4/5) with PSMA-positive scans were FDG-negative (Table 2). One patient with clinically diagnosed PCa had PSMA and FDG avidity within the prostate as well as a left lung squamous cell carcinoma, with a PSMA-positive FDG-positive sacral lesion considered attributable to either primary cancer, but it is considered more likely to be lung metastasis.

3.4. Castrate-Resistant Prostate Cancer

Among five patients with mCRPCa (Gleason 4 + 4 n = 3; Gleason ≥ 4 + 5 n = 2; Table 5), two were concordant to solitary metastases (adrenal and T11 vertebra). Within this group, FDG PET was shown to outperform PSMA PET for one patient (Patient 16) with initial metastatic disease treated with ADT and stereotactic radiotherapy, where a new solitary vertebral lesion was equivocal but more intense on FDG PET than PSMA PET. This was subsequently confirmed as a metastasis with a further PSA increase to 30 ng/mL and PSMA PET/CT evidence of intense avidity, with development of other new bone metastases (Figure 1). Patient 14 had an adrenal metastasis confirmed following surgical excision and an excellent PSA response post-operatively (17 to 0.09 ng/mL, further details reported elsewhere) [29].
Patient 15 presented with a PSA of 800 ng/mL and Gleason 4 + 5 = 9 disease on biopsy, demonstrating concordant prostatic, right pelvic, and retroperitoneal nodal PSMA and FDG avidity, with PSMA-negative FDG-positive mediastinal lymphadenopathy and PSMA-positive FDG-negative bony metastases (Figure 2). The mediastinal lymphadenopathy was considered to have a typical appearance for a granulomatous disease process; however, this was not confirmed histopathologically.
Two mCRPCa patients did not show FDG-avid PCa, both with multiple malignancies, although one was a subsequent diagnosis. One had rectal adenocarcinoma on a background of Gleason 4 + 4 PCa diagnosed 5 years prior and treated with ADT. The other patient had Gleason 4 + 4 PCa, previously treated with RP, salvage EBRT, salvage pelvic LN dissection, and continuing ADT. FDG PET was performed due to the atypical distribution of PSMA-avid mediastinal and supraclavicular lymphadenopathy, with a rising PSA from 0.05 to 0.23. The subsequent LN biopsy showed poorly differentiated adenocarcinoma, which was eventually clinically attributed to an alternative primary salivary malignancy.

4. Discussion

While the use of staging PSMA PET/CT for the detection of metastatic disease has increased in contemporary clinical practice, there are very few reports on the combined use of PSMA and FDG PET for PCa staging, outside of patient selection for RLT in mCRPCa. The results from this retrospective series found that PSMA PET had a higher detection rate than FDG PET; however, there was increased PSMA/FDG discordance with more advanced disease (high volume mHSPCa, mCRPCa).
PSMA PET/CT is highly sensitive for localised and metastatic PCa; however, 5–10% of primary tumours have low PSMA expression, potentially limiting the assessment of distant disease in these patients. Notably, Hofman and colleagues reported that for patients with biopsy Gleason Grade ≥ 4 + 4, metastases were missed (false negative) by PSMA PET/CT in six patients (3% overall, 19% of true metastases) that were detected by conventional imaging [10]. Thus, this PSMA-negative group may benefit most from FDG PET staging in the mHSPCa setting. Furthermore, PSMA-negative FDG-positive disease may be an aggressive subtype, demonstrated by very poor prognosis in mCRPCa and higher FDG uptake associated with worse survival in mHSPCa [30].
The additive benefit of FDG PET/CT was observed in a prospective single-arm trial in high-risk M0 CRPCa that reported FDG after PSMA PET/CT increased the detection of metastases from 65% to 73% and that PSMA-negative FDG-positive disease was more common in CRPCa (33%) than in HSPCa (6%) [27]. In our results, FDG-avid disease was seen in one-fifth of (20%) patients with mHSPCa as opposed to three-fifths of (60%) patients with mCRPCa.
In men with BCR following RP with negative PSMA PET/CT, the presence of FDG-avid disease was predicted by higher PSA levels and Gleason score (p < 0.001) in one study, with positive FDG PET seen in 90% of men with PSA ≥ 2.3 ng/mL and Gleason score ≥ 8, while it was seen in 0% of men for reciprocal criteria [31]. We observed a similar relationship for two patients in this study series. The first had high-risk CRPCa (PSA 24.4 ng/mL, Gleason 4 + 4) with T11 vertebral body uptake that was equivocal on PSMA PET/CT and so underwent FDG PET that also showed uptake in the same location, although this was also inconclusive. This lesion was then subsequently confirmed as a PCa metastasis, displaying high uptake on repeat PSMA PET 12 months later with the development of new bony lesions (Figure 2). The second patient had dual negative PSMA/FDG PET with a PSA of 0.57 ng/mL at 17 years following radical prostatectomy (unknown Gleason score). Therefore, FDG PET may assist the assessment of patients with high-risk features (high PSA levels and Gleason score) and suspected metastatic disease but have negative PSMA PET, particularly in the CRPCa setting.
Use of both PSMA/FDG PET may also be helpful in the presence of concurrent non-prostate malignancies, which were present in 9 out of 16 patients in this series (56.3%) [32]. FDG PET can be complementary as PSMA avidity is reported in many other non-PCa malignancies, usually due to PSMA expression by malignancy-associated neovascular endothelial cells rather than tumour cells [32]. Three patients in this series had lung masses which were all dual PSMA-positive FDG-positive. One patient had an incidental dual PSMA-positive FDG-positive renal mass found on staging for high-risk PCa. Growing evidence demonstrates the applicability of PSMA PET as a staging modality in renal cell carcinoma (RCC), particularly in recurrent disease [32,33]. Three patients had rectal adenocarcinoma in addition to PCa, all of whom had FDG uptake in the primary rectal lesion and PSMA uptake identified in only one out of three cases. PSMA uptake has been sparsely reported in rectal adenocarcinoma, with immunohistochemistry in one case showing PSMA expression in neovasculature but not in tumour cells [34,35].
The strengths of this study include an intra-individual comparison of PSMA and FDG PET across a spectrum of PCa disease states, with all imaging performed at a single high-volume tertiary centre. The limitations of this retrospective series are selection bias, small sample size, and significant heterogeneity in the indications for use of PSMA and FDG PET. Interpretation was also often confounded by multiple malignancies, which is an area of ongoing research [32]. In these cases, the combined use of FDG and PSMA PET/CT was not necessarily able to conclusively determine the origin of distant metastases based on imaging findings alone. There appeared to be greater utility in the subsequent addition of FDG PET after PSMA PET for the assessment of incidental synchronous malignancies, but these must be interpreted with caution. Furthermore, scant follow-up data limited the comparison of uptake patterns relative to oncological outcomes. FDG uptake (SUVmax > 15) was correlated with worse 12-month PFS (p = 0.05) and poor response to RLT (disease progression in 12/15 men), which translated to poor overall survival (median 2.3 months) in a different study of similar patients with advanced mCRPCa who did not receive RLT [28,36].

5. Conclusions

FDG PET was of low utility when compared to PSMA PET for localised and mHSPCa. The highest additional yield for detection of metastases with FDG PET was observed in mCRPCa, where PSMA-negative FDG-positive PCa metastases were more common in patients with higher PSA levels and higher Gleason scores. Improved disease characterisation is important for these patients, given the poor prognosis of PSMA-negative FDG-positive mCRPCa. Further research is needed on the role for combining FDG and PSMA PET across the spectrum of PCa, particularly in castration-resistance and high-risk patients with negative PSMA PET.

Author Contributions

Conceptualization, D.A.P., P.A.T. and M.J.R.; methodology, D.A.P., P.A.T., M.J.R. and S.M.; formal analysis, S.M.; investigation, S.M., D.A.P. and M.J.R.; data curation, S.M.; writing—original draft preparation, S.M. and M.J.R.; writing—review and editing, S.M., D.A.P., N.D., P.A.T., J.W.Y. and M.J.R.; visualisation, S.M. and M.J.R.; supervision, M.J.R. All authors have read and agreed to the published version of the manuscript.

Funding

This research was funded by a Royal Brisbane and Women’s Hospital Foundation project grant.

Institutional Review Board Statement

The study was conducted in accordance with the Declaration of Helsinki and approved (13 August 2020) by the Institutional Ethics Committee of Royal Brisbane and Women’s Hospital (LNR/2020/QRBW/67789).

Informed Consent Statement

The study was reviewed by the Royal Brisbane and Women’s Hospital Human Research Ethics Committee (LNR/2020/QRBW/67789) and was approved (13 August 2020) for a consent waiver due to conduct as a clinical audit.

Data Availability Statement

Supporting data are included in Table 3, Table 4 and Table 5.

Acknowledgments

The authors thank Andrew Jiang for data collection. M.J.R. is supported by a Clinician Research Fellowship from the Metro North Office of Research, Queensland Health, research support package from The University of Queensland and Viertel Clinical Investigator Award from the Sylvia and Charles Viertel Charitable Foundation.

Conflicts of Interest

The authors declare no conflicts of interest.

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Figure 1. Patient 16 with very mild uptake in T11 vertebra due to tumour deposit (white arrow) on (A) Ga68-PSMA PET/CT which was higher on (B) FDG PET/CT, and subsequently became highly avid on repeat F18-PSMA PET/CT (C) one year later.
Figure 1. Patient 16 with very mild uptake in T11 vertebra due to tumour deposit (white arrow) on (A) Ga68-PSMA PET/CT which was higher on (B) FDG PET/CT, and subsequently became highly avid on repeat F18-PSMA PET/CT (C) one year later.
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Figure 2. Patient 15, with PSA of 800 ng/mL and Gleason 4 + 5 = 9 PCa previously treated with bilateral orchidectomy showing multiple metastases (white arrows). Coronal PET/CT illustrates (1A) PSMA-avid retrocrural and para-aortic lymphadenopathy, with (1B) concordant FDG avidity of retrocrural and para-aortic nodal disease, but discordant FDG-avid mediastinal lymph nodes. Axial PET/CT of the pelvis shows (2A) PSMA-avid bilateral common and external iliac lymph node metastases, whilst (2B) FDG uptake is only seen in the right common and external iliac lymph nodes. Sagittal PET/CT illustrating (3A) intense PSMA uptake within the prostate and PSMA-avid spinal metastases, with (3B) no FDG uptake seen in bone lesions.
Figure 2. Patient 15, with PSA of 800 ng/mL and Gleason 4 + 5 = 9 PCa previously treated with bilateral orchidectomy showing multiple metastases (white arrows). Coronal PET/CT illustrates (1A) PSMA-avid retrocrural and para-aortic lymphadenopathy, with (1B) concordant FDG avidity of retrocrural and para-aortic nodal disease, but discordant FDG-avid mediastinal lymph nodes. Axial PET/CT of the pelvis shows (2A) PSMA-avid bilateral common and external iliac lymph node metastases, whilst (2B) FDG uptake is only seen in the right common and external iliac lymph nodes. Sagittal PET/CT illustrating (3A) intense PSMA uptake within the prostate and PSMA-avid spinal metastases, with (3B) no FDG uptake seen in bone lesions.
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Table 1. Patient characteristics, grouped by disease status into non-metastatic (localised; local recurrence; biochemical recurrence, BCR), metastatic hormone-sensitive (mHSPC), and metastatic castrate-resistant (mCRPC). ADT—androgen deprivation therapy; Ca—cancer; EBRT—external beam radiotherapy; GS—Gleason score; LR—local recurrence; Pt—patient; PLND—pelvic lymph node dissection; RP—radical prostatectomy; SBRT—stereotactic body radiotherapy.
Table 1. Patient characteristics, grouped by disease status into non-metastatic (localised; local recurrence; biochemical recurrence, BCR), metastatic hormone-sensitive (mHSPC), and metastatic castrate-resistant (mCRPC). ADT—androgen deprivation therapy; Ca—cancer; EBRT—external beam radiotherapy; GS—Gleason score; LR—local recurrence; Pt—patient; PLND—pelvic lymph node dissection; RP—radical prostatectomy; SBRT—stereotactic body radiotherapy.
PtAgePrior PCa TreatmentDisease StatusIndication for Dual TracerYear of PCa DiagnosisGSPSA (ng/mL)
158NoneLocalisedOther Ca (renal)20204 + 515
266RP, EBRTBCROther Ca (lung)20083 + 40.39
356NoneLocalisedOther Ca (lung)20183 + 48.6
477ADTLocalisedOther Ca (colorectal)20134 + 41.7
577RP, EBRTLRAtypical lesion (s)Early 1990sN/A10
677RPBCRAtypical lesion (s)2003N/A0.57
782NonemHSPCOther Ca (lung, lymphoma)2019N/A6.7
869NonemHSPCOther Ca (colorectal)20194 + 49.6
982OrchidectomymHSPCOther Ca (melanoma)20084 + 50.04
1061RP, EBRT, ADTmHSPCOther Ca (salivary)20104 + 512
1177EBRT, ADTmHSPCAtypical lesion (s)20054 + 34
1280EBRT, ADTmCRPCOther Ca (colorectal)20134 + 46.6
1365RP, salvage EBRT, salvage PLND, ADTmCRPCAtypical lesion (s)20124 + 40.19
1479EBRT, ADTmCRPCAtypical lesion (s)20114 + 51.9
1582Orchidectomy, ADTmCRPCAtypical lesion (s)20114 + 5800
1667High dose rate brachytherapy, EBRT, ADT, pelvic lymph node SBRTmCRPCNegative PSMA PET20094 + 424
Table 2. Dual tracer PET indication according to prostate cancer disease status; non-metastatic (localised; local recurrence; biochemical recurrence, BCR), metastatic hormone-sensitive (mHSPC), and metastatic castrate-resistant (mCRPC).
Table 2. Dual tracer PET indication according to prostate cancer disease status; non-metastatic (localised; local recurrence; biochemical recurrence, BCR), metastatic hormone-sensitive (mHSPC), and metastatic castrate-resistant (mCRPC).
Non-MetastaticmHSPCmCRPCTotal
Multiple malignancies4419 (56.3%)
Atypical lesions2136 (37.5%)
Negative PSMA PET0011 (6.3%)
Total6 (37.5%)5 (31.3%)5 (31.3%)16
Table 3. Comparison of lesions by avidity (SUVmax indicators <3: −, 3–4.9: +, 5–9.9: ++, 10–14.9: +++, >15: ++++)—non-metastatic disease.
Table 3. Comparison of lesions by avidity (SUVmax indicators <3: −, 3–4.9: +, 5–9.9: ++, 10–14.9: +++, >15: ++++)—non-metastatic disease.
PtIndication for Dual TracerLesionsPSMAFDGPCa Avidity Pattern
1Right renal mass on PSMA PET/CT for high-risk PCaProstate++++PSMA+ FDG−
Right kidney mass++++
2Lung SCC seen on PSMA PET/CTRight pulmonary hilar LNs+++++PSMA– FDG−
Right lung mass++++++
Thyroid++
3Concurrent lung adenocarcinoma and PCaRight lung mass+++++PSMA− FDG−
Left parietal lobe of cerebrum+*
Right lower paratracheal LNs+++
Left pulmonary hilar LNs+++
Coeliac LNs++
Right supraclavicular LNs++
Right seventh rib+
Right ischium+++
Left acetabulum+
L1 vertebrae++
4Rectal cancer and history of PCaProstate+++++PSMA+ FDG−
Rectum+++++
5Rising PSA and complex liver lesionProstate bed+++PSMA+ FDG−
Liver mass+++
6Rising PSA and non-PSMA avid retroperitoneal LNsRight maxillary sinus+++PSMA− FDG−
Superior mesenteric LNs+++
Paraaortic LNs++
Aortocaval LNs+++
Right thoracic cutaneous lesion+
* Indiscernible from background uptake.
Table 4. Comparison of lesions by avidity (SUVmax indicators <3: −, 3–4.9: +, 5–9.9: ++, 10–14.9: +++, >15: ++++)—mHSPCa.
Table 4. Comparison of lesions by avidity (SUVmax indicators <3: −, 3–4.9: +, 5–9.9: ++, 10–14.9: +++, >15: ++++)—mHSPCa.
PtIndication for Dual TracerLesionsPSMAFDGPCa Avidity Pattern
7Synchronous lung SCC, small cell lymphoma, and clinically diagnosed PCaProstate, laterally++PSMA+ FDG+
(Sacral lesion favoured to be lung metastasis but with no histopathological diagnosis made)
Prostate, posterior apex++
Left lung mass+++
Right subpleural nodule+
Right vallecula++
Sigmoid colon++
Left inguinal LNs++
Right sacral ala++
8Synchronous PCa and colorectal cancerRight prostate lesion++++PSMA+ FDG−
Left prostate lesion++
Right external iliac LN+
Rectum+++++
Liver lesion*+++
9Metastatic melanoma and mHSPCaLeft pulmonary hilar LNs++PSMA− FDG−
C7 vertebrae++
Right tenth rib+
10Parotid SCC with nodal metastases, and background of mHSPCa on ADTLeft infraclavicular LN+++PSMA+ FDG−
Left paraaortic LN++
Left ear+
11Liver lesion with background of mHSPCaProstate++++PSMA+ FDG−
Right acetabulum++
Caecum++
* Indiscernible from background uptake.
Table 5. Comparison of lesions by avidity (SUVmax indicators <3: −, 3–4.9: +, 5–9.9: ++, 10–14.9: +++, >15: ++++)—CRPCa.
Table 5. Comparison of lesions by avidity (SUVmax indicators <3: −, 3–4.9: +, 5–9.9: ++, 10–14.9: +++, >15: ++++)—CRPCa.
PtIndication for Dual TracerLesionsPSMAFDGPCa Avidity Pattern
12Metachronous prostate cancer and rectal cancerProstate++++PSMA+ FDG−
Right external iliac LN++
T9 vertebrae++
Rectum+++
13mCRPCa and metastatic adenocarcinoma of unclear primary, possibly salivaryLeft external iliac LN++PSMA+ FDG−
Right pulmonary hilar LN+++++
Mediastinal LN+++++++
Left supraclavicular LNs++++
14Rising PSA and 4 cm adrenal lesion (metastasis vs. primary adrenal lesion)Right adrenal mass++++++++PSMA+ FDG+
(Concordant)
15Mediastinal and pulmonary hilar LNs on PSMA PETProstate++++++PSMA+ FDG+
Right external iliac LNs+++++++
Right common iliac LNs++++++
Left external iliac LNs++++
Left common iliac LNs++
Para-aortic LNs+++++
Retrocrural LNs+++++
Mediastinal LNs+++
Right pubis+++
T8++++
L2++++
L4++++
16Rising PSA with negative PSMA PETT11 vertebrae++PSMA+ FDG+
(Equivocal; later confirmed as metastasis)
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McGeorge, S.; Pattison, D.A.; Dhiantravan, N.; Thomas, P.A.; Yaxley, J.W.; Roberts, M.J. Intra-Individual Comparisons of [18F]fluorodeoxyglucose and Prostate-Specific Membrane Antigen Positron Emission Tomography in Prostate Cancer Patients Across Different Disease States: New Insights into Disease Heterogeneity. Uro 2025, 5, 1. https://doi.org/10.3390/uro5010001

AMA Style

McGeorge S, Pattison DA, Dhiantravan N, Thomas PA, Yaxley JW, Roberts MJ. Intra-Individual Comparisons of [18F]fluorodeoxyglucose and Prostate-Specific Membrane Antigen Positron Emission Tomography in Prostate Cancer Patients Across Different Disease States: New Insights into Disease Heterogeneity. Uro. 2025; 5(1):1. https://doi.org/10.3390/uro5010001

Chicago/Turabian Style

McGeorge, Stephen, David A. Pattison, Nattakorn Dhiantravan, Paul A. Thomas, John W. Yaxley, and Matthew J. Roberts. 2025. "Intra-Individual Comparisons of [18F]fluorodeoxyglucose and Prostate-Specific Membrane Antigen Positron Emission Tomography in Prostate Cancer Patients Across Different Disease States: New Insights into Disease Heterogeneity" Uro 5, no. 1: 1. https://doi.org/10.3390/uro5010001

APA Style

McGeorge, S., Pattison, D. A., Dhiantravan, N., Thomas, P. A., Yaxley, J. W., & Roberts, M. J. (2025). Intra-Individual Comparisons of [18F]fluorodeoxyglucose and Prostate-Specific Membrane Antigen Positron Emission Tomography in Prostate Cancer Patients Across Different Disease States: New Insights into Disease Heterogeneity. Uro, 5(1), 1. https://doi.org/10.3390/uro5010001

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