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
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.
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.
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.
Pt | Age | Prior PCa Treatment | Disease Status | Indication for Dual Tracer | Year of PCa Diagnosis | GS | PSA (ng/mL) |
---|
1 | 58 | None | Localised | Other Ca (renal) | 2020 | 4 + 5 | 15 |
2 | 66 | RP, EBRT | BCR | Other Ca (lung) | 2008 | 3 + 4 | 0.39 |
3 | 56 | None | Localised | Other Ca (lung) | 2018 | 3 + 4 | 8.6 |
4 | 77 | ADT | Localised | Other Ca (colorectal) | 2013 | 4 + 4 | 1.7 |
5 | 77 | RP, EBRT | LR | Atypical lesion (s) | Early 1990s | N/A | 10 |
6 | 77 | RP | BCR | Atypical lesion (s) | 2003 | N/A | 0.57 |
7 | 82 | None | mHSPC | Other Ca (lung, lymphoma) | 2019 | N/A | 6.7 |
8 | 69 | None | mHSPC | Other Ca (colorectal) | 2019 | 4 + 4 | 9.6 |
9 | 82 | Orchidectomy | mHSPC | Other Ca (melanoma) | 2008 | 4 + 5 | 0.04 |
10 | 61 | RP, EBRT, ADT | mHSPC | Other Ca (salivary) | 2010 | 4 + 5 | 12 |
11 | 77 | EBRT, ADT | mHSPC | Atypical lesion (s) | 2005 | 4 + 3 | 4 |
12 | 80 | EBRT, ADT | mCRPC | Other Ca (colorectal) | 2013 | 4 + 4 | 6.6 |
13 | 65 | RP, salvage EBRT, salvage PLND, ADT | mCRPC | Atypical lesion (s) | 2012 | 4 + 4 | 0.19 |
14 | 79 | EBRT, ADT | mCRPC | Atypical lesion (s) | 2011 | 4 + 5 | 1.9 |
15 | 82 | Orchidectomy, ADT | mCRPC | Atypical lesion (s) | 2011 | 4 + 5 | 800 |
16 | 67 | High dose rate brachytherapy, EBRT, ADT, pelvic lymph node SBRT | mCRPC | Negative PSMA PET | 2009 | 4 + 4 | 24 |
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-Metastatic | mHSPC | mCRPC | Total |
---|
Multiple malignancies | 4 | 4 | 1 | 9 (56.3%) |
Atypical lesions | 2 | 1 | 3 | 6 (37.5%) |
Negative PSMA PET | 0 | 0 | 1 | 1 (6.3%) |
Total | 6 (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.
Pt | Indication for Dual Tracer | Lesions | PSMA | FDG | PCa Avidity Pattern |
---|
1 | Right renal mass on PSMA PET/CT for high-risk PCa | Prostate | ++++ | − | PSMA+ FDG− |
Right kidney mass | ++ | ++ |
2 | Lung SCC seen on PSMA PET/CT | Right pulmonary hilar LNs | + | ++++ | PSMA– FDG− |
Right lung mass | ++ | ++++ |
Thyroid | + | + |
3 | Concurrent lung adenocarcinoma and PCa | Right 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 | − | ++ |
4 | Rectal cancer and history of PCa | Prostate | ++++ | + | PSMA+ FDG− |
Rectum | + | ++++ |
5 | Rising PSA and complex liver lesion | Prostate bed | +++ | − | PSMA+ FDG− |
Liver mass | − | +++ |
6 | Rising PSA and non-PSMA avid retroperitoneal LNs | Right maxillary sinus | − | +++ | PSMA− FDG− |
Superior mesenteric LNs | − | +++ |
Paraaortic LNs | − | ++ |
Aortocaval LNs | − | +++ |
Right thoracic cutaneous lesion | − | + |
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.
Pt | Indication for Dual Tracer | Lesions | PSMA | FDG | PCa Avidity Pattern |
---|
7 | Synchronous lung SCC, small cell lymphoma, and clinically diagnosed PCa | Prostate, 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 | + | + |
8 | Synchronous PCa and colorectal cancer | Right prostate lesion | ++++ | − | PSMA+ FDG− |
Left prostate lesion | ++ | − |
Right external iliac LN | + | − |
Rectum | + | ++++ |
Liver lesion | * | +++ |
9 | Metastatic melanoma and mHSPCa | Left pulmonary hilar LNs | − | ++ | PSMA− FDG− |
C7 vertebrae | − | ++ |
Right tenth rib | − | + |
10 | Parotid SCC with nodal metastases, and background of mHSPCa on ADT | Left infraclavicular LN | +++ | − | PSMA+ FDG− |
Left paraaortic LN | ++ | − |
Left ear | − | + |
11 | Liver lesion with background of mHSPCa | Prostate | +++ | + | PSMA+ FDG− |
Right acetabulum | ++ | − |
Caecum | − | ++ |
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.
Pt | Indication for Dual Tracer | Lesions | PSMA | FDG | PCa Avidity Pattern |
---|
12 | Metachronous prostate cancer and rectal cancer | Prostate | ++++ | − | PSMA+ FDG− |
Right external iliac LN | ++ | − |
T9 vertebrae | ++ | − |
Rectum | − | +++ |
13 | mCRPCa and metastatic adenocarcinoma of unclear primary, possibly salivary | Left external iliac LN | ++ | − | PSMA+ FDG− |
Right pulmonary hilar LN | ++ | +++ |
Mediastinal LN | +++ | ++++ |
Left supraclavicular LNs | ++ | ++ |
14 | Rising PSA and 4 cm adrenal lesion (metastasis vs. primary adrenal lesion) | Right adrenal mass | ++++ | ++++ | PSMA+ FDG+ (Concordant) |
15 | Mediastinal and pulmonary hilar LNs on PSMA PET | Prostate | ++++ | ++ | 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 | ++++ | − |
16 | Rising PSA with negative PSMA PET | T11 vertebrae | + | + | PSMA+ FDG+ (Equivocal; later confirmed as metastasis) |
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