Prostate MRI. FINDINGS: Status post prostatectomy.. There is a new small enhancing nodule in the left superior prostatectomy bed in the region of the left seminal vesicle. This measures approximately 0.9 x 0.4 cm (image 17, series 6 and image 49, series 9).). There are no enlarged or morphologically abnormal lymph nodes. The urinary bladder is unremarkable. No suspicious osseous abnormalities are identified. Stable small postoperative fluid collection in the left external iliac region.
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LowT
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A prostate bed focus might possibly represent a local recurrence which would not have the same implication as a metastasis. A local recurrence, theoretically would have a chance of cure, by a local ablative procedure such as surgery or as accepted, radiation therapy. ------- Though, it is not available in the US and still experimental, there is a novel approach, contingent on the solitary focus being PSMA avid, of doing PSMA radioguided surgery - with one of the same advantages that prostatectomy has as an initial curative intent therapy, that if surgery fails, one still has salvage radiotherapy with or without ADT in the toolbox. Admittedly, this is still in its infancy, and has yet to proven. And admittedly testing has been, via conventional imaging detection, on lymph node metastasis with no significant success - but lymph node metastasis is not the same as a presumed local recurrence.
That low T's BCR took 6 years to happen speaks to a relatively indolent relapse, further favoring local recurrence or conceivably oligometastasis over conventional widespread (cows out of the barn) metastases; the latter not considered amenable to directed therapy. Furthermore, even in the widespread de novo metastatic state, albeit only in the low volume subset, cytoreduction of the primary site, shows benefit.
There is no way to ascertain whether cancer cells are only in what you call the "solitary focus." In fact, the treatment area is moving toward widening rather than focal. I'm talking about prostate bed relapse, not regional (pelvic lymph node) metastatic relapse in this case.
The 2010 RTOG guidelines completely or partially missed cancer in 33% of the patients
The 2020 GFRU guidelines completely or partially missed cancer in 10% of the patients"
That means in their unselected study 66-90% of patients are cured by RT ablative therapy only. So for those patients, the proof is in the pudding - they had only a prostate bed recurrence.
For the others, what do you do? Well the patient is not just any patient. We know specific things about him. His recurrence is 6 years post-primary treatment. That is an incredibly long time. And he is 80 years old. This suggests the patient has a benign recurrence. This patient could afford to do "active surveillance"; monitoring his PSA Doubling Time and if and when it becomes concerning he could opt for salvage RT and ADT at that time. If on active surveillance he may never need treatment period.
If he is 80 yo and in good health, he may want to have SRT now rather than waiting for later - tissue recovery is always better in younger men. There is no such thing as a "benign recurrence." It is malignant, not benign.
On the flip side of pursuing an aggressive approach for curative intent, for a PSA DT of greater than 9 months and time to BCR of 6 years; observation -- kind of akin to active surveillance in the initial diagnosis state, is an accepted approach, as one's prognosis is actually excellent.
Normal detection limits of a PSMA scan is about 4mm, so with respect to size, it should be sufficient to confirm if this nodule of 9mm x 4mm is the source of rising PSA. But your PSA is too low for a PSMA scan to be sensitive enough to have a high percentage chance of confirming this nodule — PSA needs to be closer to 0.5 and above, but it helps that the main tumor out of the way and there is a lower background noise threshold. If confirmed, probably salvage RT is in order, but I would consider salvage Brachy if the SV is involved (as was mine).
Yes, for a PSMA scan. If negative, check my Bicalutamide maneuvers thread. You may buy time, while keeping your PSA very low, via a miniscule dose of Bicalutamide. Coming November will be one year for me.
That is a permanent big dilemma for me. To take the PSMA scan I should let the PSA climb to at least 0.1. Prior to Bicalutamide my PSADT was 9.5 months. So, each month I get tempted to stop taking it so as to proceed in due time with the scan, but the popular wisdom of "Don't change the winning team" prevails and kicks the can further down the road. But some day I will have to just do it.
Additional clinical information that needs to be included in planning approach.
This will be lengthy but no other way. And its not the entire story.
Treated hypothyroidism.
History of late onset hypogonadism with trail of clomiphene seven years ago which had to be discontinued after 2 months due to eye SEs. This increased T nicely, dropping FSH and LH, but PSA went from 5 to 8 in six weeks which led to ultimate Dx of PCa.
Nine months after RARP (78 gm gland; GS 3+4; GG 2; extensive ECE; - margins; -SV) with post op uPSAs running < 0.006. Tumor in unusual post mid line location surrounding ejaculatory ducts.
24 large 3-5 cm lymph nodes were removed. All negative.
Began low dose T gel 9 months post op due to low T symptoms with frequent monitoring to keep level in 400 range. Went well until month 26 when T spiked to 970 and uPSA first became detectable at 0.0150. Was unable to monitor T while traveling for 2 months.
T gel stopped and uPSA fell to <0.006 but subsequently began a slow rise over the years to present value. Frequent lab monitoring.
FSH 3x high normal limit and LH 2x high normal limit except when on Tgel. And even now with no Tgel for three years these remain the same.
Discovered PRL was elevated with a slow rising trend. I have read this is not good in the setting of PCa and with recent increasing uPSA levels a trial of Cabergoline was tried but stopped after six weeks do to visual problems. It did lower PRL to < 1 from 25.4. It has now returned to 18.7 since stopping the Cabergoline.
Have had brain MRI with focus on sella turcica which was normal.
Had been on high dose pravastatin for many years but stopped it 2 yrs ago thinking it may be contributing to low T symptoms. Resulted in marked improvement in symptoms (strength, pain, coordination, brain, etc.) and rise in Cholesterol and T levels. Cholesterol being a substrate of T. However, with rise in T to as high as 700, the FSH and LH remain elevated.
There have been extreme spikes in E2 over the years but recently I may have determined that was due Biotin in multivitamin which I no longer take. E2 now runs 25-30.
Free T has always been extremely low except when on Tgel it rose to low normal range.
There appears to be a correlation with slow rising T since stopping the statin and increasing rate of rise of uPSA.
Six weeks ago begin a very low dose of different statin to bring cholesterol down and maybe the T as well which may impact uPSA level. We’ll see.
One more point of information is recent use of 5 alpha Reductase Inhibitors with DHT now <4,
Thoughts on putting this together in some meaningful way are greatly appreciated. I am being schedule for PSMA PET CT in the near future.
Before taking any medication my (endogenous) total T was in the 820-850 range. After starting taking Avodart it has raised to 930-1480 range (average 1150). Currently, under my additional feeble Bicalutamide dose it is in the 1650-3100 range (average 2230). Typical control loop under-run situation i.e. when some "sensor" receives lower than anticipated input it instructs the "generator" to produce more.
That is beyond my pay grade to understand. I’ve never had T vales like that, endogenous or otherwise. Except when it shot up to 970. Circumstances surrounding that was pharmacy provided a third brand of gel and as we were leaving country for two months trip and having just received last T of < 300, I just applied one packet to chest/upper arms during that time. By the time I returned home and drew my T again, my body hair was like a wooly oxen. Have pictures to prove it!
This morning got last free T level back and it is at 4. Low normal range begins at 6. Usual results for me have been 2-4 range. Except when on Tgel which brought it up into low end of normal range.
I really watched my lab values while on the Tgel, using partial packets, varying application sites, etc. trying to avoid spikes etc. (My experience was absorption was chest-upper arms> abdomen> thighs.). Also my insurance provided three different brands while I was using it so probably different vehicles might affect absorption.
Because of the PCa I was compulsive about watching these levels
A point of interest is, currently I feel great!
The uPSA levels is my concern as is the elevated PRL, FSH, LH, in the setting of rising PSA.
I think this thing is way too complicated to but together with current star of knowledge/understanding.
My have read these elevated levels (PRL, FSH, LH) in the context of PCa is not desirable.
Looks like the cancer is very hormone sensitive (expected).
For some reason the testicles seemed unable to keep up T production without being stimulated by the high FSH/LH. But now with normal T (fT still low) they should have come down.
I’ve seen no less than five endocrinologist ms (they don’t treat cancer), one oncologist (doesn’t treat endocrine diseases) urology who does not treat either one.
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