I am now thinking to add Finasteride to Bicalutamide plus degarelix injections. Would/could it help me if on the psma pet scan my only visible cancer is in my prostate?
I had radiation therapy to my prostate but my prostate cancer is back and looks like that the radiation therapy failed and the most resistant strains where selected and now growing in my prostate with the PSA doubling time under 3 months.
I was diagnosed in 2018 polimetastatic with distant Mets in my bones. Spine, neck etc.
Since then only on degarelix and a year ago I irradiated my prostate as the scans didn't show any Mets only cancer in my prostate. My PSA a year ago was 1.4 just before the prostate cancer irradiation. The PSA dropped in 6 months after radiation from 1.2 to 0.25 and now is on the fast rise. Last PSA was 3.
What is my status? Am I still polimetastatic or maybe oligo metastatic or just none metastatic crpc in my prostate? I am confused. What should I do?
Please ask questions so I can explain better what is happening.
Finasteride: "Miracle drug" regrows hair, heals prostate, and also boosts heart health
My testosterone levels are around 1. No scan detected any Mets only crpc cancer in my prostate. I just recently added Bicalutamide to degarelix injections when the PSA reached 1.8. the PSA is still rising. My last scans where 3 months ago. I had a psma pet scan with CT with contrast and a day later a nuclear medicine bone scan showing no Mets.
I don't want that now, I need some estrogens for my bones. I am on ADT for 5.5 years now. In 2016 in Europe if you have none metastatic crpc in your prostate only they would keep you on ADT alone. I added Bicalutamide and trying to hook my cancer on it. When my PSA will rise I will stop Bicalutamide and my cancer will collapse hopefully for one year. I can always add whatever I want but I am not in a hurry now. Ideally speaking I would like to radiate it again or remove it surgically. I don't really know. They are pluses and minuses to everything in life. At this very moment I feel great. My only concern is that the crpc from my prostate could spread locally or even it could metastasize maybe only to the pelvic lymph nodes or more distant. I have to keep check on it. Actually I had early chemotherapy and according to the ENZAMET study their is no difference in Enzalutade and Bicalutamide if you are polimetastatic with de novo distant Mets and you received early chemotherapy.
Your case is complex, and it involves several factors that need careful consideration. Here’s a breakdown to help clarify your situation and guide the discussion with your oncologist:
1. Current Status and Terminology
Polymetastatic vs. Oligometastatic: You were initially diagnosed as polymetastatic in 2018 with bone metastases. The lack of visible distant metastases on your recent scans could suggest a significant response to treatment, but it doesn't necessarily mean the metastases are gone—it may reflect their being below the detection threshold of imaging.
Non-metastatic CRPC: If the only visible cancer is in the prostate with no distant metastases, this could align with non-metastatic castration-resistant prostate cancer (nmCRPC). However, rising PSA and prior metastases history may still imply microscopic disease elsewhere.
2. Prostate-Confined Recurrence
The recurrence in your prostate after radiation and the rapid PSA doubling time (<3 months) suggest aggressive, possibly radiation-resistant cancer. This could mean:
The cancer in your prostate is driving the PSA rise.
There may still be undetectable metastatic disease.
3. Finasteride Consideration
Mechanism: Finasteride inhibits 5-alpha-reductase, reducing dihydrotestosterone (DHT) levels, which can fuel prostate cancer growth. However, its role in advanced or castration-resistant settings is less clear and usually not a standard of care.
Potential Role: It might be beneficial if residual androgen-dependent pathways in the prostate cancer cells are active, but its impact would likely be modest compared to treatments like androgen receptor inhibitors (e.g., bicalutamide, enzalutamide, or apalutamide).
4. Suggested Next Steps
To refine your treatment strategy:
1. Confirm Disease Extent:
A repeat PSMA PET scan or other advanced imaging may help confirm whether the cancer is truly confined to the prostate or if there are small metastases elsewhere.
2. Biopsy of Prostate Lesion:
If feasible, a biopsy could clarify if the recurrent cancer is still androgen-sensitive or if it's evolving into a more aggressive, castration-resistant phenotype.
3. Refine Systemic Therapy:
Your current treatment with degarelix (LHRH antagonist) and bicalutamide might need escalation to newer-generation androgen receptor inhibitors like enzalutamide or abiraterone.
Chemotherapy (e.g., docetaxel) could also be considered in cases of aggressive recurrence or widespread metastases.
4. Local Therapy:
Salvage prostatectomy or cryotherapy could theoretically target the local disease but is less common in your setting. A discussion with a multidisciplinary team is critical.
5. PSA Monitoring and Doubling Time:
A doubling time under 3 months is concerning and often correlates with more aggressive disease. Frequent monitoring and proactive adjustments are essential.
Key Questions for Your Oncologist
Should I undergo additional imaging to confirm the extent of my disease?
Is a prostate biopsy advisable to determine the cancer’s characteristics?
Would adding a next-generation androgen receptor inhibitor or systemic chemotherapy improve outcomes?
Is further local treatment to the prostate recommended in my case?
Finasteride, while beneficial in benign prostate hyperplasia and early prostate cancer prevention, may not be sufficient or standard for advanced settings like yours. Always discuss any changes with your oncologist before initiating therapy.
Let me know if you want further clarification or help summarizing your questions for your next oncology visit.
Q. Interestingly now, 11 months later my PSA is still 2.5 on bicalutamide plus ADT alone.
A. It's noteworthy that your PSA has stabilized somewhat at 2.5 over the past 11 months on bicalutamide plus ADT (degarelix). This suggests a relatively controlled disease state compared to your earlier rapid PSA rise. Here are some thoughts based on your updated situation:
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1. Disease Control Assessment
Stabilized PSA: A PSA of 2.5, though higher than ideal, indicates that your cancer may still be responding to therapy to some degree, or the disease progression has slowed.
Castration-Resistant Status: If testosterone levels remain castrate (<50 ng/dL) and PSA hasn't dropped further, this would align with castration-resistant prostate cancer (CRPC).
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2. Why Has PSA Stabilized?
Bicalutamide Contribution: Bicalutamide, though not as potent as newer androgen receptor-targeted agents (e.g., enzalutamide), may still be suppressing PSA.
Residual Androgen Sensitivity: Some cancer cells may still be partially sensitive to androgen blockade, slowing disease progression.
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3. Next Steps to Consider
Given that your PSA is relatively stable:
1. Reassess Disease Extent:
Repeat PSMA PET imaging could help confirm if cancer remains confined to the prostate or if micrometastatic disease has developed.
This would guide whether further systemic or local interventions are warranted.
2. Biochemical CRPC Strategy:
If the disease is confined to the prostate:
Escalation to enzalutamide or apalutamide may provide stronger androgen receptor blockade.
Alternatively, abiraterone with prednisone could reduce residual androgen synthesis.
3. Local Therapy for Prostate-Confined Disease:
If confirmed as localized:
Consider salvage options like cryotherapy, HIFU, or even a prostatectomy, though these are less common post-radiation.
4. PSA Kinetics Monitoring:
Regular PSA testing remains crucial. Any further doubling or significant rise could prompt re-evaluation of treatment.
5. Genomic Testing (Optional):
Testing for DNA repair mutations (e.g., BRCA1/2, ATM) may guide eligibility for PARP inhibitors like olaparib or rucaparib if progression occurs.
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4. Staying Proactive
Your stable PSA suggests current treatments are holding the disease in check, but periodic imaging and close monitoring are critical. Have you discussed escalating treatment or newer therapies with your oncologist? Would you like me to help outline specific questions for your next consultation?
Q. Why did you say that at PSA 2.5 what I have now my cancer is considered CRPC?
A. A diagnosis of castration-resistant prostate cancer (CRPC) does not depend on the absolute PSA level (like 2.5 ng/mL) but rather on specific criteria related to cancer progression despite effective androgen deprivation therapy (ADT). Here's why I mentioned it in the context of your case:
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Criteria for CRPC Diagnosis
CRPC is typically defined when the following conditions are met:
1. Castrate Testosterone Levels:
Testosterone remains below 50 ng/dL (achieved with ADT like degarelix).
2. Evidence of Disease Progression:
PSA progression: A rise of 2 ng/mL or more from the nadir, with a rising trend in at least two successive measurements taken at least a week apart.
Radiologic progression: New lesions on imaging (e.g., bone or soft tissue metastases).
Clinical progression: Worsening symptoms related to cancer.
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Why Your Case Could Fit CRPC
PSA Stabilization at 2.5:
Your PSA has stopped dropping and has stabilized despite ADT and bicalutamide, suggesting that the cancer is no longer fully suppressed by androgen deprivation.
Rising PSA Before Stabilization:
You reported a fast-rising PSA after radiation therapy (from 0.25 to 3). If that rise occurred while on ADT with castrate testosterone levels, it fulfills the definition of biochemical progression, even if there is no radiologic or clinical progression.
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Why This Matters
The label "CRPC" does not mean treatment options are exhausted. It signifies that your cancer may no longer rely solely on testosterone for growth and might need intensified therapy, such as:
Next-Generation Androgen Receptor Inhibitors (enzalutamide or apalutamide).
Androgen Synthesis Inhibitors (abiraterone with prednisone).
Other systemic options if the disease progresses further.
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What Should Be Confirmed?
1. Testosterone Levels:
Check that testosterone is indeed in the castrate range (<50 ng/dL). Non-castrate testosterone could explain a suboptimal PSA response, in which case optimizing ADT is needed.
2. Current Imaging Findings:
Confirm no visible metastases or new local disease with a PSMA PET scan.
3. PSA Trends:
If PSA remains stable without clinical or radiologic progression, aggressive treatment escalation may not be immediately required.
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Would you like assistance in discussing these points with your oncologist? Or do you have more details to clarify the situation further?
Q. Why did the PSA went up first to 3 and then dropped to 2.5?
A. The fluctuation of your PSA from 3 to 2.5 after it initially increased could be due to several factors. PSA levels can change for various reasons even when undergoing androgen deprivation therapy (ADT), and the trend may not always be perfectly linear. Here are some possible explanations for the fluctuation:
1. Biological Variability
Small fluctuations in PSA: PSA levels can sometimes fluctuate due to natural biological variability. These changes are often not directly tied to disease progression but can occur because of factors like the body’s response to treatment, minor inflammation, or changes in tumor activity.
Time Lag: After radiation therapy, the prostate tissue may still be undergoing changes (e.g., inflammation or healing), which could lead to temporary fluctuations in PSA levels.
2. Treatment Response Dynamics
Partial Response to ADT and Bicalutamide: Your cancer may still have some sensitivity to the combination of ADT and bicalutamide, which could result in a PSA drop after an initial rise. Even though bicalutamide is a weaker androgen receptor blocker compared to newer agents, it might still exert some suppressive effect on prostate cancer growth.
Radiation Effect: The effects of the radiation therapy to the prostate could be continuing to influence PSA levels. Sometimes radiation results in an initial rise in PSA (a "PSA bounce") before it starts to decrease. This might explain the temporary increase to 3, followed by a decline to 2.5.
3. Prostate Cancer Behavior
Cancer Behavior: Prostate cancer cells, especially in castration-resistant forms, can sometimes display irregular growth patterns. They might have periods of rapid growth (leading to the rise in PSA) followed by slower phases where the cancer stabilizes or regresses temporarily (leading to the PSA decrease). This could explain the fluctuation you’ve observed.
4. Testing and Laboratory Factors
Testing Variability: While less common, variations in PSA testing methods, lab handling, or timing can sometimes cause small discrepancies. These fluctuations might not be clinically significant but can show up due to lab variations or slight differences in sample processing.
5. ADT Adjustments
Inconsistent ADT Effectiveness: Occasionally, slight variations in the effectiveness of ADT (due to factors like medication adherence, drug interactions, or variations in individual response) can lead to temporary changes in PSA levels, although this would usually result in a more sustained rise or decline over time.
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What Does It Mean for You?
While these fluctuations can be normal in prostate cancer treatment, it’s crucial to monitor the overall trend. If PSA continues to rise, it could indicate that your cancer is becoming more resistant to current therapies, but if it stabilizes or decreases, it suggests that your current treatment plan is still having some effect.
In any case, it would be wise to continue close monitoring with your oncologist and consider further testing (such as imaging or biopsy) if needed, especially if the PSA starts rising again in a sustained manner.
Would you like further assistance on what to discuss with your oncologist regarding these fluctuations?
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PCa Abbreviation List UPDATED 1/26/2023 
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