So I was diagnosed over the summer with PCa at age 52. After several years of steady rises I was 5.5 and a biopsy found it. Gleason 8 (4+4) in four of 12 cores. I had RALP about a month ago (10/2019), and I will be going in for my first PSA test in about two weeks. The pathology showed that the cancer had spread to the seminal vesicles, but otherwise i had clean margins, no EPE and no lymph node involvement (9 nodes were examined).
At this stage I realize recurrence chances are high, but hope springs eternal.
I know about uPSA tests every three months, and getting salvage radiation once it reaches 0.1. I have also read about radiation before any rise, with our without ADT. Those seem to be my four choices at the moment.
Assuming I am undetectable (<0.1 for the first PSA test) is there anything new/upcoming I should be doing to maximize positive outcomes? It seems all of the treatment trials are for later stages, but the internet is vast and I am brand new.
Be sure not to take anything from the internet that might interfere with PSA readings. Even a small amount of interference with your PSA may lead you down the wrong path:
Your links to the statin studies showing an association of statins with increased risk of prostate cancer (at least post-RP, if I'm reading them right) was really alarming to me. I've been on statins for 11 years, about the same number of years I've been dealing with PC. I'm bouncing around like a pinball reading studies that contradict each other. I'm not capable of judging whether a given study is a good one, or lacking somehow, or what. It's curious to me that statins could somehow promote cancer since they lower cholesterol, which is what the body uses to make testosterone, which doesn't cause cancer but certainly feeds it. Do you think the association is mainly due to statins lowering PSA, thus delaying discovery of PC, and not some more direct cause-and-effect? Can you look at these studies I'm linking to (you're probably alread familiar with them) and say whether they're as substantive or reliable as the ones you linked? I mean, I'm considering taking myself off the statin since I saw the studies you linked to and seeing what happens to my PSA. It's like, take a statin and get prostate cancer, don't take a statin and get a heart attack.
The point you should take away is that association is not causation. And that the evidence, such as it is, for prostate cancer is very weak. You are wrong to take it as evidence of inverse causation. It just demonstrates how lousy the studies are.
I could also have shown you 20 or so studies demonstrating an association with improved survival:
Thanks Allen. It's not that I see association as causation but that there's often not a lot more than association to go by in making a decision, so it's like making a decision just in case association some day might also prove to be causation. Shooting craps, in other words. Your reply is a great relief even if it doesn't completely relieve me of the concern that the statin is masking PSA. From what I've read about masking on this site, am I right to infer that the masking should be a concern mostly if post-treatment PSA is below 0.1, where even a small total amount of masking could be proportionally significant?
You are absolutely right that we often don't have definitive randomized clinical trials (RCTs) proving causation. Lacking that, there are certain criteria we can use to make judgments that may be right more often than they are wrong. These have been compiled by Austin Bradford Hill (below). I can summarize:
• Strength of Association (larger associations are more likely (but not necessarily) causal)
• Consistency of Data (independent studies all lead to the same conclusion)
• Specificity (a very specific population is differentially affected)
• Temporality (the effect has to occur after the cause)
• Biological gradient (to some extent, more drug leads to more effect)
• Plausibility (one can come up with a plausible explanation)
• Coherence (lab studies demonstrate a plausible mechanism for the observed effect)
• Experiment (has the effect been prevented by modifying the cause)
The diversity of effects of statins noted in several studies, means the purported benefits/harms of statins on PC are suspect based on the second item (consistency of data). The mendelian analysis lends further credibility to the suggestion of "no effect." Until we have RCTs, "no effect on PC" is our best assumption.
You may be right that statins mask PSA, but if so, the trend should be telling. I'd assume that the masking effect, if any, is consistent over time.
Associative, causal, or whatever, I know that after RP cholisterol and triglicerides have lowered to unseen levels for the last 30 years that I have lab data.
Please understand all these different labs that do PSA have lab error margins. A variation with a labs margin of error may require follow-up testing but, at least initially, should not be cause for great concern. Also, PSA is produced by the peri-urethral ducts and the salivary glands. This is important if, for example, one had pelvic radiation therapy. As the peri-uretheral ducts recover they will again begin producing PSA and possibly resulting in SMALL increases in total PSA.
Fyi spread to the seminial vessicles is a higher risk for re-occurrence/metastasis as the seminial vesicles are very vascular and this is thought to be a common route for metastatic spread.
FYI I am told the best imaging that is available for metastasis is PSMA but it is only for "research" so far in the USA (7 sites in the USA I know of) & I am told does not do well in detection below a PSA of 0.5.
PSA is produced in the salivary glands? I learn something new every day. But why on earth would the salivary glands produce PSA? Makes me wonder - when I see a piece of key lime pie or marionberry-rhubarb galette and my mouth starts watering, my PSA goes up? I shouldn't get my PSA tested right after I've been in a patisserie? And guys who chew gum have higher PSAs?
Run a google search for "PSMA imaging", click on "imaging" near the top of the page and you will see accumulation in the salivary glands, kidneys, ureters, bladder & liver. PSMA tracer is eliminated from the body by the urinary system as well as the liver. The urinary system is the principle mode of elimination for most PSMA tracer ligands.
According to my MO PSA is produced in small but detectable amounts in the salivary glands. So it would not be surprising PSMA imaging "lites up" the salivary glands .... and it does. Furthermore, if I am not mistaken, Lu-177 treatment has a "dry mouth" side effect .... which makes sense due to PSA production and PSMA imaging accumulation. I just pointed this out with peri-urethral PSA production and lab variability to point out that small moves in PSA of for example 0.03 to 0.06 (a doubling) might not be "real" and could be artifact.
"PSA concentrations in men post-cystoprostatectomy were also assessed. The 44 men in the study group ... PSA concentrations were <0.01 ng/mL in 42 out of the 44 specimens (95.4%) with values of 0.01 and 0.02 ng/mL in two specimens (Figure 3). The other 42 results were detectable with a median of 1.67 pg/mL (0.00167 ng/mL) and interquartile range of 0.68- 4.10 pg/mL (0.00068-0.0041 ng/mL)."
You and I have similar diagnoses except I have 20 years on you. 4+4 Gleason, no lymph nodes per MRI and no bone Mets per bone scan, My oncologist showed me a chart developed by big names in PC that took multiple factors into account and then showed recommended treatment with greatest probability of cure. In my case the rec was ADT for 1 1/2 to 3 years plus external radiation (44 treatments). I had first shot last week with radiation to start in8 weeks after first hormone shot.
Obviously not right for everyone but my oncologist I has a great reputation so I’m trusting him, the radiation oncologist and some dietary changes to get me thru this.
I am 74 years and have Gleason 5+5, PSA of 250, one ECE and seminal vesicles invasion. I was put on Firmagon which brought down the PSA to 1.47 in 4 months. From month 5 onwards I had 39 IMRT fractions totalling 78 Gy. Today it is 1 month since completion of IMRT and all the side effects of the radiation are gone except some skin discoloration that is going away. I have a checkup in Mar and Jun with PSA and PSMA Pet Scan. The real truth on what is the result of IMRT will be known through regular PSA tests. Dr wants me to continue ADT for minimum 2 or 3 years. My Dexa year bone density after 7 months on ADT was -0.9 which is normal. I have continued regular 5 km walks, weights 3 days a week and 3 rounds of 18 holes of golf-all walking. I feel healthy and have maintained a steady weight with a good diet. Now one can only wait.
😀. That’ll make me 103 so I doubt I’ll be able to keep that date! Your however, have every chance to f doing so. I know 81 (your age in 30 years) sure seems like a doable intermediate goal for me at 73👍
First of all DO NOT PANIC!!! Second Where did you get your User ID? From the bottom line of an eye chart?
Next fill us in with a little more info about yourself. Location? Treatment Location(s)? Doctor's name(s)? All info is voluntary but helps us help you and helps us too.
Thank you. Pca is a slow growing cancer so you have lots of time to fight the MF bastards.
My user id is courtesy of my parents. First initial and last name. Anytime I sign up for something, unless my son has been there first, i am guaranteed to get the username without having to try to hard to find a unique one. In my profile I have all of the details. I live near Philadelphia and I am being treated at Fox Chase Cancer Center. Dr Chen is my surgeon/urologist. PC may be slow growing, but my sense of things is that the medical world tends to lean on that fact just a little too much. At some point the disease crosses a threshold, and nobody really seems to know when that is, but it does cross it. Primary treatment before that point and it is curative. After that point it seems to get really messy.
Thank you for your quick and detailed reply. You can take some comfort in knowing that the members here are able to help you in your fight against the monster. Regards.....
I tell this to every guy I know with our malady. Please, if at all possible, make an appointment at MD Anderson and let them have a look. When I presented my local specialists with MDAs info they both said they’d never seen it before. Yet they see it daily at MDA. You can make an appt online very easily. It could save your life. I’m convinced it has mine.
Good luck!!
I was 53 over four years ago with #4 gleason 4+4. . Slow growing? Well at stage 4 you’re already advanced . Are you stage four?
No. T3b Clean margins, no epe but unfortunately it did spread to the seminal vesicles.
• in reply to
Good ,better than 4 .. you caught it before I did .. I was stage #4 gl.4+4 but I was t-4 meaning the prostate walls were breached and the horse was out of the barn . I was told . The 8 weeks radiation and adt put me in remission now over fours years and running .. So if it worked in my worsened condition it can surely put your pc away too. Stage #4 an eminent return projected but with you being #3 you have better odds and a shot at curative . You just have to get through the treatments and live more healthy than ever before .
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In my profile I have all of the details. I live near Philadelphia and I am being treated at Fox Chase Cancer Center. Dr Chen is my surgeon/urologist. PC may be slow growing, but my sense of things is that the medical world tends to lean on that fact just a little too much. At some point the disease crosses a threshold, and nobody really seems to know when that is, but it does cross it. Primary treatment before that point and it is curative. After that point it seems to get really messy.
PSA slightly up after salvage radiation
Rising PSA - When to be concerned?
Double time seems official?
4 month Casodex + radiation
Dad has PC in pelvic nodes ? Is he on correct treatment
