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Cancer: Prostate Message Board


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Hello Zent and welcome to the Board!:)

Your father clearly has infection ("bacteria seen"), and that typically affects PSA. In fact, infection can affect PSA a lot and fast. It can drive PSA to very high levels. Then, when the infection wanes, the PSA often drops back to normal levels, only to climb again when the infection becomes more active again.

In the past week there was another patient on this board with a situation similar to your father's, and comments there would apply to your father too. Here are some thoughts for your Monday meeting.

There could be prostate cancer hidden within the rapid rise in PSA, contributing just a little. If so, and if it were the mild type of prostate cancer, most likely "active surveillance" would be appropriate for a man of 81. There is some chance that your father has aggressive prostate cancer, though it seems much more likely that the PSA rise is due to infection and not that type of prostate cancer. It could be that your father's previous infection has recurred, or it could be that he has a new infection caused by a different bacterium. You could ask your father's doctor about these possibilities.

A DRE would be wise.

Follow-up PSAs would also be wise to see if the pattern of PSA results is consistent with prostate cancer or inconsistent with prostate cancer but consistent with infection.

My own layman's impression is that a biopsy at this time would not be warranted, but your father's doctor would be a far better judge of that. An MRI, especially a "multiparametric" MRI that is now so useful in resolving prostate issues, is probably also premature; again, your father's doctor is in a better position to assess that.

The lifestyle practices your father is following seem to help in coping with prostate cancer (and health generally).

I am not sure of the meaning of the other lab results that are out of the reference range. You could ask the doctor about those too.

Good luck with helping your father. I hope this issue resolves as an infection and that he has relief from his pain.
Hi again jetski76,

This reply is to your post before your latest post. I’ll address that later.
I wanted an advanced bone scan, the NaF18 (sodium fluoride) PET/CT scan and expected to have to travel far to get it.

[U]Increase in prostate volume[/U]. I am used to cc rather than ml, but the values will be the same: 5 ml = 5 cc. First, your father had a remarkably small prostate in 2012 - 5 ml. The norm for a healthy prostate in the US is in the range of about 25 to 30. However, after treatment, it can be much smaller. Mine decreased from mildly enlarged down to 15 after treatments. The increase from

That increase of 5 to 10, a doubling, in about 6 months from October 2012 to April 2013 seems very rapid, but the prostate at that point is still unusually small. My layman's guess is that this is due to recovery from some treatment with some contribution from benign prostate growth; however, it does seem unusually rapid to my layman’s eyes. If that were all due to cancer, you would have a cancer doubling time, which is a standard characteristic universally used when represented by PSA – the “PSA doubling time" or PSAD, of 6 months. However, with a prostate volume of 15 at a point 3 ½ years later in October 2016, it is clear that that six months doubling time does NOT represent all cancer, perhaps not representing any cancer. Do you see why this is so? Also, keep in mind that these “measures” of prostate volume are often more like estimates based on DRE exams, which involve some uncertainty. On the other hand, if theses size assessments are all based on imagery, especially if the same imagery, that would build confidence in each estimate and in any trend. It is possible, if one of more of the size assessments is based on a DRE, that what you have reflects a fair amount – possibly a great amount – of uncertainty when such a small prostate is involved. It helps that the same doctor has been involved. The increase from 15 to 23 in January 2018, 15 months later, still means your father has a prostate on the small side, and it appears the doubling time for prostate growth is on the slow side even if it were caused by cancer and not benign growth. Perhaps the urologist could explain the likely rates of benign growth in older men who have had prior treatment in the prostate area for conditions that are not cancer.

You asked how good conventional MRI was at detection. My impression has been that unimproved MRI that is not multiparametric and without an endorectal coil is not so good. (Some modern multiparametric MRIs do not need an endorectal coil.) Here is a way you can find a paper that discusses this: go to www.pubmed.gov and search for : MRI AND prostate cancer AND kirkham [au] AND emberton m [au] AND 2006 [dp] .

Healthy cells – no infection, no prostate cancer – in a prostate that is only around 23 ml in size would generally produce a PSA of about 2, far below your father’s PSA. Based on the erratic PSA pattern and the overall evidence, I suspect that infection is the cause, or perhaps one of the other odd causes like infarction. A biopsy could reveal evidence of an infection, and of course also of cancer. I’ll add some ideas on this in responding to your latest post.
Hello IADT3,

Thanks again for your informative and helpful replies!! Your generosity in helping others shines through in your messages.

If you don't mind, I have some follow-ups after reading your reply:

1) You wrote,

" My impression has been that unimproved MRI that is not multiparametric and without an endorectal coil is not so good".

"My laymans' impression is that your father has no cancer, but the results to date do not rule out any stage of cancer, though they do make it even less likely."

My father had the 1.5 T MRI without an endorectal coil. Do you think a 1.5 T MRI without an endorectal coil does not have the resolution and accuracy to detect metastatic and lymp node involvement? If yes, does it make sense to get a mp-MRI right away? That way, we will know all the details like lymph node involvement, metastasis, suspicious areas, PI-Rads score etc. I would like to know if there is a test that can confirm lymph node involvement andr metastatis at this moment?

2) As mentioned in my previous message, a TURP biospy was taken on Wednesday and we will get the report in 5 days. Antibiotics have been given for my father for his bacterial infection. He will probably be discharged tomorrow. The Urologist will mostly see my father in a month and test PSA again. Since the grade of cancer is unknown at this time and the random 12 core TURP biopsy are commonly found to miss high grade prostate cancers, if we wait for a month to repeat PSA again, will that be too late as the high grade cancer could have spread beyond the prostate?


3)Is it okay to wait for the bacterial infection to clear and then do a PSA? That way, if PSA is elevated again, a mp-MRI along with fusion biopsy (in a nearby city) would describe the proper grade of the cancer. If PSA is decreasing after a month, we can hold off on the mp-MRI and repeat PSA again monthly. Does this sound reasonable?


4) I did read that low PSA (less than 2.5) cancers tend to be aggressive. My father's PSA has always been in the range of 0.522- 0.79 until Oct 2016 when it was last measured. Since it shot up to 11.22 in 1.5 years, could this be such a case? Do the low PSA cancers stay low throughout or the PSA's increase as the cancer starts to spread? My father's 21 fold increase in his otherwise low PSA values over a period of 1.5 years does concern me a lot.

5)You wrote, " However, with a prostate volume of 15 at a point 3 ½ years later in October 2016, it is clear that that six months doubling time does NOT represent all cancer, perhaps not representing any cancer. Do you see why this is so?"

By this, do you mean that if the doubling time was consistent throughout the 3.5 years, my father's prostate volume would have been around 200 ml? Since it was not the case, there is a chance that the doubling from 5 ml in October 2012 to 10 ml in April 2013 could also not be a cancer? Also, please note that all the prostate volumes from Oct 2012 and beyond are from the Ultrasounds of Abdomen and Kindey. My father's Urologist never did a DRE for the last 10+ years. NOTE: I will know my father's prostate volume in the 1.5 T MRI tomorrow. I will update.



Thank you,
Zent
Hi Zent,

I’m responding to your post #14.

1) Your father’s MRI seems to have some of the characteristics of a mpMRI, though obviously at the lower resolution 1.5T than the higher 3T. By the way, does he have any ferrous implants that could be affected by the substantially more powerful magnetic field? Does he have other implants with shapes that could cause an unacceptable heat build-up due to the more powerful magnetic field? Some patients, I believe not many, are unable to get 3T scans for these reasons. Your father did get the standard T2 images plus T1 images, but he also got diffusion weighted imaging, which is one of the customary added mpMRI parameters. I suspect the contrast agent that your father got was simply to improve resolution generally and not the DCE (Dynamic Contrast Enhanced) technology to image blood supply. The radiologist who did his imaging could probably answer these questions. Spectroscopy has been a promising additional parameter for many years (and I’ve been tuning in to news about it for more than a decade), but it seems to me that it has not been widely adopted in mpMRI imaging – not enough payoff yet beyond the value contributed by the other parameters. Also, while DCE (Dynamic Contrast Enhanced imaging) does add value in enabling the radiologist to determine what is going on regarding blood supply (tumors need more blood), there is some thought that much of its value overlaps what is provided by the other parameters and may not be worth doing because of some very small but real and serious risk that is added by the use of the contrast agent. Nonetheless, I think that DCE parameter would be worthwhile for your dad for possible imaging after the biopsy.

At the moment even full-fledged mpMRI is not considered adequate for diagnosis, and the PI-RADS score is not accepted in lieu of a Gleason score (which itself is being re-conceived so that it is simpler to use), though that change in the role of PI-RADS is under active consideration and research. The scan your father had would not be able to identify high-grade disease (nor could a mpMRI), but it should be able to spotlight areas of the prostate that could contain high-grade (or any grade) prostate cancer to guide the biopsy; a high PI-RADS, 4 or especially 5, would suggest a strong likelihood of high-grade disease but would not be conclusive.

Regarding 2): My layman’s feeling is that your father has had enough imaging to guide the biopsy; while a 3T complete mpMRI resulting in a PI-RADS report would likely have been more helpful, what your father had is probably good enough. If the biopsy does miss some high-grade cancer that is fully contained at this point in the prostate, it is possible that detected lower-grade cancer would trigger treatment that would also cure the higher-grade cancer, which would mean that no value would have been added even if the high-grade cancer had been detected earlier.

If stealthy serious cancer evades detection by biopsy, it is still likely that subsequent PSA testing and other monitoring will soon smoke it out, with a good chance that it would remain in range for radiation, as research has shown that most metastatic cancer is close enough to treat for a while. If the cancer is already metastatic, an mpMRI might not pick it up even now. Even aggressive cancer that is now contained would be unlikely to become stage IV in the amount of time to wait for more PSA evidence. Therefore, the window of benefit is fairly small for a situation that could be just infection, perhaps with some other non-cancer elements (such as infarction, calcium deposits, etc.), and with what looks like fairly good imaging to guide the biopsy.

On the other hand, there is a small chance that a 3T mpMRI might pick up an aggressive cancer that would otherwise spread to a point that treatment is difficult; if money, convenience, and willingness of the radiologist to do the additional scan are not issues, there is some chance of real benefit, though small. If I were in your situation, I believe I would not seek the mpMRI at this time, but such a decision is always more difficult when you are the one actually making the decision and not just thinking about it. I remember well that I gave a lot of thought to whether to push for mpMRI prior to radiation, even though I had already had two excellent scans; I came to realize that the radiation dose would be the same no matter what the scan found, so I went ahead without the scan. A key question to ask is “What difference will what I would like make to the next step I will be taking?” I believe that question is usually in the minds of good doctors.

If the biopsy turns out positive, at that point your dad could benefit from a mpMRI at 3T to help decide whether active surveillance would be a good choice (for low-risk cancer) or what treatment options would be a good fit for his case. Depending on potential treatment, various imaging options could be considered, including, if the case then appears challenging, some of the newer scans that are outstanding at picking up very small metastases in bone, in lymph nodes and in other soft tissue.

Regarding 3): It is now believed rather firmly, based on research, that Gleason score 6 and lower cancers – the ones most suitable for active surveillance (AS), never, or extremely rarely, change into more aggressive cancers. However, it is also known that biopsies which find only Gleason 6 cancers can miss higher grade cancers that will cause problems. The key concept of surveillance is that truly active surveillance will pick up any stealthy bad actors before they become serious. Research from many centers around the world has consistently shown that AS is excellent at doing that (and is steadily improving).

Regarding 4): This is getting ahead of the game, but I can really empathize with you as you try to visualize the future and prepare for different situations. There are now excellent bone and soft tissue scans that can very reliably (though not yet perfectly) detect and locate metastases in bone, lymph nodes and other soft tissues. Moreover, even better scans are emerging, though there seems to be not much ground for further improvement.

One of the best currently available scans is known in the US as the axumin scan. It is very good at both bone and soft tissue detection, picking up tumors of about 3 mm and larger (and even smaller, sometimes) and it does not require its radiation element to be produced on-site, which is a big advantage. I had a NaF18 PET/CT bone scan, which is very sensitive, but not so good for soft tissue. I also had a scan for soft tissue that was excellent but is no longer available due to safety concerns. Soft-tissue (and some bone value) scans that are available are the C-11 acetate and C-11 choline PET/CT scans, but both use radioactive carbon isotopes with short half-lives that must be manufactured at the imaging site, a big disadvantage in accessibility, as only a few facilities have the necessary cyclotron facility. Some other scans are also in use, I believe, and a number are in the investigational stage. All of these scans are very useful for monitoring whether metastatic cancer is developing or progressing.

CT scans can pick up tumors about the size of a pea or larger, but they will miss smaller tumors, and that means they miss a lot of tumors. The normal technetium bone scan, which is widely available, requires at least about 10% of cancer infiltration of bone at the metastasis site before it shows up on the scan, so it too is of some but limited usefulness. These two scans were routine at the time of diagnosis for all patients when I was diagnosed in late 1999, but they were soon discontinued unless the patient had higher-risk characteristics, as they were virtually always negative for men with low-risk and even most intermediate-risk prostate cancer. (Both were negative for me even though I had high risk cancer: a PSA of 113.6, all biopsy cores, positive, most 100% cancer, Gleason 4+3=7 cancer, a "rock hard" prostate, etc.)

The usual PET scan is a glucose based scan; it is useful for most cancers because they get their energy from glucose (sugar). Prostate cancer is different, getting its energy from fat, basically, until it is well advanced. Therefore, the glucose based PET scan is not useful for prostate cancer until it is well advanced. Non-glucose PET scans, for example the sodium fluoride (NaF18) PET/CT scan that I had, are useful for prostate cancer, but are not warranted unless the case has some higher-risk characteristics.

You are asking very good questions and are learning this fast. Keep it up and good luck! :)
Hello IADT3,

I hope you are doing well!!

The biopsy report will only be available later this week and my father will be seeing the Urologist on April 2. I have two questions. As you have mentioned in your earlier messages, I am asking you these questions to get a handle on the various outcomes that are possible.

[U]Question #1:[/U]

The findings on my father’s TRUS report from last week is as below:
--------------------------------------------------------------------------------------
Central Zone is heterogeneous in echotexture
Peripheral zone is normal in echotexture
No focal lesions
Bilateral seminal vesicles are normal
--------------------------------------------------------------------------------------

I read online the following points about zones and cancer in the prostate:
1)20-25% of prostate cancers occur in the central zone of the prostate and are hard to detect and also tend to be the highest grade.
2) The peripheral zone is about 70% of the cases of cancer and the rest are in the transition zone.
3)On a TRUS, the central zone is presented as a combination of central and transition zone.

If a TRUS can visualize the zones of a prostate, I take it that a pelvis MRI with T2 and diffusion weighting must be able to do the same with better resolution. Is this an accurate assumption? If yes, does , “Central Zone is heterogeneous in echotexture” on the TRUS and “Area of altered echotexture; hypointense on T2w; showing restricted diffusion noted in the left hemigland. Area measures 19 x 11.22 mm” on the MRI would more likely be a case of cancer in the central zone? Your thoughts on this?


[U]Question #2:[/U]

On March 17, a urine test was done for my father which showed the elevated PSA of 11.22 and the following abnormal results:

Urine ph - 7.5 (Reference: Acidic)
Urine leucocytes: Present
WBC pus cells: 10-15 (Reference Range: 3-5)
RBC - 2-4(Reference Range: 0-1)
Epithelial - 1-2 (Reference Range: 2-3)
Remarks: Bacteria seen

On March 19, when my father was admitted to the hospital for a cystoscopy (and eventually underwent MRI, TRUS and biopsy for elevated PSA), a sample of urine was collected for culture. He was also given antibiotics starting March 19 to be taken until March 30. The results of the urine culture came out on March 21 as, “No growth after second day”. Previously, his urine cultures always have taken 3-4 days to come back with results.

I am mentioning all of this because if there was no substantial bacteria in his urine culture and hence no UTI or infection, it seems to point to cancer as most likely to explain the findings on his MRI. Your comments?

Thank you,
Zent
Hi again Zent,

I only have time now for the first set of questions. I will try to get to the later questions at another time. Before long YOU will be the expert on this! :cool: You wrote:

Prostate Cancer/PSA Questions:

1) My father's Urologist will check his PSA again in the last week of June (3 months from his biopsy). Does it make more sense to check PSA in the coming weeks in another lab rather than wait until June 21?

2) What other tests can be done currently to check for prostate cancer if PSA is not a reliable indicator of cancer (assuming my father has chronic prostatitis)?

3) My father's biopsy showed a low grade PIN. Given the poor quality of the biopsy, it might as well have been a high grade PIN/cancer. Does PIN(high or low grade) increase PSA?

++++++++++

My impressions/answers:

Regarding 1): My layman’s impression is that it makes sense just to wait and let the effects of the biopsy go away.

Regarding 2): There are some tests, but the question is whether it would be worthwhile doing them in view of the negative findings so far and the prostatitis that may be explaining the PSA pattern; my impression is that it would be premature to do these now, but you and your dad, and his doctors, are closer to the whole situation. A multiparametric MRI could be done and interpreted by an expert radiologist; that could also help spot prostatitis and help assess its extent. One or more blood or urine tests for prostate cancer could be done, at least one of which is not sensitive to infection, Here is one published paper from Italy about PHI, PCA3, and free-PSA, the latter known to misleading if there is infection: https://www.ncbi.nlm.nih.gov/pubmed/26162485 .

Some infrequently used blood tests could be done: CGA (chromogranin alpha); NSE (neuron specific enolase); PAP (prostatic acid phosphatase, used a lot before PSA), and CEA (carcinoembryonic antigen); for most of my earlier years with the disease, these were quite useful for patients with the unusual types of prostate cancer that made little or no PSA, but that would probably not be a good fit in your dad’s case as he makes a lot. However, he could have a rare case of prostatitis that made a lot of PSA combined with a rare and stealthy prostate cancer that made little or none. One fairly frequent unfavorable consequence is that your dad might have one or more results that were enough out of the normal range to cause further tests to be performed, but with no real problem, just personal variation – normal for him but not for most others. That happened to me with CEA, which we monitored for about two years as I recall it before deciding it did not matter. (CEA is one of the better tests for colon cancer.) Perhaps others on the board will suggest some tests that they have found useful.

Regarding 3) – high (and low) grade PIN and PSA: First, here’s another paper (involving at least one of the same authors) saying that PIN does not influence the PCA3 test: https://www.ncbi.nlm.nih.gov/pubmed/23116408 (includes a link to a copy of the complete paper). Here’s a paper based on a fairly small group of patients that indicates no influence of high-grade PIN on PSA: https://www.ncbi.nlm.nih.gov/pubmed/10524873. Here’s another study that reaches the same conclusion: https://www.ncbi.nlm.nih.gov/pubmed/8650867. I got these from searching www.pubmed.gov for - high grade PIN AND elevated PSA and prostate cancer – and also glancing on the right, after clicking on promising abstracts, for similar studies.

Good luck! Jim
Hello Jim,

I hope you are doing well! I wanted to thank you again for educating me regarding my father's case last year. Your posts made a significant difference as my father is based in India and my knowledge of the issues were nonexistent! Your explanation of how little of his prostate tissue the biopsy had sampled was very helpful. The biopsy did come negative. The IHT test in April 2018 was also negative

Just wanted to give you an update regarding my father:

1) He saw his Urologist in October 2018. He still had mild pain in his penis shaft at that time. This was 7 months after the MRI and biopsy. No PSA's were done after March 2018. The Urologist told my father that his penis shaft pain will slowly recede and he will only measure his PSA in October 2019 as he is otherwise doing fine.

2) Over the next few months, his pain decreased further and subsequently went away. So far, no issues with his urination.

3) In in December 2018, my father experienced issues where he had to apply additional force to pass stool. His Gastroentologist prescribed a fiber supplement and advised we see check his PSA (along with other tests) once every year. He has been fine with stool and today his PCP checked his PSA along with the other routine tests that he usually does every 6 months.

His PSA came as : 0.196 ng/ml ( Reference Range : < 7.2).

This is the first time his PSA was checked since March 2018 when it was 11.22 ng/ml

Questions:
1) Given your extensive knowledge, can we say with reasonable confidence that his PSA of 11.22 in March 2018 was due to his UTI's from Dec 2017- March 2018?

2) Would you advise we check his PSA again in a couple of months to ensure that his current low value was not a temporary event?

Thank you,
Zent





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