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Cancer: Prostate Message Board

Cancer: Prostate Board Index

Hello Members,

Thank you for reading my message.

My father is 81 years old and lives alone. He was diagnosed with Recurrent Urethral Stricture in 2001 by his Urologist. He was on Tamsulosin and Darifenacin for a lot of years and was fine until Sept 2016, when he had pain in the entire penis shaft and part of his pelvis just above the penis. He rated the pain as 3/10. In Oct 2016, his PSA was 0.522 and the ultrasound of the kidney and abdomen was normal(with a normal prostate). His Urologist did a flexible cystoscopy and dilated his stricture and he had no pain until Dec 2017.

In Dec 2017, he had a penis pain of 3/10 and EColi infection in his urine. After antibiotics and repeat urine cultures, the urine was clear. An ultrasound of the kidney and abdomen in Jan 2018 was normal(with a normal prostate).. For the last three months, his penis pain has been 1/10 or 2/10 and his Urologist prescribed him some creams, which helped.For the last two days, his pain stayed at 2/10 and so went to see the Urologist again. The Urologist is doing a flexible cystoscopy on Monday, March 19. Several blood tests were done today. The following values were abnormal and they worry me a lot:

1)[B]Prostate Specific Antigen(PSA): 11.22 (0-6.5)[/B]

2)Prothrombin PTE: specimen blood citrate - clotting assay - 14.2 (9.5-12.5)

3)Urine ph - 7.5 (Acidic)


•Urine leucocytes: Present

•WBC pus cells: 10-15 (3-5)

•RBC - 2-4(0-1)

•Epithehleal - 1-2 (2-3)

•Remarks: Bacteria seen

He has no other symptoms. No pelvic pain or issues with urination. The urine stream is fine, no burning sensation or dibbling, change in skin color or discharge. His primary care physician does a physical every six months. The last physical was done a week ago and the tests of Complete Blood Count, Urine, Lipid Profille, HBA1C were all normal. He is 5 ft 3 inches in height, weighs 125 lbs, with a waist size of 36 inches. He walks twice a day and uses his exercise bike once daily. He is physically and socially active and eats a healthy vegetarian diet.


1) In a span of 15 months, his PSA has jumped from 0.522 to 11.22? I am very worried as a [B]21 fold increase in his PSA over 15 months[/B] could be an aggressive form of prostate cancer? What are your thoughts?

2) What specific tests should be done to get further information? 3D MRI of prostate? DRE? Biopsy?

3) I will be talking to his Urologist on Monday after his cystoscopy. What questions should I ask him about his PSA of 11.22?

Thank you,

Hello IADT3,

Thank you so much for such a detailed and helpful reply!!

I will certainly ask the questions you described in your reply to my father's Urologist this week. I will ask about DRE and repeat PSA testing and probably a newer antibiotic for his bacterial infection. In December, when a EColi was found in the urine culture, he was on Nitrofurantoin for a month. The repeat culture in January showed no bacteria. It seems like he has a new bacteria as you stated.

My father had had the same urologist ever since his diagnosis of recurrent urethral stricture in 2001. The Urologist has always stayed away from any surgical procedures for my father's urethral strictures (like urethroplasty) and had him on Tamsulosin and Darifenacin for almost 15 years without much issues for my father. The Urologist is thorough in testing etc.

If you don't mind, I have some follow-up questions for you:

1) How well can a Urologist see the prostate when a cystoscopy is done? Is the resolution as good as a trans-rectal ultrasound? I am asking this because my father's hospital probably does not have a multi-parametric MRI (have not checked - has regular MRI's, CT and PET scans), but probably has trans-rectal ultrasound.

2) If a prostate looks suspicious during cystoscopy, is a trans-urethral biopsy as good as a trans-rectal biopsy in selecting parts of the prostate that may have cancer? Since a cystoscopy is being done currently, if the prostate looks suspicious, does it make more sense to do a trans-urethral biopsy now?

3) The Urologist has not performed a DRE on my father for 10+ years. He would do periodic (once in 6 months) ultrasound of his abdomen and kidney and urine tests to check on his strictures. The ultrasounds always had a normal prostate and my father has never had any prostate issues before. I realize DRE is a quick test in the office, but if the prostate is better visualized in a cystosocpy, is a DRE needed?

4)My sense from knowing my father's Urologist is that he will dilate my father's stricture tomorrow, prescribe antibiotics for a month or so and then repeat the urine culture and PSA. Is this adequate for now?

Thank you!!
Hello IADT3,

My father was discharged today. He has been on antibiotics since Monday and will continue taking them. Urine culture was also done on Monday. The reports of culture must be available by Monday, but the biospy might take more time. My father was asked to see the Urologist on Monday.

The pelvis MRI is 1.5 T with an array coil. The cystoscopy was done a few hours before the MRI. I am not sure how that would affect the MRI accuracy. As per my amateur readings on PubMed, 1.5 T with an array coil is on par with 1.5 T with an endorectal coil. It may not be as good as a 3T Multiparametric MRI. The MRI report is described below:

[B][U]Plain and Contrast Enhanced MRI of the Pelvis[/U][/B]

[B]Clinical Indication[/B]: Raised PSA levels. To rule out Prostate Cancer.

[B]Comparison[/B]: none
Technique[/B]: Using a phased array coil, small field-of-view imagining of the prostate was performed using the following sequences: axial T1-weighted, axial T2-weighted, sagittal T2-weighted, oblique coronal T2-weighted, diffusion-weighted.

Axial T1-weighted images with and without fat suppression through the prostate were obtained before and dynamically after the intravenous administration of contrast.

Using a large field-of-view, the entire pelvis to the level of aortic bifurcation was imaged with the following sequences: post-contrast fat suppressed T1-weighted, diffusion weighted, fat suppressed T2-weighted, STIR.


[B]Prostate:[/B] Size 3.2 x 2.8 x 3.9 cm

Volume: 17.472 cc

Area of altered echotexture; hypointense on T2w; showing restricted diffusion noted in the left hemigland. Area measures 19 x 11.22 mm. No extracapsular extension.

[B]Seminal vesicles[/B]: Normal signal on T2-weighted images in bilateral seminal vesicle. No abnormal enhancement.

[U]Extracapsular extension[/U]: No loss of interface with the right neurovascular bundle.

[U]Bladder[/U]: Normal wall thickness and signal intensity. No invasion.

[U]Lymph Nodes:[/U] No pelvic lymphadenopathy noted.

[U]Bones[/U]: Normal in signal intensity.


Area of altered echotexture; hypointense on T2w; showing restricted diffusion noted in the left hemigland. Area measures 19 x 11.22 mm. No extracapsular extension.

Suggested histopathological evaluation.


If you don't mind, I have a few questions again:

1) I have read in your earlier posts that restricted diffusion on a MRI is a classic sign of cancer. Also, my father's prostate volume has decreased from a 23 ml on Jan 8 to 17.472 ml on March 19. I have read on PubMed that cancers are usually found in lower prostate volumes rather than higher. Given the above facts, do the abnormal findings below in the MRI mean a cancerous tumor of 19 x 11.22 mm?
Area of altered echotexture; hypointense on T2w; showing restricted diffusion noted in the left hemigland. Area measures 19 x 11.22 mm. No extracapsular extension.[/B]

2) I am certain that the biospy was a TURP and not a MRI-fusion biopsy. The MRI was done on March 19 and the biopsy on March 21. Without the software for fusing MRI images on a rectal ultrasound, can an experienced Urologist biopsy the right parts of the prostate using TURP when the MRI says, "showing restricted diffusion noted in the left hemigland. Area measures 19 x 11.22 mm"? The concern here is that TURP being a random biopsy will miss high grade cancers if the Urologist is unable to biopsy the suspicious parts of the prostate.

3) Given the results of the MRI, can we make any judgements about metastasis and lymph node involvement?

Thank you!!
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,
Hello IADT3,

Sorry to bother you again! I have a question about my father's persistent penis pain. If you have any insights about it, I am eager to know:

My father first had pain in his penis (a 4 on a scale of 1 to 10) in Dec 2017. His Urologist did a Urine culture and the results indicated EColi infection greater than 10000 CFU/ml. Antibiotics were given and a repeat urine culture in January was normal.

His pain oscillated between a 1/10 and 2/10 in February and March. He was prescribed a few creams which made the pain manageable. When the pain persisted at 2/10 for a couple of days in the third week of March, the Urologist ordered urine and blood tests (11.22 PSA, positive for bacteria, urine had elevated WBC and leukocytes). A cystoscopy was performed on March 19, which did not find anything abnormal.

The elevated PSA took us down the path of ultrasound, MRI and biospy. For about a week after his cystoscopy (March 19- March 26), he felt no pain. This might be due to all the NSAID's he was give during his 5 days hospital stay (March 19-March 22).

His pain returned on April 2 and is currently between 1/10 and 1.5/10. Since the last few days, the pain is felt more in the tip of his penis than shaft. He saw the Urologist on April 9 and when I emailed his Urologist, he said that the pain will slowly recede. My father has no growth, no discharge, no changes in skin color or redness/rash or anything of that kind on his penis. He has no pelvic pain. His urine stream is fine.

My father had a similar complaint of penis pain in Oct 2016 and a cystoscopy was done in Nov 2016. He had no pain in his penis from Nov 2016 to Dec 2017. So, I am unsure why the pain is persisting so far.

1) Does UTI in December explain the penis pain in Dec-Jan?
2) Does the detected UTI on March 17 explain the penis pain in Jan-March?
3) Since several antibiotics have been given March 17 for his UTI, can the Cystoscopy itself be the cause of his current penis pain due to inflammation of his urethra ?
4) Any other reasons for his persistent pain? I would be grateful for any comments from you.

Thank you!!

Hi again Zent,

This is a reply to your post of April 15.

I learned a lot more about prostatitis. However, I'm not sure what I learned will be of much help. One lesson was that prostatitis is an understudied area, unlike prostate cancer. Apparently there is no really good treatment for most prostatitis, though existing treatments often help somewhat, and, for the infrequent cases caused by bacteria (8%, which surprised me), antibiotics often are highly effective.

Here are my responses, as a layman, to your questions.

1) Possibly, but there are other explanations.

2) The same answer as 1).

3) The speaker identified "trauma", giving biopsy as an example, as sometimes the cause of inflammation and/or pain. My layman's impression is that a cystoscopy could similarly result in "trauma" and be the cause of your father's pain, but I have no idea how likely this would be, and the research seems scanty. I did a search - one of several - of using - cystoscopy AND penile pain - and filters for Abstract, Humans, Male, Aged: 65+ years, Adult: 19-44 years and found 37 papers. One paper, at, indicated a very low incidence for patients having a catheter, which is about as close as I could get. ("Iatrogenic" in the paper's title means "caused by a doctor".) Though rare, at least with catheters it does happen.

4) I also heard that what actually causes prostatitis is that you have to be a susceptible individual - anatomically, genetically, and then you have to have an event; that event could be an infection. It could be a trauma; that trauma could be a biopsy. It could be sitting on a bicycle seat. It could be radiation. It could be an radical prostatectomy, a TURP. All these things could start it. And then a cascade of events occurs, either an infection, or your immune system starts to act up and causes sort of an arthritis of the prostate. Nerves get involved, they get more active; muscles get involved; you have spasm. And then you end up with a disabled patient with chronic pelvic and prostate pain.

Sometimes the pain is caused by nerves and is not related to infection or inflammation. Some of us even have prostatitis symptoms when we no longer have prostates. Removal of the prostate is not encouraged with the idea of a side benefit (or main purpose) of curing prostatitis. Some have a lot of pain after removal of the prostate to cure prostatitis.

In other words, what I learned is it not only did not work, it made things worse. It was noted note that this was not based on studies. That leaves open the possibility that such a prostatectomy to relieve prostatitis might work some or much of the time but that some men do not benefit and seek out a specialist in prostatitis pain. The doctor stated his experience might mirror reality. He said there were some treatments that help somewhat with pain that was caused by nerves (neuropathic).

Regarding PSA, apparently it takes about six months for PSA to come back to normal when the cause of prostatitis is bacteria that have been effectively treated. If there is chronic prostatitis, PSA will be all over the place and won't be useful as a warning for prostate cancer.

Published research has found that the drugs finasteride and dutasteride (Proscar and Avodart in the US) tend to help reduce the risk of developing prostatitis and help make it less intense.

I hope this helps.
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: .

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: (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: Here’s another study that reaches the same conclusion: I got these from searching 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

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