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Harv V lives in North Carolina, USA. He was 52 when he was diagnosed in February, 2009. His initial PSA was 3.00 ng/ml, his Gleason Score was 6, and he was staged T1c. His initial treatment choice was Surgery (Robotic Laparoscopic Prostatectomy) and his current treatment choice is None. Here is his story.

THERE WAS NO RESPONSE TO AN UPDATE REMINDER IN 2014 SO THERE IS NO UPDATE.

After three years of PSA tests exceeding 3, my Urologist thought it was too high for someone my age and arranged for a biopsy. My first biopsy, two weeks after my PSA reading of 3.0, came back HGP (High Grade PIN). I opted for a second confirmatory biopsy soon thereafter. This one came back with one core positive. Immediately, I thought I would go to one of the major university medical centers for a radical prostatectomy. My local Urologist seemed taken aback that I would not have his small practice do it in the local hospital, but I didn't want to entrust such a surgery to a small-practice surgeon doing a small number of RLPs.

I spoke to several surgeons in the region at major university medical centers Duke and UNC. All but one recommended that I should have the tumor destroyed soon via one method or another. The exception was a surgeon who was salaried and noted that he had nothing to gain by advocating any particular treatment option. He suggested that I look seriously at the active surveillance option.

Ten weeks post-biopsy, I had my PSA drawn by my PCP and analyzed by the same lab. It had shot up to 5 from 3 (a 67% increase!) in just 18 weeks and, being aware that PSA velocity was an indicator for action, I panicked. [Whilst Harv's reaction is understandable, PSA can vary signficantly over a short period of time - see this experiment and PSA 101.] I returned a doctor I had spoken to previously. He assured me that the PSA is NOT a good measure and I shouldn't be looking at it over such a short time-frame, and it could even be high due to irritation from the biopsy 10 weeks before. If PSA is not a good measure, then I figured there's no way I'm going to pursue active surveillance using PSA as my signal to treat the cancer, on such a sparse time frame. He mentioned his work in focal cryotherapy. This is where, for select patients, he thoroughly maps the prostate (think 60-80 cores!!) and freezes the cancerous tissue, leaving most of the prostate functional. [One of the YANA mentors, Steve Z had this kind of biopsy and focal cryotherapy.] But my concern over the risk that biopsies pose for leaking cancer cells or letting them escape into the bloodstream quickly eliminated that possibility. That concern/paranoia is based on the question of--how does prostate cancer persist after a prostatectomy where the margins are all negative? To me, biopsies seem like the most likely avenue for escape, and for my low-volume, low Gleason statistics, I'll try to avoid biopsies. [The question of tumours being spread by biopsy has been discussed many times. There is no clear answer and although there is a good deal of merit in what Harv has to say, logic indicates that with the very high number of biopsy procedures being carried out since the use of PSA for tests, the number of diagnosed prostate cancer cases would have climbed rapidly. It has not.]

Two weeks after my high PSA test, I took a confirmatory PSA test, which showed my PSA had dropped back by 20% to 3.9. Both tests were analyzed by the same lab, and I had been easy on my prostate (celibate, no bike-riding, no bowel movements) for at 48 hours before each test. I can now see that FREQUENT PSA readings might be helpful--within a year I would have 12 data points, one per month, where I could see the normal variability of PSA, and presumably at some point, I would be able to see an abnormal rise and be able to take action sooner than I would be able to by monitoring semi-annual or annual PSA measures.

I next went to see a surgeon at Johns Hopkins.. He quoted me a 75-80% potency rate w/o meds at 24 months and >95% continence rate, and noted that the various surgeons there have the same success rates. [It is important when discuss rates of potency and continence to establish just how these are measured and how they can be demonstrated. Many studies use definitions that would not be accepted by most men as adequate.] I asked him about focal procedures that treat only the cancerous portion of the prostate, and he replied that prostate cancer tends to be multi-focal, so he did not favor focal procedures.

I returned to Duke where I met with a team comprised of a medical oncologist, urological surgeon, and radiologist. Perhaps this is where I should have started. All were down-to-earth, straightforward, and open to my ideas about treatment. The surgeon was amenable to my monthly PSA active surveillance. The oncologist confirmed the non-existence of evidence that biopsies leak cancer. He noted that a classic Swedish study found that the death rate for men my age who were on active surveillance protocols was twice as high as those who had chosen surgery, 20 years down the road. [It is not clear as to which study is being referred to here. The Swedish Holmberg study titled A RANDOMIZED TRIAL COMPARING RADICAL PROSTATECTOMY WITH WATCHFUL WAITING IN EARLY PROSTATE CANCER showed that while radical prostatectomy significantly reduced disease-specific mortality, but there was no significant difference between surgery and watchful waiting in terms of overall survival. (N Engl J Med 2002;347:781-9.)] So, he believes I should be treated soon.

Finally, I met with the Radiologist, who informed me about IGRT (Image Guided Radiation Therapy) and IMRT (Intensity Modulated Radiation Therapy). My concept of radiotherapy was outdated and I hadn't realized that radiation could now be focused in a fixed three-dimensional area the size of the prostate. I asked about proton beam therapy, as a "Brotherhood of the Balloon" uncle has been touting this approach and he was pleased with it, having had the treatment years ago. The Radiologist's reply was that proton beam was attractive at one time, but since the advent of IGRT/IMRT that can confine the radiation to a small mass, the proton beam therapy no longer has that advantage. I have read the BOB advocate book "You Can Beat Prostate Cancer" and it does seem quite biased (as expected) and outdated, especially in its depiction of RP surgery (blood transfusions and all). Furthermore, I understand there is still no evidence that PBT produces superior outcomes (except, perhaps, in profit!). Still, I was unhappy about the prospects for retaining continence and potency from IGRT/IMRT since the goal is to eradicate the cancer and in so doing, tends to cook the margins that hold the nerves that drive potency and continence.

At this point, I am pursuing my monthly PSA monitoring active surveillance while I look at advances in RP that suggest superior margin, continence and potency rates and try to separate the truth from hype.

UPDATED

August 2009

Update Aug '09:

After my last contribution, I consulted with surgeons elsewhere in the country who claim very high 1-year post-surgery continence and non-medication potency rates due to athermal and other newer techniques. However, other surgeons do not know how these high rates can be achieved, even with the newer techniques. I read an account of a patient who was never surveyed by one of these super-achieving surgeons post-surgery, so I wonder if patients are surveyed selectively.

I found this article from Johns Hopkins. It is worth a read and suggests that "vitamin D is a most promising area for prostate cancer research.". I started taking larger doses of Vit D3 hoping that this might help to keep the cancer in check.

UPDATED

July 2010

I continue to closely monitor my PSA and Vitamin D3. My PSA stayed low at 3.2 until I stopped taking 50K IU of Vitamin D3 per week (instead, I was taking 1K/day per my primary care physician). My PSA then shot up to 4 the next month. I resumed taking 5K IU/day and after another month my PSA settled down to 3.2-3.4. It has stayed there since, and I am now getting both PSA and Vit D3 checked every other month. I've just noticed this pattern between D3 and my PSA levels with me, real or coincidental. Certainly, the studies e.g. Johns Hopkins (previous update) support the possibility of the link being real.

For me, Vit D3 supplements pose problems in that some metabolite of the D3 or the increased calcium uptake from the D3 causes unquenchable thirst at night. For this reason, I try to expose my skin more (easy in the spring & summer), which is worse for my skin but I think better for my health.

As I've said before, I am careful to have my PSA drawn under similar circumstances. No exercise that puts pressure on my prostate (e.g., cycling) or sex within 48 hours of the test; both of these can cause an increase in PSA in the blood. Also, if I have a bowel movement, I will wait for another day as I believe this, too, puts pressure on the prostate.

I read the book "Anticancer: A New Way of Life" by David Servan-Schreiber and have tried to adopt its diet and exercise regimen to the extent feasible. I recommend it.

As my oncologist recently pointed out, when I started this adventure with early PCa, the rule was to get rid of the cancer and the exception was active surveillance. Now, he says, it's exactly the opposite--a surgeon has to have a much better reason for a prostatectomy than simply the presence of early PCa. A lot changes in a year...

UPDATED

July 2011

Over the last year, my PSA gradually increased from a steady 3.4 to 3.9, despite my Vitamin D therapy. In May, I had another biopsy, my first in over three years, and that unfortunately showed a Gleason 3+4 in one core and more positive cores than found previously.

I am now at the point where I am no longer low risk, but still believe surgery or radiation is over-treating these small tumors. Immunotherapy for intermediate-risk PCa is not available in the US; nobody is even conducting any clinical trials on it yet for intermediate risk. Yet I'm not confident enough to wait another several years until someone, somewhere, has an effective immunotherapy program for lower-risk PCa. So, while I really believe it's overtreatment, I will most likely pursue surgery at Duke or UNC in the next couple of months.

UPDATED

December 2011

I had RLP in late July, 2011 at University of North Carolina medical center. Surgery went well. Pathology showed positive margin in one small area, but no indication that cancer had spread from the capsule.

Many complications followed surgery; total blockage 2 weeks post-surgery resulting in ER visit and catheter again for another 2 weeks, multiple strain-resistant UTIs, and then bladder neck contracture. The contracture was caused by scar build-up, which gradually blocked the urethra. A minor but rather painful urethral dilation procedure stretched the scar tissue, followed by another cath for a week. This was followed by daily self-caths for a month or so to ensure the urethra stayed open.

At this point, I have moved my care to a local practice, as my post-surgery experiences with continuity and coordination of care were below expectations. My PSA is zip and I have no significant problems with incontinence, but ED is as expected.

UPDATED

April 2012

My PSA is still 0 and I am no longer encountering unexpected side-effects

UPDATED

June 2013

Continuing to improve. No evidence of PCa. Only minimal leakage after lifting heavy objects. ED improving although some nerves still MIA and libido is very low.

Harv's e-mail address is harvhealth at (replace "at" with @) yahoo dot (replace "dot" with .) com


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