Low PSA with a Gleason 8 diagnosis

I was diagnosed with prostatitis and BPH (Benign Prostate Hyperplasia) in 2001, but since my PSA level remained around 1.5 for the next seven years, my primary care physician always assumed it was simply an enlarged prostate she was feeling via the DRE (Digital Rectal Examination) at my annual physical.

In September 2008 I experienced a bout of hematuria (blood in the urine), which led to an appointment with a urologist, which led to a biopsy and cystoscopy in late 2008. The biopsy revealed 11 cancerous cores (out of 12 samples) and a Gleason grading of 4+4=8, i.e., aggressive PCa. My PSA was still 1.5.

Upon finding a lesion in my urethra via cystoscopy, my urologist subsequently performed a urethral biopsy, which revealed (to quote my urologist),"extensive cancer," staging me as T4N0M0

In the memorable words of the same doctor, "You're definitely not a candidate for surgery--and I'm a surgeon" since the cancer was very close to my urethral sphincter. At the time of diagnosis he prescribed Casodex, an anti-androgen at triple the normal dose (150 mg/day), which I stayed on for two months, and resulted in significant shrinkage of my prostate. In March 2009, we ended the Casodex, and I received a one-year implanted dose of Vantas, a LHRH agonist, aka androgen deprivation therapy (ADT). At that time I was also diagnosed with osteopenia, a precursor to full-blown osteoporosis, so I enjoyed three years of quarterly Zometa infusions.

I began Radiation therapy (RT) in April, 2009, which consisted of 25 sessions of intensity-modulated RT (IMRT) pus 17 sessions of image-guided RT (IGRT), for a total of 79 Grays of radiation. The Vantas did not decrease my testosterone sufficiently, so I went back on Casodex. In March 2010, I became the first patient in my doc's practice to start on Firmagon, which was quite effective and I continued with its monthly injections for 2 more years. My last monthly injection was February 2012.

The very good news is that my PSA became undetectable in November 2009, and it has remained undetectable ever since. (Most recent test: February 2016). The bad news is that even though I had my last Firmagon shot four years ago, I have also remained castrate ever since. So much for a "hormone holiday." My testosterone seems to have permanently left the station. Or in the memorable words of my doc, "It looks like your pituitary-hypothalamic axis is trashed." I have fewer hot flashes, but have night sweats almost every night. Needless to say, my libido has also left the station, but my wife has been amazingly understanding and we've found other ways to be intimate.

Since the cancer invaded my urethra, radiation directed there has resulted in a stricture, which needs to be treated via balloon cystoscopy every year or so. I will soon be learning how to do self-catherization, not because I'm incontinent but because I have to keep the pipe open. But it's really a minor tradeoff given the aggressiveness of my cancer

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  • Many oncologists leave their patients thinking quality of life via restored testosterone is a certainty after stopping adt or "taking a holiday." Your experience is a - sober - reminder that each of our treatment outcomes are unique and unpredictable.

  • My history seems like the flip side of yours. My GP found a nodule on my prostate by DRE when I had a physical on turning 55. My PSA was 2.4. He said the only way to know if it was PC was biopsy and referred me to a urologist. He said the same thing and if it was PC with early detection and prompt treatment there was chance of cure. I opted for biopsy which showed PC with a Gleason score of 8 (4+4). A literature search in 1999 showed with a radical prostatectomy I had about 48% chance of cure and without it probable aggressive mestastasis in a short time. I chose surgery because if that didn't work I could have a second shot at cure with radiation. I've posted my treatment history for the last 17 years. Good luck with your future treatment. The journey continues.

    It's not the years in your life, it's the life in your years. Live it!

  • Hi Craig,

    The PSA cutoff for a biopsy (4.0 when I was biopsied) was designed to find cancer in ~20% of that population. What many don't realise is that, while far less cancer is found at lower PSAs, the Gleason profile is not much different. High grade cancer can be found at very low PSAs. Just another reason why we need a panel of tests with more specificity. Not only to eliminate the 80% of biopsies that are negative, but to find agressive PCa that puts out little PSA.

    My own story is a bit odd. In 2000, I took advantage of an intensive company medical before retiring (age 52). The doctor told me that I'd probably have no prostate problems, because it was the size of someone in his 20's.

    Two years after retiring (age 54), I went to my doctor for a checkup & told him that I had some discomfort in the prostate region. He did a DRE. Said that the gland was enlarged - "normal" for my age. Visibly upset, he told me that there was a nodule. Blood had been drawn & the PSA came back as 0.8.

    In the week or so before I saw a urologist, I used a "prostate health" mix from a health store. When the urologist examined me, he said that my prostate size was that of a 23 year old. The biopsy came back negative.

    However, within a few 3-month visits, without the prostate gaining in size, the PSA had gone to 1.7 & then 3.0. My urologist used an out-of-state lab because so many labs were returning erratic results (>12 years ago - different now). Nevertheless, I asked for a retest. Within a week, it had gone from 3.0 to 3.3. So I had the biopsy & GS=4+3 was found. Later confirmed by pathology.

    I opted for surgery. Ironically, no cancer was found in the nodule. Supposedly, no cancer outside the gland, but it was very close to the margin. My first post-op PSA was 0.3 & 0.8 three months later.

    I still can't make sense of it. Without the (non-cancerous) nodule, my PSA of 0.8 might have caused me to put off my next PSA for years. Perhaps I should have asked for a 2nd biopsy when the PSA was 1.7? Things seem screwed up when, under the care of a urologist, & using PSA as the guideline for biopsy, cancer wasn't found until it was already GS=4+3 & invasive. Well, I got over it & moved on.

    I must admit that occassionally, I wonder what effect that first biopsy had on the sequence of events? I had blood in the ejaculate for well over a month. The procedure has to cause inflammation. There are some reports of "tracking", etc. It all seems so primitive.

    -Patrick

  • I have often wondered whether biopsy of the prostate gland before metastasis outside the prostate might not be the very event that allows early escape of prostate cancer tumor cells from the capsule of the prostate. And, without that event it might well be months or years before PC spreads outside the prostate on its own. Why isn't removal of the prostate and then biopsy used after PSA rise and DRE or scan or MRI confirms a tumor? Why can't a blood test tell if there are circulating tumor cells before biopsy?

  • I remember, years ago now, when I researched the PCa risk from vasectomy, that some follow-up studies reeked of damage control & political correctness. Unthinkable that men should reject vasectomy because of PCa risk. While the risk seems to be small for most men, a pair of studies convinced me that early age vasectomy (I was in my 20's) or 20 years since vasectomy (me too) were, indeed, risk factors. But the subject is essentially dead these days.

    Similarly, there was an unseemly rush to whitewash biopsies, IMO. The studies that recognized & quantified risk, found that risk to be very low, but there are an awfully large number of biopsies performed in the U.S. each year. & the subject of dormancy never comes up.

    At the beginning of the PSA era, PCa mortality actually increased. That wasn't supposed to happen. Lupron shots were so profitable that doctors were somehow able to rationalize early use. Early use evidently meant not only early resistance, but also accelerated mortality in some cases. When Medicare removed the profit motive, doctors rethought the wisdom of early ADT. Some still do it but most don't. The hump in the mortality curve is quite distinctive. After that hump, we see a steady decline in mortality, as expected, well below pre-PSA era levels. (That downward slope is the case for continued PSA screening.)

    The profit motive is, I believe, a barrier against moving out of the PSA era. Urologists make a lot of money from biopsies. In the pre-PSA DRE era, that was not the case. Urologists make no money from blood tests. With a test like the 4K test that I mentioned last week, their income would decline. The argument against a panel test, following an elevated PSA result, is: "Let's do a biopsy, just to be sure!" A biopsy is a sample - there is nothing "sure" about it. With a suitable panel test, I question whether a biopsy would even be needed.

    I'm not trying to trash the profession. Cognitive dissonance is a powerful thing. The guys who say that the current protocol is ideal, probably believe it & don't see the self-interest conflict. If Medicare insisted on a 4K test first, incomes would decline but most practitioners would, I hope, eventually admit that the old way was barbaric.

    -Patrick

  • What is a 4 k test?

  • The 4Kscore test is a blood test that gives you a percent risk score that reflects your chance of having aggressive prostate cancer. This test provides additional information for you to use, along with any other information like a PSA and DRE result, to decide on what might be your next treatment or diagnostic next step.

    If your risk factor score is low the chances of you having aggressive prostate cancer are also low so you might decide not to have a biopsy or to go to active surveillance if you have had a positive biopsy.

  • I don't know if I'd call the old way barbaric but it was crude. When I had my biopsy at age 62 in 2001 they took 6 samples and

    there was probably no set location for those but even if there was it's unlikely they would find a positive sample unless the cancer was already beyond the early stage. I know there is a better way to do biopsies these days- at least for cryosurgery.

    It requires full anesthesia and the number of samples is at least

    20 or more- they use something similar to battle ship if you remember that game from the 60's or 70's. It's much more likely to find positive samples if they're there.

  • Patrick, There is no evidence that a prostate biopsy contributes to the spread of prostate cancer. The needle used for a biopsy is designed so that it enters the prostate as a solid piece of metal; once in the prostate it opens up and "bites off" a sliver of prostate tissue and then closes and comes out again as a solid piece of metal.

    In the popular (not medical) world it is often discussed that the cancer cells track along the needle's path, but there is no evidence of this happening. Could it happen in some instances, yes it might and yes it certainly is possible that it did in your situation, but for you and at this moment it really doesn't matter. What is important is that you are where you are today and that is what you need to be concerned about.

    Looking back with even the smallest regret is simply a waste of your energy.

    A bigger issue for biopsies is the increasingly higher incidence of biopsy related infections we are seeing men get. These infections re sometimes life threatening.

  • Joel,

    The oldest paper on the subject of tracking/seeding is from Johns Hopkins [1]. Bastacky et al reported a 2% incidence of tracking, with another 3.7% being equivocal for extension along the needle track.

    In a recent review of the literature [2], Volanis et al looked at 26 papers where tracking was reported. They concluded that "the incidence of seeding appears to be <1%" With maybe a million biopsies a year in the U.S., "<1%" is hardly reassuring. The authors conclude that:

    "... seeding along the needle track is a rare complication after prostate biopsy. Its actual incidence is presently difficult to quantify."

    So we don't actually know how rare it is.

    -Patrick

    [1] ncbi.nlm.nih.gov/pubmed/201...

    J Urol. 1991 May;145(5):1003-7.

    Needle biopsy associated tumor tracking of adenocarcinoma of the prostate.

    Bastacky SS1, Walsh PC, Epstein JI.

    Author information

    Abstract

    We reviewed 350 previously biopsied completely submitted clinical stage B radical prostatectomy specimens resected between January 1, 1987 and December 31, 1988 in an attempt to identify the incidence of needle biopsy associated tumor tracking into periprostatic soft tissue. We identified 7 cases (2.0%) of needle biopsy associated tumor tracking, 3 in which the only tumor penetration in the gland was limited to the needle track. The maximal soft tissue extension from the biopsy site ranged from 0.1 to 1.2 cm. and approached the nearest soft tissue margin to within 0.5 mm. in 4 cases. In contrast to prior reports showing clinically evident tracking only with transperineal biopsies from high grade tumors, 6 of our 7 cases were of intermediate grade (in the glandular and tracking components) and 6 had transrectal biopsies. Needle biopsy associated tumor tracking occurred with core (14 gauge) and biopsy gun needles (18 gauge). An additional 13 cases (3.7%) showed some features of needle biopsy associated tumor tracking but they were equivocal. These findings have significant implications in light of recent proposals advocating serial mapping of prostate cancer using the biopsy gun with potential conservative observation of smaller tumors.

    PMID: 2016779 [PubMed - indexed for MEDLINE]

    [2] ncbi.nlm.nih.gov/pubmed/249...

    BJU Int. 2015 May;115(5):698-704. doi: 10.1111/bju.12849. Epub 2014 Oct 22.

    Incidence of needle-tract seeding following prostate biopsy for suspected cancer: a review of the literature.

    Volanis D1, Neal DE, Warren AY, Gnanapragasam VJ.

    Author information

    Abstract

    With the widespread clinical use of prostate-specific antigen (PSA), biopsy of the prostate has become one of the most commonly performed urological procedures. In general it is well tolerated, although there is some morbidity and risk of infection. In recent years, there have been increasing concerns that prostate biopsy may lead to tumour seeding along the needle tract. The aim of the present paper was to review the evidence on the prevalence of tumour seeding after prostate biopsy and to define the risk of this event in the context of current clinical practice. A PubMed literature search was conducted in January 2014 according to the Preferred Reporting Items for Systematic Reviews and Meta-analysis (PRISMA) statement. Literature was examined with emphasis on the incidence of seeding, clinical presentation and on risk factors including type of needle used, transrectal vs transperineal approach, as well as tumour grade and stage. In all, 26 publications were identified reporting needle-tract seeding after prostate biopsy. In all, 42 patients with needle-tract seeding were identified. In most cases, seeding was reported after transperineal biopsy of the prostate, while nine cases occurred after transrectal biopsy. Based on the reviewed series the incidence of seeding appears to be <1%. The increase in the number of biopsies and cores taken at each biopsy over the years has not resulted in an increase in the reported cases of seeding. In conclusion, seeding along the needle track is a rare complication after prostate biopsy. Its actual incidence is presently difficult to quantify. It is reasonable to advise appropriate counselling and take measures to reduce this event where possible; however, we do not advocate avoidance of biopsies as the benefits of appropriate cancer diagnosis and management outweigh any potential risks from seeding.

    © 2014 The Authors. BJU International © 2014 BJU International.

    KEYWORDS:

    biopsy; local extension; prostate; seeding; tracking

    PMID: 24958224 [PubMed - indexed for MEDLINE]

  • Craig, I discontinued Firmagon 4 months ago. Testosterone stayed castrate. Have been on testosterone replacement, 100 mgs injection every 2 weeks, for hypogonadism. Now have stopped Xtandi and Avodart. I am feeling much better, physically and mentally. I am trying this, as my psa went fom 0.35 to 2.4 in 5 months. I figure, if these drugs are causing me many side effect and seem to be failing, let's see what happens over the next few months. My psa may rise, but what if it doesn't!!! I get blood tests every 2 months and both of my doctors are watching this with much interest. I have always been a rebel and am fortunate to have doctors that respect me and are willing to listen to my reasoning. If nothing else, I am enjoying my vacation already. If it has negative effects, I don't know at this time, what is next. I have it noted in my file that I will never have radiation or chemo. My psa is 2.4 and my testosterone is 22.

  • Thank you for your various replies which form a fascinating thread that demonstrates the diversity of both the men with PCa as well as the diversity of the disease itself.

    I have stood vigil at the bedside of a friend diagnosed and treated too late, and who died an excruciating death from a very aggressive form of this disease.

    I have also had the tremendous opportunity to be a Consumer Reviewer for the Prostate Cancer Research Program, reviewing research proposals that have—and will—make an important impact on transforming advanced PCa from a death sentence into a manageable chronic disease. During that time I have been privileged to meet and work with some of the really, really smart and creative scientists and doctors who have dedicated their careers to conquering this cancer.

    Among the top goals of today's research are getting beyond the PSA regime and eliminating the uncertainties inherent in biopsies. Progress is being made on both fronts, but we are not there yet.

    If I have learned nothing else from these two very different experiences, it is that PCa is an enormously complex array of diseases that manifests itself from barely discernable to rapidly lethal. One other thing I know: there will be no single solution that will be applicable to every man with this disease. But progress on many fronts will continue to be made.

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