One Active Surveillance journey, thus far:
2002: Had a biopsy in response to PSA increases from 1.6 in 1994 to 4.6 in 2002 (statistical doubling time 8 years). Results negative. PSAs affected by acute prostatitis attack.
2006: PSAs continued to slowly rise to 5.5 in 2006. Statistical doubling time remained about 8 years. Repeated milder prostatitis episodes. Repeat biopsy May 2006: 1 core positive, less than 5%, Gleason 3+3. Upon first biopsy in 2002, had done considerable research as to prostate cancer and treatments.
Had previously decided if ever diagnosed, would select Da Vinci surgery by Dr. Mani Menon, Detroit, one of the early Da Vinci "artists". Sent diagnostics to Dr. Menon along with biopsy slides for second opinion on pathology (confirmed Gleason 6). Dr. Menon responded that although I was a good candidate for Da Vinci surgery, with a very early low-level cancer I could also consider, with minimal risk, doing nothing for the immediate future. This resulted in my pursuing more extensive research into prostate cancer-- diagnosis, growth kinetics, treatment options, and, what the heck is Active Surveillance...
June 2006 to January 2007: Had consults with a conventional surgeon, a cryoablationist, proton radiologist at Loma Linda. Had an endorectal MRI with spectroscopy at UCSF (one small area 'suspicious' for cancer in same quadrant as positive biopsy), and a color Doppler Ultrasound (CDU) by Dr. Bahn in Ventura (single lesion identified in right mid PZ, 8x6 mm, right mid to base, probable biopsied tumor, no significant blood flow). Dr. Bahn suggested Active Surveillance or focal cryotherapy.
With spouse reviewed research, consults, imaging results. Decided to defer treatment while pursuing Active Surveillance. AS protocol- quarterly PSA, annual % free PSA and PAP (prostatic acid phosphatase, potential indicator of metastasis), periodic CDU scans, compute PSA density from PSA and CDU prostate volume. Set up Excel spreadsheet to track PSA kinetics, including linear model used by Sunnybrook, Toronto, for following AS patients. Addressed diet (drastically reduce dairy products, further reduce red meat), Started low-dose generic lovastatin to reduce LDL (dropped from 150 to 75; total cholesterol from 200 to 130). Dropped average weight from 170 to 155. Tested for serum vitamin D and found low (21.8). Increased Vit D3(OH) to average of 50 by D3 supplements, gradually increasing to 10,000 IU/day.
2007-2009: PSAs bounce up and down between 4.16 and 7.24; average about 5.8. Elevate during prostatitis episodes; drop with Leviquin treatment. Statistical PSA doubling time drops to over 20 years but with very low correlation coefficient (i.e. no real trend). Prostate size 58 to 62 cc. PSA density between 0.07 and 0.12; % free PSA stays around 15%; PAP stays less than 2.0. Series of CDU scans indicated suspected 'index tumor' has slight increase in size and vascularity. Another potential lesion noted near right base- believed to be due to prostatitis, no signs of lesions outside of capsule or near neurovascular bundles, no nodules found on DRE.. 2008 request for repeat biopsy postponed due to noted prostate inflammation.
March 25 2009: PSA 5.66, prostate volume 60 cc, PSAD 0.09, no DRE nodule. Repeat biopsy using CDU to target suspicious areas. In addition to the 'index tumor' and previously noted potential lesion, a third site identified by CDU sampled as well as 5 other cores for spatial sampling.
Right base:CDU- 9x4 mm, no vascularity; biopsy- Gleason sum 6, 40 or 60% (Bostwick) involvement, DNA ploidy.
Right base to mid: CDU- 12x6 mm, 2+ vascularity; biopsy Gleason 6, 10% involvement.
Right apex: CDU- not seen; biopsy- Gleason 6, 15% or 10% (Bostwick) involvement Left mid: CDU- small, nonspecific; biopsy- less than 5 mm ASAP or Gleason 6 (Bostwick)
Consult and decision: Cancer multi-focal in right hemisphere, very small lesion in left may be ASAP (Atypical Small Acinar Proliferation - a condition that is sometimes misread by inexperienced pathologists as adenocarcinoma or cancer) or Gleason 6. Stage now T2c Decided to reassess in 6 months after followup CDU and MRSI at UCSF.
July 6 2009: MRSI at UCSF, 3.0T magnet. "Stable right to mid gland prostate tumor with corresponding metabolic abnormalities seen on spectroscopy. There is no evidence of extracapsular invasion or lymphadenopathy". "...no evidence of seminal vesical invasion." Specific results identical to January 2007 1.5 T scan: Tumor estimated as 13 x 6 x 1 mm, 0.4 cc, small size 'close to the limit of resolution of spectroscopy." Although the results of the March biopsy were provided, the MRSI found no evidence of any but the original index tumor.
October 29 2009: CDU No significant change since March for lesions in right base, right base to mid (index tumor); right apex 5x7 mm; left mid small. No changes in vascularity. PSA 6.3, prostate volume 63 cc. PSAD 0.1, no nodule detected on DRE. Sample taken for PCA3 urine test; result 47.3.
Consult and decision: CDU results show no progression in any of tumors since March biopsy. July MRSI showed no change in index tumor since January 2007 and could not detect the other biopsy-determined tumors. Upon review of all current papers on PCA3, it appears that no current study shows any correlation between PCA3 levels and cancer Gleason sum or volume upon biopsy or surgical pathology. No statistical change in PSA trend. Although cancer is clearly multifocal, all evidence is that it continues to be slow growing. Decided to reassess in 6 months.
May 26, 2010: CDU No change in size or vascularity in tumors in right base right base to mid. Right apex.6x4 mm. Left mid 6x6 mm. PSA decreased to 5.2 January 28, then back to 6.4. (May 11)-- essentially no change in trend. Prostate volume 63 cc, PSAD 0.1. PAP 1.5 on May 11. No value seen in a repeat PCA3 test.
Consult and decision: No evident change in tumors in last 14 months. Decided to continue AS. If no change in PSAs, repeat CDU at 12 months. Meanwhile continue evaluation side effects and cancer control for treatment options.
Last November/December I participated in a clinical trial at UCSF testing a new intravenous contrast agent for prostate endorectal MRI scans. A KGO TV news report on the trial is available.
I was in an early group with the lowest concentration of the pyruvate contrast agent and it did not improve the MRI resolution for my tumors This may be due to the small tumor size (the largest is only about 0.4 cc) and low Gleason (3+3). However, the researchers are encouraged that the results are improving with higher pyruvate concentrations.
The clinical trial is still recruiting. I'd encourage anyone on Active Surveillance with no prior treatment to consider participating. It involves two endorectal MRI scans- the first a baseline study with spectroscopy and the 3.0 T magnet. Then a scan with the intravenous tracer. I had no side effects from the tracer.
For more information on the trial, contact UCSF: Christopher Soto at 415-353-9452.
However, with my small tumors and low Gleason, I still find the color Doppler Ultrasound scans with Dr. Duke Bahn (Ventura CA) more informative than the current endorectal MRSI scans. Hopefully the final results of the UCSF clinical trial will show the experimental contrast agent to provide significantly higher resolution for small early tumors.
My latest PSAs are in the high 6's low 7's, up a bit from the prior two years (bounces between 5 and 6.5). I'll be getting another color Doppler Ultrasound scan this spring to check on the little beasties.
Meanwhile life is good! I'm building a new kayak, re-building an old expedition-grade strip canoe built in the mid '70s, and cross country skiing when the current series of storms in the Sierras abate enough to let us get up to the high country.
The Best to You and Yours!
Jon in Nevada
April 2011: Annual color Doppler Ultrasound (CDU) by Dr. Bahn shows little change in previous lesions. PSA bouncing between high 6's and low 7's. PCA3 urine test increased from 47.3 (2009) to 71.3, a potential sign of progression, but literature on the value of specific PCA3 scores for indicatiing aggression continues to be rather ambiguous.
April 18 2012- PSAs now in the range of 7 to mid 8's with no specific indications of prostatitis. Annual CDU imaging by Dr. Bahn. We agreed that it was time for a repeat biopsy using CDU to target the individual lesions. Biopsy pathology by Bostwick Labs with personal review by Dr. Bostwick. Pathology suggests progression of cancer. 65% of core in right base cancer; Gleason 3+4, 10% of cancer pattern 4. 50% of core in right-base to mid Gleason 3+4; 40% pattern 4. 3% of core in right mid Gleason 3+3, 12% of core in left mid Gleason 3+3. Some good news- DNA ploidy still diploid, CDU shows no sign of penetration of seminal vesicles, perineural invasion, or penetration of prostate capsule. Biopsy results due to progression or sampling different tissue than in 2009? Uncertain. Discussed options with Dr. Bahn and decided to start Avodart to shrink prostate as 65 cc may be too large for brachytherapy if that treatment is decided.
May-June 2012- PAP test 2.9, an increase from 1.5 in 2010. Real increase or within PAP analytical variance (was 2.1 in Sept. 2009, 1.6 a month later)? Will do another PAP test in July. Review of PSA kinetics for period 2009 to present indicates doubling time of 5.6 years. Not bad but with current values in mid to high 8's, a PSA of 10 is predicted in 18 to 24 months.
Time to move on from AS! All indications are that the cancer has progressed from the initial 'very low risk' in 2006 to now intermediate risk. My trigger points for moving from AS to treatment always were the presence of significant Gleason pattern 4 in a biopsy and/or a PSA of 10.
Proceeding with consults for brachytherapy or CyberKnife radiation. Papers by the Prostate Cancer Results Study Group (2011, 2012) indicate 10 to 15 year cancer control by brachytherapy has been as good or better than surgery. Surgeons may argue, but my conclusion is that the reviews by this panel (which includes urologists, radiation and clinical oncologists, and pathologists) is about as objective as possible for our complex disease.
Dr. Katz (Flushing Radiology) has provided slides from a recent AUA presentation showing 5-year results by CyberKnife equaling or bettering surgery or brachytherapy. Will start with consults with local brachytherapy and CyberKnife centers and expand to 'centers of excellence' in Seattle and San Diego. Goal is to have treatment by the end of 2012.
May to December 2012: treading water in the U.S. health-insurance swamp.
With the April 2012 color-Doppler (CDU) targeted biopsy indicating progression of some of the tumors from Gleason 3+3 to 3+4, my PSAs rising to over 8, and the PSA doubling time for the past year decreasing from over 8 to 3.3 years, I decided to move from Active Surveillance to treatment. I started Avodart to shrink the prostate (60 cc) and potentially arrest progression while selecting treatment and obtaining insurance coverage. After considerable research, I decided upon Stereotactic Body Radiation (SBRT), specifically CyberKnife, and in June 2012 started the process with Dr. Jonathan Tay at Reno CyberKnife.
However, my insurance company, Government Employees Hospitalization Program (GEHA), one of the companies in the Federal Office of Personnel Management\'s (OPM) Federal Employees Health Benefits (FEHB) insurance exchange. denied Dr. Tay's pre-treatment authorization, saying the SBRT treatment of the prostate was 'investigational'. This was a shock as I had switched to GEHA in November 2012 because they told me in a telephone inquiry that SBRT treatment would be covered.
I started a rather long and frustrating process of appealing the GEHA denial, first with GEHA and ultimately with OPM, providing both agencies all the current medical literature on SBRT for prostate cancer. In January 2013, OPM's final review of my appeals upheld the GEHA denial, saying "... the use of stereotactic radiation therapy is considered investigational, not medically appropriate and is not consistent with standards of good medical practice in the United States..." But, during my appeal process I had contacted all the other OPM health insurance programs and found that the Security Agent's Benefit Association (SAMBA) was affiliated with Cigna, and covered SBRT for the prostate as per Cigna's Medical Coverage Policy Statement 0110, 6/15/2012. So, while OPM was upholding one of their FEHB insurance program\'s denial of SBRT, another of their programs did cover it. This inconsistency is contrary to OPM's own internal policy guidance on attaining consistency "in applying the experimental /investigational brochure exclusions" (OPM letter to FEHB program carriers, Letter 2001-27). Clearly the OPM reviewer did not consider the full range of available information on SBRT treatment of prostate cancer.
During the November 2012 FEHB Open Season, I quietly switched from GEHA to SAMBA, effective January 1, 2013. So the ultimate January 2013 OPM denial of my appeals for SBRT treatment by one of their supposedly supervised insurance carriers did not prevent me from obtaining treatment from one of their other carriers. Another example of the well-informed cancer patient's creed-- Persistance Pays Off.
Next: Avodart holding action on prostate cancer progression.
May 2012 to February 2013: Avodart holding action on prostate cancer progression
Dr. Bahn proscribed 0.5 mg/day Avodart (dutasteride) in April 2012 to reduce the size of my prostate (from 60 cc) in preparation for treatment and to potentially arrest further development of the prostate cancer while pursuing treatment. Although there has been some controversy in the past about use of 5-alpha reductase inhibitors (that inhibit conversion of testosterone to dihydrotestosterone) to prevent or arrest prostate cancer progression, increasingly in the past year studies have suggested that there is a positive effect on cancer progression.
Dosage: Avodart has a rather long half-life in the serum (blood) of 5 to 5 1/2 weeks. However, it can take up to three months to establish a steady-state serum concentration. I took Avodart daily through January 2013, then switched to 3/week. In May I dropped back to 2/week. I'll monitor my DHT levels at least quarterly-- the goal is to maintain the DHT below 6 ng/dl.
Data on my experience is listed below. Was Avodart effective in slowing my cancer progression? The PSA data and color Doppler estimates of lesion size and vascularity suggest a positive effect. However, the January CDU imaging suggesting the start of cancer infiltration into the prostate margin may suggest otherwise. As too often the case with our disease, my data are not conclusive. In oder to maintain consistent post-treatment PSA kinetics, my intention is to stay on Avodart for at least 6 months to a year after SBRT treatment.
Date Lab Results
04/18/12 CDU scan, targeted biopsy, prostate vol. 60 cc
05/23/12 PSA 8.9 ng/ml, PAP 2.9 ng/ml
05/21/12 Start Avodart
07/13/12 PSA 4.5, PAP 2.1, DHT 1.4 ng/dl, Total T 296 ng/dl, Free T 6.4 ng/dl
08/17/12 PSA 4.2, PAP 1.3, DHT <1.0, Total T 254, Free T 6.5
09/10/12 CDU, prostate vol. 53 cc, no change in size or vascularity of lesions
12/06/12 PSA 3.8, PAP 1.3, DHT <1.0, Total T 421, Free T 8.9
01/14/13 PSA 3.9, PAP 1.4, DHT 1.3, Total T 303, Free T 6.4
01/29/13 CDU, prostate vol. 50 cc. No change in size or vascularity of lesions but. for the first time, the largest (index) lesion suggests start of penetration into the prostate margin
Typo correction: in the preceding post regarding insurance issues, my switch to GEHA was November 2011, not November 2012.
Jan.- May 2013 SBRT (CyberKnife) radiation
Over the years, radiation treatments have become more effective in cancer control by increasing the dosage and thus damage to the cancer DNA. However, there is a challenging balance between increasing damage to cancer DNA from higher dosage versus increasing damage to surrounding healthy tissues. Stereotactic Body Radiation Therapy (SBRT) attempts to increase damage to cancer DNA by increasing the dosage in numerous individual radiation beams during each treatment (hypofractionation), while decreasing damage to healthy tissues by more precise beam control and lower total radiation dosage for the entire treatment. While a typical IMRT treatment plan may involve 40 sessions of about 2 Gray (Gy) each (providing a total dosage of up to 80 Gy), a typical SBRT treatment plan might involve only 5 sessions of 7 Gy each (more than 3 times the dose per session) but a total dosage of 35 to 36.25 Gy (half the total dose of IMRT or protons).
CyberKnife (CK) is one of several proprietary technologies for applying SBRT radiation using a computer-controlled linear accelerator mounted on an industrial robotic arm and near-real-time tracking of the individual radiation beams.
My CK treatment called for 5 sessions (T, F, M, T, W), each with 159 individual beams and the following total treatment dosages following a "homogenous" distribution plan:
Site/Organ Minimum Mean Maximum
in any part overall in any part
------------ --------- ---------- ------------
Prostate Target Volume 30.9 Gy 40.4 Gy 44.2 Gy
(Prostate + 3mm margin along the rectum, 5 mm margin elsewhere
Bladder 22.0 16.2 41,1
Rectum 19.4 11.5 37.4
Penile Bulb 3.1 7.1 14.1
Testes 1.8 2.9 2.5
Bowel 1.6 5.1 29.1
Right Neurovascular Bundle 14.0 30.5 39.7
Left NVB 20.0 31.9 39.3
Urethra (in prostate) 37.8 41,1 43.9
The first step is implanting 4 gold fiducials, small pellets, in the prostate to guide planning and treatment.
Ten days later a CD and MRI scan are taken and combined into the 3D computer software to develop the treatment plan.
Treatment (and MRI/CT scan) preparation consisted of a low-fiber diet the preceding day and a Fleet enema two hours before treatment. Each treatment took from 30 to 40 minutes, depending upon whether small shifts in the actual prostate position (usually due to intestinal gas or small patient movements) varied from the plan. There is no restraining "body cradle", instead just a loose stap to prevent falling off the treatment table if one falls asleep from boredom. For every third radiation beam, two low-intensity x-ray projectors in the ceiling compare the position of the fiducials with the plan. If there is a discrepancy, the treatment stops until the actual prostate position is re-registered with the computer plan. Re-registration is accomplished by automatic adjustments of the robotic arm and/or the treatment table. Actual CK treatment is rather boring. Post-treatment, Flomax was prescribed to facilitate urination during potential prostate swelling due to radiation inflammation.
As with any radiation treatment, there are potential short-term (called "acute" in the literature) and long-term ("chronic", or "late") urinary (GU) and bowel/rectum (GI) side effects. Radiation side effects are graded. Grade 0 is none noticed by the patient; Grade 1 is noticeable but not requiring a prescription to alleviate; Grade 2 is a prescription required to manage symptoms; Grade 3 is requiring more serious medical intervention.
A recent paper reported 53.0% short-term GI (bowel) Grade 2 and 0.7% Grade 3 side effects for IMRT. In contrast, two recent CK papers reported 2.1 to 8.5% Grade 2 and 0% Grade 3 short-term GI side effects. For short-term GU (urinary) side effects, the rate for IMRT was 44 Grade 2 and 2.6% Grade 3 compared to CK results of 1.4 to 20% for Grade 2 and 0 to 0.7% Grade 3.
So much for expectations. In my case I had rather severe urinary frequency (every 60 to 90 minutes) and pain the weekend after my first two CK radiation sessions. These symptoms were controlled within 3 days by prescribing phenazopyridine for the pain (really worked!) and doubling the Flomax. My bowel/rectal issues increased during the first week after the last treatment and peaked the second week. Chronic dull pain in the anal area-- felt like someone hit it with a hammer. Frequent urges for painful bowel movements, but only a few soft 'pellets' produced. "Had to go" as frequently as every 90 minutes with very little time to make it to the bathroom. Always felt like there was 'more to come' with no result. By 7 days after the last treatment, I was discouraged that the symptoms (radiation proctitis) seemed to be getting worse. ProctoFoam (topical and intra-rectal Hydrocortizone) was prescribed for the bowel issues and warm soaks of the 'bottom' and prune juice as a mild laxative, as well as eating Activia yogurt to re-establish the bowel microbes. Gradually the proctitis symptoms waned, by the fourth week after treatment urinary and bowel functions were completely normal (for me at age 70: never getting up in the middle of the night to urinate and 3 normal bowel movements per day).
So, my short-term side effects seemed to be in the usually low Grade 2 GI and GU statistics. Rather unexpected and very unpleasant, but controllable with low-level prescriptions and resolved by the fourth week after the last treatment. The urinary issues may have been escalated by the fact that I had a mild prostatitis infection prior to the start of treatment. The more severe than expected bowel radiation proctitis may have been due to my higher than average mean dosage (40.27 Gy vs. 35 to 36.25 Gy) to the prostate and close margins due to my cancer having moved from low-risk to intermediate risk and the potential for penetration of the prostate capsule.
Cancer control: The expectation after CK treatment is for the PSA to decrease by at least 50% in the first 6 months after treatment, to 1.0 or less at 12 months, and 0.1 or less by 18 to 24 months. Reported 5-year biochemical control (no PSA-evidence of recurrence) in recent CK papers ranges from 91 to 96 % for low-risk cancers, 86 to 92 % for intermediate risk, and 65 to 80 % for high risk. This is comparable to, or better than, 5-year biochemical control rates reported for current IMRT or proton treatments.
Usually the first PSA after CK treatment comes at 3 months to allow recovery from potential radiation inflammation. After my rather intense PSA monitoring during Active Surveillance, I did not wait that long. My results so far are:
PSA (with Avodart) Estimated PSA (doubled) without Avodart
01/14/2013 3.9 7.8
03/06/2013 ------ Last CK session ------------------
04/05/2013 1.4 2.8
05/02/2013 1.1 2.2
So far, so good.......
Efstathiou et al, 2013; Proton beam therapy and localized prostate cancer: current status and controversies; Br J Cancer. 2013 Apr 2;108(6):1225-30
Katz, 2012; Stereotactic Body Radiation Therapy Offers a Safe, Non-invasive Treatment for Prostate Cancer Patients Over 70 Years Old; Int. J. Radiation Oncology Biol. Phys. Vol. 84, No. 3, p. S361
Katz et al, 2012; Five-year Biochemical Control Rates for Stereotactic Body Radiation Therapy for Organ-confined Prostate Cancer: A Multi-institutional Pooled Analysis; Int. J. Radiation Oncology Biol. Phys. Vol. 84, No. 3, pp. S147-S148.
Meier et al, 2012; Stereotactic Body Radiation Therapy for Intermediate-risk Organ-confined Prostate Cancer: Interim Toxicity and Quality of Life Outcomes From a Multi-institutional Study; Int. J. Radiation Oncology Biol. Phys. Vol. 84, No. 3, p.
Oliai et al, 2013; Stereotactic body radiation therapy for the primary treatment of localized prostate cancer, J Radiat Oncol (2013) 2:63–70.
Vora et al, 2013; Nine-Year Outcome and Toxicity in Patients treated with IMRT for Localized Prostate Cancer, J Urology 2013.02.012.
UPDATE 18 MONTHS AFTER CYBERKNIFE RADIATION
Immediately after the CyberKnife radiation (see previous posts) while Avodart was still suppressing the DHT to near zero, my PSA dropped much faster than expected from SBRT radiation, reaching a low of 0.5 ng/ml in September, 2013. Once the Avodart was stopped and the DHT recovered (to 33 to 37), the PSA slowly rose to a maximum of 1.1 in December, 2013. This was right on the expected average post-CyberKnife PSA curve It has declined since them to 0.5 in May and July, 2014, about average post-CyberKnife.
I had some delayed radiation symptoms in April-May, 2014: increased urinary urgecy with mild 'burning' feeling, more urgent bowel movements. Was able to control with Aleve for urinary discomfort and Activia for bowel symptoms. Back to normal by June 2014. 'Normal' since my late '60s is not having to get up at night, but increased daytime urinary frequency and urgency compared to 10 years ago. Can't say that, except for episode above, these issues are any worse after the CyberKnife radiation than before. Sexual function has been declining since my late '60s, perhaps accelerated post-CyberKnife, but still tolerable within our 49 1/2 year marriage. I do not take Cialis or Viagra.
Otherwise I'm rather healthy and active for approaching 72. Still capable of rather strenuous physical labor and still enjoying mountain hiking and high-Sierra kayaking.
I'll do a set of blood tests (PSA, DHT, free and total T, PAP) in October and post the results.
Best wishes to all!
My PSA continues to decline following the CyberKnife radiation. It is interesting that there still is some variability in the PSA data post treatment, which points out that one should not 'panic' over apparent increases between two consecutive PSA measurements, even after treatment.
9/18/14 0.6 Total T 286; Free T 4.4; DHT 41; PAP 0.8
4/29/15 0.4 Total T 187; Free T 4.6; DHT 26; PAP 1.0
10/28/15 0.2 Total T 313; Free T 9.3; DHT 38
The low Testosterone (T) reading in April 2015 was a concern. Perhaps due to time of day (was afternoon, whereas blood draw for T should be before 10 am)? Radiation is known to often result in an increase in T, but, of course, so is aging. The T for Dec. 2015 is perhaps not abnormal for age 73. I do not have any of the classic symptoms of low T.
No further episodes of urinary or rectal radiation symptoms. ED is an increasing issue but still tolerable within my long-term (50-year) marital relationship. I still have an active lifestyle focusing on outdoor recreation in the Sierra Nevada.
Out of curiosity as to the radiation effects on the prostate gland I had a post-treatment Color Doppler Ultrasound (CDU) by Dr. Bahn in May 2015. The gland margins were still obvious, volume 53 cc. There was no sign of the smaller turmors previously monitored during Active Surveillance, however there still was evidence of the largest 'index' tumor in the right base to mid, with significantly decreased but still visible vascularity. Given the continued decline in PSA it is probable that the tumor is continues to slowly ablate from the radiation. I will do another CDU scan in a year as a followup.
Thus far I am fully satisfied with the outcome of the CyberKnife treatment.
The Best to You and Yours!
A bit over 3 years since SBRT (CyberKnife) radiation my PSA has declined to 0.1 ng/ml.
At this point it is challenging to sort out potential radiation side effects from aging (75).
Little long-term urological or rectal issues. Daytime urination urgancy had been increasing before the radiation and is not noticably worse since. I do not have to get up at night to urinate.
My total testosterone has decreased to around 250 ng/dl. Radiation treatment is known to lower testosterone (never discussed by my doctors!), but this is also a common consequence of aging. I do not have any of the fatigue or mental symptoms of low testosterone. For my age I am fit and active with a Body Mass Index of 24.
My ED is almost total. Again, difficult to sort out to what extent this is a radiation side effect due to radiation damage to nerves/vascualture or a consequence of low testosterone (whether from aging or radiation or both) or aging. With respect to my current quality of life this is something I can live with.
My personal 'bottom line' is that I have no regrets from postponing treatment for 7 years during AS (Active Surveillance). However, as noted above my AS routine was very 'active.' The payoff from imaging and targeted biopsies was that it provided confidence during AS that the cancer was progressing very slowly while also providing evidence as to when it was time to leave AS and seek treatment. Active research led me to chose either brachytherapy (seeds) or SBRT if/when it was time to be treated. I have no regrets in my final decision to have SBRT (CyberKnife). Only 5 radiation treatments over a week and a half, minimal short-term and few long-term side effects, less expensive than IMRT, so far good evidence of cancer control.
The Best to You and Yours!
Jon in Nevada
Jon's e-mail address is: ccnvww AT gmail.com (replace "AT" with "@")