Prostate ...

[MR10X]

I hear ya. I KNOW your dilemma. I have a buddy that is about 10 year older than me and in his early 50's. I advertised to him over the past 8 years which I have been involved with TRT VERY CAUTIOUSLY, but encouragingly, as I KNEW that I really dont know the implications of WHAT I MAY be doing to myself. And especially with a family PC history. Really, I wonder the sanity - but i continue to stick to my plan. WHICH IS - (as chicken or egg). Does the loss of hormone production with natural aging associate directly as "an unavoidable cost of aging" which CAN INDEED by circumvented by SIMPLY REPLACEMENT; and thus eliminating the development of cancer by supplementation of what otherwise lacked....? OR - Will the addition of hormones exogenously profoundly complicate and exacerbate the potentially INEVITABLE and/OR Unavoidable - as strict genetic CONSEQUENCE (meaning as not really yet scientifically overtable short of DNA manipulation, etc..)

SO - You are asking YOURSELF - WOULD I be sentencing my dad to a premature death sentence; OR would I be bolstering his life.?

My Thoughts:
1.) What is the REAL VALUE of TRT with regard to age and natural genetic specific progression. HOW Valuable COULD it be to him. Would he even notice it?
2.) WOULD IT POSSIBLY EVEN HELP HIM, and both psychologically as well as physically and ALL-ROUND even.? (Wouldn't it be funny if he started TRT and would up with the nursing home title - "The Aging Raging Bull"..?! LOL
3.) But what are the potential negatives? Cancers and more specifically - DNA perversions/failures ALREADY in place and action that could potentially be greatly increased. And PERHAPS even due to a failure of other systems that TRT cant influence, but NOW become a negative aspect of TRT. (Thyroid, Etc.., Could he even over exert himself and rupture a tendon due to increased muscular action that TRT wont necessarily bolster, or at least at the same rate.
4.) Would TRT just flat our prove pointless due to aged insulin activity, or other, and possibly even stretching that simply old pancrease to full blown diabetes now costing him an eye or a foot in three years. (as a scaled down example SHORT or progression of potential cancer in wait)
5.) The list goes on.. But the point is YOU REALLY CARE on this one. And MORE than just an objective patient - ITS YOUR DAD...!

Back of the subject of that buddy of mine who I hinted around to and even encouraged to look into it at times. He also had the common notion (as a negative in his head) that "injections = STEROIDS" thus further complicating his possible objectivity. THE OLD WITCH BURNING DEMONIZATION AGAIN STILL AFFECTING SOCIETY..!!!! The long and short - is that when I met him he was early forties and one of these guys NOT ONLY with a full head of hair, but young skin - the works. He was ten years older and could have passed for younger than me. So I always thought he would be 65 and passing for 40 still. BUT NO. I recently saw him and was shocked. He was half crippled and has essentially retired from his favorite past time of golf - due to same. Looking gray (never imagined possible). Most importantly kinda flabby, chubby, but not in healthy way. Also note this man was an INCREDIBLE athlete when young, and in top 5-10 percentile of population i suspect which could have played semi-pro out of school if he really wanted. I caught up with him again the other day. Even after toning it down to a minor, "man, you should just see a doc about a patch and test the water, back when we played that last round of golf a year ago - HE SIMPLY WOULD NOT EVEN RESPOND TO MY INQUIRY AS TO DID HE EVER TRY (in text comm.). So I have never pressed him, but always suggested AND ONLY BECAUSE HE DID INITIALLY EXPRESS INTEREST. I feel it would have helped him. But who knows, perhaps he would be dead of prostate cancer if he had. I JUST DONT KNOW. I'm really kinda glad he never did in the end, cause I would not have wanted to wonder if he did turn up ill in that time on, would I have caused by encouraging.. When still, it could have been a genetic development UNAVOIDABLE,,,, I would have to deal with the thought process, as there is simply not enough scientific evidence either way...

WE... Are the Beta group. Its almost like Bill Gates runs the medical science industry. As all microsoft final releases were really just the next beta now aren't they... LOL

I dont know. Like I said, I feel your dilemma. My dad had his prostate successfully removed 20 years ago at early fifties. I would not have told him to do it at any time in my experience over the last 8-9 years of research. I DONT speculate SPECIFICALLY WHY I would not. But I wont...

Hope that helps some..

I will say this,i was without test for over a year and theres a lot more that test does for your body than you realize untill you dont have .It effects a lot of things in your body and i noticed my skin was looking older than it use to,no energy,joints hurt,no endurance,no libido,less self confidence,muscle loss and actually think it effected my memory. All i can say is i feel 100% better with just a little test in my body TRT dose.

 

[Michael Scally MD]

Five Prostate Cancer Quiz Questions for Your Patients
Dr. Alan Partin offers answers and explanations.
Five Prostate Cancer Quiz Questions for Your Patients : PracticeUpdate

Question 1: After discussion with their physician, all men should consider getting a PSA checked and a digital rectal exam at age 50 years unless they have a family history of prostate cancer or are African-American, in which case they should be checked at an earlier age, between 40 and 45 years. A first PSA value of < 4.0 ng/ml at this young age is considered completely normal.

Answer: FALSE

An initial PSA value for a man aged < 50 years should be < 0.6 ng/ml to be considered completely normal. Values higher than this should prompt closer observation or referral to an urologist.

Question 2: It is not possible to do surgery for prostate cancer after radiation treatment.

Answer: FALSE

Granted, prostate surgery is rarely indicated as adjuvant/salvage treatment after failed initial radiation treatment. This is because the best treatment at that stage would require systemic (whole body) treatment(s), such as androgen deprivation and/or chemo- or immunotherapy; it—surgery—is indeed possible.

Salvage prostatectomy after radiation is only indicated if the initial tumor presentation was low-intermediate risk disease, PSA levels following radiation failed to maintain a sustained decrease to below the nadir (lowest value after treatment), and the post-radiation biopsy demonstrates microscopic evidence of active cancer cells.

Question 3: Transrectal ultrasound (TRUS)–guided prostate biopsy has a great chance of spreading prostate cancer cells into the bloodstream and rectum.

Answer: FALSE

An excellent question. While it is not completely 100% free of possibility, the actual evidence that this might occur suggests that it is a very low probability. The reasoning is best described in Dr. Walsh’s book, where he addresses the question of needle tracking of tumor cells at biopsy and notes that if this was a serious risk, the concept of early diagnosis and treatment would be moot and that many thousands of patients have benefited from this intervention.

Dr. Walsh also notes that if the cancer is confined to the prostate, the few cells that might be dislodged into the blood stream during biopsy are unlikely to survive if they do not have the metastatic capability. For these reasons, we feel that it is very unlikely that prostate biopsy spreads cancer or causes disease to grow in the rectum.

Question 4: My friend was diagnosed with prostate cancer and began radiation treatment within 3 weeks. I was just diagnosed and was told by my physician that I didn’t need treatment at all—I just needed to be “watched.” My doctor gave me bad information.

Answer: FALSE

When prostate cancer is detected on a biopsy and is felt by the pathologist and urologist to represent very-low risk disease (outlined below), it is often recommended that these men participate in a treatment option called “active surveillance”—an option in which no actual treatment is given; just a well-designed surveillance protocol.

Prostate cancer is the most prevalent male cancer, but the majority of men with the disease do not die of prostate cancer. Studies suggest that 30% to 50% of men > 60 years diagnosed with prostate cancer today by PSA screening undergo a treatment (either surgery or radiation) that will not extend their life or improve its quality. This does not mean that prostate cancer does not kill men, but, rather, some men who are older and/or in poor health with a slowly progressive form of the disease may not need immediate treatment. The key is to accurately identify those men who, for now, can safely forego treatment. Eligible men should meet the following criteria for very–low or low-risk disease:

• Life expectancy < 20 years
• Cancer not felt on digital rectal examination (stage T1c)
• PSA density (PSA divided by prostate volume) < than 0.15
• Gleason score ? 6 with no Gleason pattern 4 or 5
• No more than 2 cores with cancer, or cancer involving ? 50% of any core on at least a 12-core biopsy

Question 5: Robotic-assisted prostatectomy provides superior long-term cancer cure and better quality of life (urinary continence and sexual function) when compared with the traditional open surgical approach.

Answer: FALSE

Many studies have reported the outcomes of robotic surgery. None to date has been randomized (a statistical method to limit selection and other bias), thus limiting our ability to draw a strong conclusion related to this question. The largest study which looked at men in the national SEER database suggested that, while blood loss and length of stay within the hospital were improved by the robotic method, there was an actual increase in treatment for some of the quality-of-life issues related to prostate surgery (eg, incontinence and erectile dysfunction) in the short term. No long-term matched or randomized comparative data exist to determine if either approach (traditional open or robotic) is better with respect to cure of cancer. At this time, it is safe to say that both approaches to removal of the prostate have similar risks and benefits. A careful discussion with your prostate surgeon will best determine the method that is best for you.

 

[Michael Scally MD]

Wu JN, Fish KM, Evans CP, deVere White RW, Dall'Era MA. No improvement noted in overall or cause-specific survival for men presenting with metastatic prostate cancer over a 20-year period. Cancer. http://onlinelibrary.wiley.com/doi/10.1002/cncr.28485/abstract

BACKGROUND Prostate cancer mortality in the United States has declined by nearly 40% over the last 25 years. However, to the authors' knowledge, the contribution of prostate-specific antigen (PSA) screening for the early detection of prostate cancer remains unclear and controversial. In the current study, the authors attempted to determine whether improvements in survival over time among patients with metastatic prostate cancer have contributed to the decline in mortality.

METHODS Men aged???45 years who presented with de novo metastatic prostate cancer from 1988 to 2009 were identified within the California Cancer Registry. Overall survival and disease-specific survival were estimated using the Kaplan-Meier method. A multivariate analysis with Cox proportional hazards modeling was performed to adjust for different distributions of variables between groups.

RESULTS A total of 19,336 men presented with de novo metastatic prostate cancer during the study period. On multivariate analysis, overall survival was found to be better for men diagnosed from 1988 through 1992 and 1993 through 1998 than for men diagnosed in the most recent era (hazards ratio, 0.78; 95% confidence interval, 0.72-0.85 [P?<?.001] and HR, 0.79; 95% confidence interval, 0.74-0.86 [P?<?.001]). There was no improvement in disease-specific survival observed when comparing the most contemporary men (those diagnosed between 2004 and 2009) with those diagnosed between 1988 and 1997.

CONCLUSIONS In this analysis of men presenting with de novo metastatic prostate cancer, no consistent improvement in overall or disease-specific survival could be demonstrated over time. These data suggest that improvements in survival for patients with advanced disease have not contributed substantially to the observed drop in prostate cancer mortality over the PSA era and that stage migration secondary to PSA screening plays a more prominent role.

 

[Michael Scally MD]

Nelson AW, Tilley WD, Neal DE, Carroll J. Estrogen receptor beta in prostate cancer: friend or foe? Endocrine-Related Cancer. http://erc.endocrinology-journals.org/content/early/2014/01/08/ERC-13-0508.abstract

Prostate cancer is the commonest, non-cutaneous cancer in men. At present, there is no cure for the advanced, castration-resistant form of the disease.

Estrogen has been shown to be important in prostate carcinogenesis with evidence resulting from epidemiological, cancer cell-line, human tissue and animal studies. The prostate expresses both estrogen receptor alpha and estrogen receptor beta.

Most evidence suggests that estrogen receptor alpha mediates the harmful effects of estrogen in the prostate whereas estrogen receptor beta is tumour-suppressive, but trials of estrogen receptor beta-selective agents have not translated into improved clinical outcomes.

The role of estrogen receptor beta in the prostate remains unclear and there is increasing evidence that isoforms of estrogen receptor beta may be oncogenic. Detailed study of estrogen receptor beta and estrogen receptor beta isoforms in the prostate is required to establish their cell-specific roles, in order to determine if therapies can be directed towards estrogen receptor beta-dependent pathways.

In this review we summarise evidence on the role of estrogen receptor beta in prostate cancer and highlight areas for future research.

 

[Michael Scally MD]

Wenisch JM, Mayr FB, Spiel AO, Radicioni M, Jilma B, Jilma-Stohlawetz P. Androgen deprivation decreases prostate specific antigen in the absence of tumor: implications for interpretation of PSA results. Clin Chem Lab Med 2014:1-6. Androgen deprivation decreases prostate specific antigen in the absence of tumor: implications for interpretation of PSA results : Clinical Chemistry and Laboratory Medicine

Background: Prostate-specific antigen (PSA) is used as an outcome measure for relapsed disease in prostate cancer. Nonetheless, there are considerable concerns about its indiscriminate use as a surrogate endpoint for cell growth or survival. We hypothesized that treatment with a luteinizing hormone releasing hormone (LHRH) analog would decrease PSA levels even in the absence of malignant disease.

Methods: We determined testosterone and PSA levels in 30 healthy volunteers after a single intramuscular injection of a LHRH depot formulation. Testosterone and PSA levels were quantified by radioimmunoassay and electrochemi-luminescence immunoassay, respectively.

Results: After an initial flare-up during the first 3 days testosterone decreased reaching castration levels in 18 of the 30 young men (60%). After the nadir on day 28, testosterone levels increased to normal again. Changes in PSA paralleled those of testosterone. Castration reduced PSA levels by 29% (95% CI 19%-39%) compared to baseline (p<0.0001).

Conclusions: LHRH superagonists decrease PSA levels by testosterone deprivation. Conferring these findings to tumor patients, decreases in PSA after treatment with LHRH analogs might not only reflect disease regression but also a direct testosterone mediated effect on PSA. Thus, PSA levels should be cautiously interpreted when patients receive hormonal therapy.

 

[Michael Scally MD]

Kaplan AL, Trinh Q-D, Sun M, et al. Testosterone Replacement Therapy Following the Diagnosis of Prostate Cancer: Outcomes and Utilization Trends. The Journal of Sexual Medicine. http://onlinelibrary.wiley.com/doi/10.1111/jsm.12429/abstract

Introduction Late-onset hypogonadism may impair quality of life and contribute to metabolic and cardiovascular comorbidity in aging men. Testosterone replacement therapy is effective in treating hypogonadism. However, for the millions of men with a history of prostate cancer, exogenous testosterone has long been considered contraindicated, even though little data in such men are available. Clarification of this safety issue could allow treatment to be considered for a sizeable segment of the aging male population.

Aim The aim of this study is to examine population-based utilization and impact of testosterone replacement therapy in men with prostate cancer.

Methods Using linked Surveillance, Epidemiology, and End Results-Medicare data, we identified 149,354 men diagnosed with prostate cancer from 1992 to 2007. Of those, 1,181 (0.79%) men received exogenous testosterone following their cancer diagnosis. We used propensity scoring analysis to examine the effect of testosterone replacement on the use of salvage hormone therapy and overall and prostate cancer-specific mortality.

Main Outcome Measures We assessed overall mortality, cancer-specific mortality, and the use of salvage hormone therapy.

Results Following prostate cancer diagnosis, testosterone replacement was directly related to income and educational status and inversely related to age (all P?<?0.001). Men undergoing radical prostatectomy and men with well-differentiated tumors were more likely to receive testosterone (all P?<?0.001). On adjusted analysis, testosterone replacement therapy was not associated with overall or cancer-specific mortality or with the use of salvage hormone therapy.

Conclusions In this population-based observational study of testosterone replacement therapy in men with a history of prostate cancer, treatment was not associated with increased overall or cancer-specific mortality. These findings suggest testosterone replacement therapy may be considered in men with a history of prostate cancer, but confirmatory prospective studies are needed.

 

[Michael Scally MD]

Cui Y, Zong H, Yan H, Zhang Y. The effect of testosterone replacement therapy on prostate cancer: a systematic review and meta-analysis. Prostate Cancer Prostatic Dis. Prostate Cancer and Prostatic Diseases - Abstract of article: The effect of testosterone replacement therapy on prostate cancer: a systematic review and meta-analysis

Background: Testosterone replacement therapy (TRT) is a widely accepted form of treatment worldwide for aging men with late-onset hypogonadism syndrome. Urologists have been concerned about the possibility of TRT causing prostate cancer. The aim of this study was to assess the relationship between TRT and prostate cancer.

Methods: A literature review was performed to identify all published, randomized controlled trials (RCTs) of testosterone treatment for hypogonadism. The search included the MEDLINE, Embase and the Cochrane Controlled Trials Register databases. Fixed-effect model was chosen for homogeneous studies; otherwise, a random-effect model was used. Inconsistency was quantified by using the I2 statistic, which tests the proportion of heterogeneity across studies.

Results: Results of 22 RCTs involving a total of 2351 patients were analyzed. Eleven RCTs were short-term (<12 months) and 11 were long-term (12-36 months) comparisons of TRT with a placebo; TRT was administered transdermally, orally or by injection. Respective odds ratio (OR) and 95% confidence interval (CI) values for injection, transdermal administration and oral administration of short-term TRT were as follows: prostate cancer: 0.39 (0.06-2.45), 1.10 (0.26-4.65) and no oral; biopsy: 5.28 (0.24-113.87), 2.11 (0.32-13.73) and no oral; and prostate nodule: 1.01 (0.13-7.60), no injection and oral. Respective OR and 95% CI values for injection, transdermal administration and oral administration of long-term TRT were as follows: prostate cancer: 2.09 (0.18-24.73), 3.06 (0.12-76.70) and 0.19 (0.01-4.03); biopsy: 2.09 (0.18-24.73), 3.65 (0.88-15.20) and 0.97 (0.13-7.03); and prostate nodule: 3.13 (0.12-80.68), 1.00 (0.06-16.41) and 0.97 (0.13-7.03). Though for some routes of administration and some end points, the OR associated with testosterone administration were >1 indicating increased risk, none of these reached or even approached statistical significance (all P>0.10), which was consistent with the results of subgroup analyses and sensitivity analysis. Besides, sensitivity analysis indicated that short-term TRT was more likely to increase PSA levels than treatment with placebo (P<0.00001).

Conclusions: This meta-analysis shows that regardless of the administration method, TRT is the short-term safety and does not promote prostate cancer development or progression but long-term data are warranted with justifiable end points.

 

[BBC3]

Maybe on topic, Maybe not. Dad has just been diagnosed with liver cancer in his mid seventies. He had his prostate COMPLETELY REMOVED around 52. At first he was talking about "they were looking to see where it was coming from". I said, "duhh, your liver". LOL JK. But seriously I am not so sure what all that was about and just had me thinking that it was Prostate Cancer catching up 20+ years later and spreading to liver. He stated after surgery that "they got it all" and that they did not think prostate related. I don't think I have spoken with him about the official pathology report yet - even after surgery. So that is pending in my mind.

More on target with PC. For many years now he has been stating that he has a PSA count and the doc is scratching his head stating there is no Prostate, and therefore there should be no PSA to count. I shrugged it off thinking yea whatever, that's just an indication that there was some prostate left behind. (I mean, how the hell do you go in an manually cut out every single bit of prostate?!? But it does beg the interesting point that if it was just only a tiny bit, when he finally told me he was getting a read of (.8)!!!! That kinda blew my mind. But that says something about the value of SERUM COUNTS now don't it.!!!!

So for what its worth I will advise back if it turns out in pathology that the cancer is prostate related or not.

FOR THE SAKE OF THIS THREAD. Just how DO YOU get a PSA count when the prostate has supposedly been entirely removed??? Can someone technically astute please expound??

ON A SIDE NOTE...: The gut that I mentioned in a post back who had his prostate removed at like 40 (remarkably early for PC), who was just completely destroyed about not being able to get wood has apparently found his miracle in a pin. I think he tried everything under the sun including some kind of "dikhole" lozenge to help with erectile capacity and NOTHING worked - he was miserable. I spoke with a bud the other day that said he finally tried caverject and states nice 4 hour diamond cutters / as all the hype I had heard. Very expensive (like 100 bucks perhaps per wood/not sure). But it is apparently his second found sex life (which he holds DEARLY)....

So dont forget the point up top. Anyone??

 

[ELOX50]

I had the PCA3 test when my urologist indicated we should try it because my PSA was at 1.2. I'm 50 with a family history of Prostate cancer. My father passed at 67 one year after diagnosis with a very aggressive form. The PCA3 came back positive which resulted in a biopsy. I can't tell you how tough it was waiting two weeks for the results. Happy ending! Biopsy resulted in a negative result. Weww! Doc recommended avodart for prevention. I declined and take a prostate complex rooted in saw palmetto and some other stuff. It has been 4 years and my PSA last check was 1.8. This was down from previous check of 2.2.

 

[MR10X]

When i was treated for PCa there were a few options.Removing the prostrate had a very low rate of success and some potentually bad side effects like mentioned.Removing the prostrate might not get all the cancer,there might some cancer outside the prostrate in the surrounding tissue. Seed implants with external radiation treatments has the best by far success of getting all the cancer,even what it outside the prostrate.My PSA before seed implants and radiation treatment was 11.4 and after treatments it was 0.09. Its been a year since my treatment and i get a PSA done in march to how sucessful it was,my last PSA was 0.09.

 

[BBC3]

FROM THE EXCEPT of the ARTICLE presented in this post (NOT stated by Scally but posted as citing the article by this Dr. Alan Partin....)

I always HEARD that the "most prevalent cancer in men" was Testicular Cancer???! I also heard it was the most curable...?

"

Five Prostate Cancer Quiz Questions for Your Patients
Dr. Alan Partin offers answers and explanations.
Five Prostate Cancer Quiz Questions for Your Patients : PracticeUpdate



Prostate cancer is the most prevalent male cancer, but the majority of men with the disease do not die of prostate cancer. Studies suggest that 30% to 50% of men > 60 years diagnosed with prostate cancer today by PSA screening undergo a treatment (either surgery or radiation) that will not extend their life or improve its quality. This does not mean that prostate cancer does not kill men, but, rather, some men who are older and/or in poor health with a slowly progressive form of the disease may not need immediate treatment. The key is to accurately identify those men who, for now, can safely forego treatment. Eligible men should meet the following criteria for very–low or low-risk disease:"

 

[BBC3]

Now In my early 40's and having a family history of PC I am finally starting to understand what the prostate is, as I have experienced my first few bouts of "BPH type inflammation" as urinary difficulty and possibly erectile dysfunction. While I was always into supplements and even used saw palmetto as a youngster, I would not have had the experience to determine if Saw Palmetto had ANY effect on my prostate or not. The longest and most stable period I ever took SP was at 37 and for about 1.5 months and noted nothing then either - but still never KNOWING prostate dysfunction type interaction. Other experience prior was EXTREMELY limited to getting some supps and taking a bit before trashing after it sat there forever. So I am planning another and a serious run with SP to see how it actually applies - soon...

I had the PCA3 test when my urologist indicated we should try it because my PSA was at 1.2. I'm 50 with a family history of Prostate cancer. My father passed at 67 one year after diagnosis with a very aggressive form. The PCA3 came back positive which resulted in a biopsy. I can't tell you how tough it was waiting two weeks for the results. Happy ending! Biopsy resulted in a negative result. Weww! Doc recommended avodart for prevention. I declined and take a prostate complex rooted in saw palmetto and some other stuff. It has been 4 years and my PSA last check was 1.8. This was down from previous check of 2.2.

 

[MR10X]

I was diagnosed with high grade cancer a year and a half ago.I never had any prostrate issues at all,the only way i knew i had it was a PSA test that was 5.5 and 6 months later it had increased to 11.4.It was confirmed with a biopsy and ultrasound.I have done AAS since 1980 and never had prostrate issues. I guess and the doc also said the only way to monitor my treatment success is by PSA and right now my last PSA score was 0.09.What i would do since it is a history in your family is get PSA test every 6 months,i asked my urologist what the youngest patient he treated was and he said he was in his 40's. The reason i suggest every 6 months is because mine increased from 5.5 to 11.4 in 6 months.The most important thing is to catch it early before it spreads.....

 

[MR10X]

The reason i asked the doc how old the youngest person he treated for PCa was i had a PSA test done when i was about 50 which came out good.The next time i had a PSA done i was 65 and it came back 5.5 Both of my kids will turn 40 and 41 this year and since i had PCa they should be testing early.

 

[Michael Scally MD]

Highlights
• PCa patients had higher tPSA and PHI, but lower %fPSA, tT, fT, and bioT
• PHI showed largest AUC for detection of PCa
• AUC of PHI increased by including bioT or tT in a binary logistic regression model
• Patients with testosterone concentration of < 8 nmol/L had greatest benefit

Friedersdorff F, Manus P, Miller K, Lein M, Jung K, Stephan C. Serum testosterone improves the accuracy of Prostate Health Index for the detection of prostate cancer. Clin Biochem. Serum testosterone improves the accuracy of Prostate Health Index for the detection of prostate cancer

OBJECTIVE: Prostate cancer (PCa) detection suffers from low specificity when using prostate-specific antigen (PSA) alone. The aim of this study was to investigate the applicability of total testosterone (tT), free testosterone (fT), the fraction (%) of fT to tT (%fT), and bioavailable testosterone (bioT) in serum to improve the diagnostic validity of serum (-2)pro-PSA-based prostate health index (PHI).

DESIGN AND METHODS: Total and free PSA (tPSA, fPSA), (-2)pro-PSA, testosterone, and sex-hormone-binding globulin were measured by automated immunoassays from serum of 193 men scheduled for prostate biopsy (99 PCa, 94 without PCa). FT and bioT were calculated using an online calculator.

Statistical analyses were performed by non-parametric tests (Wilcoxon signed rank, Mann-Whitney, Kruskal-Wallis), binary logistic regression, and receiver operating characteristics (ROC) analyses.

RESULTS: Compared with the non-malignant controls, PCa patients had significantly higher tPSA concentrations and PHI values, but lower %fPSA values and lower concentrations of tT, fT, and bioT.

PCa could be differentiated from controls by PHI, tT, fT, bioT, and %fPSA. PHI showed the largest area under the ROC curve (AUC=0.73) that was increased further by the inclusion of bioT or tT in a binary logistic regression model. The AUC of PHI in patients with tT concentrations of <8nmol/L (indicating biochemical hypogonadism) was significantly larger than in patients with higher tT values (0.86 vs 0.70; P=0.024).

CONCLUSIONS: The PHI-based discrimination between PCa patients and non-malignant controls could be improved by the simultaneous determination of testosterone. Patients with testosterone concentration of <8nmol/L have the greatest benefit.

 

[MR10X]

Do have any information on whether its not a good ides to use HGH after you had prostrate cancer.I read in the Genotropin HGH insert that you are not suppose to use it if you have cancer but didn't state which type but i'm guessing cancer in general.

 

[MR10X]

After 3 months of TRT at 120mg a week of Test E which resulted in a level of 1580 taken after 3 days of the injection my latest PSA came back 0.60,although its higher i believe this would be normal since i had no Testosterone for over a year which should lower PSA numbers. My PSA after ADT and PCa treatments was 0.10.
My test results were
TT 1580 346-1197
FT 26.7 6.6-18.1
E2 17.2 25-50

 

[Michael Scally MD]

The Great Prostate Hoax: How Big Medicine Hijacked the PSA Test and Caused a Public Health Disaster
[ame=http://www.amazon.com/The-Great-Prostate-Hoax-Medicine-ebook/dp/B00HBQ6NY8/]Amazon.com: The Great Prostate Hoax: How Big Medicine Hijacked the PSA Test and Caused a Public Health Disaster eBook: Richard J. Ablin, Ronald Piana: Kindle Store[/ame]

 

[Michael Scally MD]

Preston MA, Wilson KM, Markt SC, et al. 5alpha-Reductase Inhibitors and Risk of High-Grade or Lethal Prostate Cancer. JAMA Intern Med. http://archinte.jamanetwork.com/article.aspx?articleid=1878668

IMPORTANCE 5alpha-Reductase inhibitors (5ARIs) are widely used for benign prostatic hyperplasia despite controversy regarding potential risk of high-grade prostate cancer with use. Furthermore, the effect of 5ARIs on progression and prostate cancer death remains unclear.

OBJECTIVE To determine the association between 5ARI use and development of high-grade or lethal prostate cancer.

DESIGN, SETTING, AND PARTICIPANTS Prospective observational study of 38 058 men followed up for prostate cancer diagnosis and outcomes between 1996 and 2010 in the Health Professionals Follow-up Study.

EXPOSURES Use of 5ARIs between 1996 and 2010.

MAIN OUTCOMES AND MEASURES Cox proportional hazards models were used to estimate risk of prostate cancer diagnosis or development of lethal disease with 5ARI use, adjusting for possible confounders including prostate specific antigen testing.

RESULTS During 448 803 person-years of follow-up, we ascertained 3681 incident prostate cancer cases. Of these, 289 were lethal (metastatic or fatal), 456 were high grade (Gleason sum [GS] 8-10), 1238 were GS 7, and 1600 were low grade (GS 2-6). A total of 2878 (7.6%) men reported use of 5ARIs between 1996 and 2010. After adjusting for confounders, men who reported ever using 5ARIs over the study period had a reduced risk of overall prostate cancer (hazard ratio

---

, 0.77; 95% CI, 0.65-0.91). 5ARI users had a reduced risk of GS 7 (HR, 0.67; 95% CI, 0.49-0.91) and low-grade (GS 2-6) prostate cancer (HR, 0.74; 95% CI, 0.57-0.95). 5ARI use was not associated with risk of high-grade (GS 8-10) prostate cancer (HR, 0.97; 95% CI, 0.64-1.46) or lethal disease (HR, 0.99; 95% CI, 0.58-1.69). Increased duration of use was associated with significantly lower risk of overall prostate cancer (HR for 1 year of additional use, 0.95; 95% CI, 0.92-0.99), localized (HR, 0.95; 95% CI, 0.90-1.00), and low-grade disease (HR, 0.92; 95% CI, 0.85-0.99). There was no association for lethal, high-grade, or grade 7 disease.

CONCLUSIONS AND RELEVANCE While 5ARI use was not associated with developing high-grade or lethal prostate cancer, it was associated with a reduction in low-grade, GS 7, and overall prostate cancer. Because the number of patients with high-grade or lethal prostate cancer in our cohort was limited, we cannot rule out potential risk of harm with 5ARI use.

 

[Michael Scally MD]

Phillips I, Shah SI, Duong T, Abel P, Langley RE. Androgen Deprivation Therapy and the Re-emergence of Parenteral Estrogen in Prostate Cancer. Oncol Hematol Rev 2014;10(1):42-7. http://www.touchoncology.com/sites/www.touchoncology.com/files/ebooks/OncHemUS101/files/44.html / http://www.touchoncology.com/articles/androgen-deprivation-therapy-and-re-emergence-parenteral-estrogen-prostate-cancer

Androgen deprivation therapy (ADT) resulting in testosterone suppression is central to the management of prostate cancer (PC). As PC incidence increases, ADT is more frequently prescribed, and for longer periods of time as survival improves. Initial approaches to ADT included orchiectomy or oral estrogen (diethylstilbestrol [DES]). DES reduces PC-specific mortality, but causes substantial cardiovascular (CV) toxicity. Currently, luteinizing hormone-releasing hormone agonists (LHRHa) are mainly used; they produce low levels of both testosterone and estrogen (as estrogen in men results from the aromatization of testosterone), and many toxicities including osteoporosis, fractures, hot flashes, erectile dysfunction, muscle weakness, increased risk for diabetes, changes in body composition, and CV toxicity. An alternative approach is parenteral estrogen, it suppresses testosterone, appears to mitigate the CV complications of oral estrogen by avoiding first-pass hepatic metabolism, and avoids complications caused by estrogen deprivation. Recent research on the toxicity of ADT and the rationale for revisiting parenteral estrogen is discussed.