TRT and prostate cancer

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madman

Super Moderator
Introduction: It has been well established that male hypogonadism has a significant impact on patient quality of life and that replacement of testosterone can markedly improve symptoms and potentially offer a protective effect. The connection between testosterone replacement therapy (TRT) and prostate cancer (CaP) risk has long been a contentious subject among urologists. With the relatively recent introduction of the saturation model hypothesis by Morgentaler to explain androgen binding in CaP along with a growing body of retrospective studies, there has been a mounting challenge to the entrenched paradigm that TRT in hypogonadal men stimulates CaP. This review is a relevant update for the practicing urologist seeking to gain a better understanding regarding the risk and benefit profile to TRT in a variety of CaP settings.

Objective: To perform a literature review and provide a clinically relevant update to characterize the relationship between TRT and risk of prostate cancer (CaP) in the following clinical settings: developing de novo prostate cancer, patients with known untreated localized CaP, after definitive therapy for CaP with curative intent, and in advanced prostate cancer. In providing this evidence-based update to the practicing urologist, we seek to potentially impact practice patterns through a more comprehensive understanding of the risks/benefits of TRT.

Methods: A literature review using the PubMed database was performed using the following independent search terms: “prostate cancer,” “testosterone therapy,” “testosterone replacement therapy,” “hypogonadism,” “radical prostatectomy,” “radiation therapy”, “advanced prostate cancer,” “metastatic castrate-resistant prostate cancer,” “bipolar androgen therapy” and “high dose testosterone therapy”. We identified English language studies and past review articles to evaluate the role of testosterone in the development of CaP, the use of TRT after CaP to treat hypogonadism, and the use of TRT as directed therapy in the advanced prostate cancer setting.

Results: The vast majority of studies reviewed were retrospective in nature with relatively short follow-up periods. TRT was found to be safe and does not appear to increase the incidence of prostate cancer de novo. In men with a history of treated or untreated CaP, TRT does not appear to increase the risk of recurrence or progression of CaP. Supraphysiologic TRT appears to show clinical benefit to mCRPC patients. Well-designed randomized studies with longer-term follow-up are lacking at present.

Conclusions: The concerns regarding TRT causing/worsening CaP appears to be unsupported by the available retrospective studies and urologists may give consideration to treating symptomatic hypogonadal men with a history of CaP. There also appears to be an emerging role for supraphysiologic TRT as a therapy in the advanced prostate cancer setting. Further well-designed randomized studies are warranted.
 
Defy Medical TRT clinic doctor
Introduction: It has been well established that male hypogonadism has a significant impact on patient quality of life and that replacement of testosterone can markedly improve symptoms and potentially offer a protective effect. The connection between testosterone replacement therapy (TRT) and prostate cancer (CaP) risk has long been a contentious subject among urologists. With the relatively recent introduction of the saturation model hypothesis by Morgentaler to explain androgen binding in CaP along with a growing body of retrospective studies, there has been a mounting challenge to the entrenched paradigm that TRT in hypogonadal men stimulates CaP. This review is a relevant update for the practicing urologist seeking to gain a better understanding regarding the risk and benefit profile to TRT in a variety of CaP settings.

Objective: To perform a literature review and provide a clinically relevant update to characterize the relationship between TRT and risk of prostate cancer (CaP) in the following clinical settings: developing de novo prostate cancer, patients with known untreated localized CaP, after definitive therapy for CaP with curative intent, and in advanced prostate cancer. In providing this evidence-based update to the practicing urologist, we seek to potentially impact practice patterns through a more comprehensive understanding of the risks/benefits of TRT.

Methods: A literature review using the PubMed database was performed using the following independent search terms: “prostate cancer,” “testosterone therapy,” “testosterone replacement therapy,” “hypogonadism,” “radical prostatectomy,” “radiation therapy”, “advanced prostate cancer,” “metastatic castrate-resistant prostate cancer,” “bipolar androgen therapy” and “high dose testosterone therapy”. We identified English language studies and past review articles to evaluate the role of testosterone in the development of CaP, the use of TRT after CaP to treat hypogonadism, and the use of TRT as directed therapy in the advanced prostate cancer setting.

Results: The vast majority of studies reviewed were retrospective in nature with relatively short follow-up periods. TRT was found to be safe and does not appear to increase the incidence of prostate cancer de novo. In men with a history of treated or untreated CaP, TRT does not appear to increase the risk of recurrence or progression of CaP. Supraphysiologic TRT appears to show clinical benefit to mCRPC patients. Well-designed randomized studies with longer-term follow-up are lacking at present.

Conclusions: The concerns regarding TRT causing/worsening CaP appears to be unsupported by the available retrospective studies and urologists may give consideration to treating symptomatic hypogonadal men with a history of CaP. There also appears to be an emerging role for supraphysiologic TRT as a therapy in the advanced prostate cancer setting. Further well-designed randomized studies are warranted.

These studies are all great but when I ask my physician friends, one who is an oncologist,they all say the same thing, greater risk for prostate cancer. I would blow it off except it’s hard to dismiss it when an actual oncologist says it.
 




















 
Last edited:
Controversies with testosterone therapy (2020)
Mohit Khera, MD
Department of Urology, Baylor College of Medicine, Houston, Texas, USA



Conclusions

Clinicians prescribing testosterone should be aware of the current controversies associated with TTh. Controversies associated with TTh include the potential risk of developing prostate cancer and the worsening of LUTS. In addition, there are concerns about TTh potentially increasing CV risk.
The current literature does not suggest that there is a significant risk with TTh and prostate cancer, LUTS, and CV events. However, more studies, including randomized placebo-controlled trials, are needed. Clinicians prescribing TTh should also be aware that the majority of hypogonadal patients currently being treated with TTh are being treated off-label. Finally, lifestyle modification, such as weight loss and improvement in sleep, as well as varicocelectomy, can improve serum T values. Patients should be counseled appropriately regarding the indications for T therapy and the benefits of lifestyle modification prior to initiating TTh.
 
Safety of testosterone therapy in men with prostate cancer (2019)
Abraham Morgentaler & Monica Caliber


Areas covered: This review outlines the historical underpinnings of the historical belief that TTh “fuels” PCa and the experimental and clinical studies that have radically altered this view, including a description of the saturation model. The authors review studies of TTh in men with PCa following radical prostatectomy and radiation therapy, in men on active surveillance, and in men with advanced or metastatic PCa.


Expert opinion: TTh provides important symptomatic and overall health benefits for men with PCa who have TD. Although more safety studies are needed, TTh is a reasonable therapeutic option for men with low-risk PCa after surgery or radiation. Data in men on active surveillance are limited, but initial reports are reassuring.
 
These studies are all great but when I ask my physician friends, one who is an oncologist,they all say the same thing, greater risk for prostate cancer. I would blow it off except it’s hard to dismiss it when an actual oncologist says it.
My primary care doc says the same thing. And they are always so dang sure of themselves too.
 
Ask your doctors what they think about this.

Good stuff Nelson. BTW he also believes that testosterone causes BPH, enlarged prostate. I told him that from what I've read, there is a growing trend towards questioning this conventional wisdom. But I let it go at that. I am not likely to change his mind.
 
Ask your doctor what he or she thinks about this

 
post #12


PCa

*There is no evidence of increased PCa risk in men on TTh


*Recent evidence fails to support the longstanding fear that T therapy will increase prostate cancer risk or cause rapid growth of occult cancer

*The relationship between testosterone and prostate cancer appears to follow a saturation curve, present in many biological systems, in which growth corresponds with a concentration of a key nutrient until a concentration is reached in which an excess of the nutrient is achieved (Figure 2).
Clinical data indicate the saturation point for serum T is approximately 250 ng/dL (8.68 nmol/L)

*There is no evidence that TTh will convert sub-clinical prostatic lesions to clinically detectable PCa

*Nonetheless, in the absence of large-scale, long-term controlled studies, it is impossible to definitively assert the safety of TTh with regard to PCa.

*Therefore, prior to starting TTh, a patient’s risk of PCa must be assessed using, at a minimum measurement of serum prostate-specific antigen (PSA). Pretreatment assessment should include PCa risk predictors such as age, family history of PCa, and ethnicity/race. If suspicion of PCa exists, it may be reasonable to perform a prostate biopsy if warranted by clinical presentation. Testosterone therapy may be initiated in these men if a prostate biopsy is negative

*After initiation of TTh, patients should be monitored for prostate disease with measurement of serum PSA at 3–6 months, 12 months, and at least annually thereafter. In a subject with an increased risk of PCa urologist supervision is required

*An initial increase of prostate-specific antigen (PSA) and prostate volume with TTh is frequently seen over the first 2–6 months because the prostate is an androgen-dependent organ. The increase in PSA will be greatest in men with marked TD and least (or absent) in men with milder degrees of TD. The PSA level at 6 months after initiation of TTh should be used as the new baseline

*Referral to a urologist for prostate evaluation and possible biopsy during TTh should be made with the development of a new palpable prostate abnormality on DRE or with a worrisome rise in PSA.
Recommendations regarding what constitutes a concerning rise in PSA include an increase of 1.0 ng/ml over baseline PSA or a PSA velocity greater than 0.35 ng/ml per year.
 
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