The Prostate Saturation Point after Testosterone Replacement Therapy in Testosterone Deficiency Patient

2021 ◽  
Vol 104 (9) ◽  
pp. 1465-1470

Background: The effect of testosterone on the prostate gland is an unresolved question. The prostate saturation model is a recent hypothesis explaining that the stimulation of prostate tissue by testosterone is limited to a certain level of testosterone due to the limited number of androgen receptors. However, data from the Thai patients related to this issue are still lacking and need to be explored. Objective: To investigate prostate changes after testosterone replacement therapy (TRT). Materials and Methods: A retrospective study including testosterone-deficient patients who had TRT between 2011 and 2017 at Ramathibodi Hospital was conducted. The change in prostate-specific antigen (PSA) levels before and after TRT, or after a 1-year observation, was measured and analyzed as the primary objective. As a secondary objective, the authors measured and evaluated normal PSA velocity (PSAV) in the patients after TRT. Results: One hundred eleven testosterone deficient patients were included for analysis. The mean age was 62 years old. The baseline testosterone level and PSA level at the beginning were 247 ng/dL and 1.16 ng/mL, respectively. After undergoing TRT for one year, the results showed that the testosterone and the PSA levels were 307 ng/dL and 1.46 ng/mL, respectively. In addition, the subgroup analysis illustrated that patients who had low baseline testosterone levels such as 247 ng/dL or less, had significant increase of PSA level after treatment. However, when the baseline testosterone level was more than 247 ng/dL, the PSA levels were steady after treatment. For the secondary-objective results, the PSAV of the testosterone deficiency patients after TRT was 0.3 ng/mL/year. Conclusion: The evidence clearly indicates that TRT significantly increased the serum testosterone level. However, it had a limited effect on PSA change. The present study results supported the hypothesis of the prostate saturation model. The authors believe that a testosterone level of 247 ng/dL can saturate all androgen receptors in the prostate gland and no longer increase prostate stimulation. Keywords: Prostate-specific antigen; Prostate cancer; Testosterone replacement Therapy; Prostate saturation

2014 ◽  
Vol 32 (4_suppl) ◽  
pp. 229-229
Author(s):  
Aksam Yassin ◽  
Dany-Jan Yassin ◽  
Peter Hammerer

229 Background: There is controversy over whether testosterone replacement therapy is a risk factor for prostate cancer. Herein, we evaluate whether testosterone deficiency (TD), testosterone replacement therapy (TRT) or 5-alpha reductase inhibitor (5-ARI) therapy affect the risk of prostate cancer. Methods: Data were collected from 224 male patients who had an indication for prostate biopsy: Prostate specific antigen (PSA) greater than 4, PSA-Velocity >=0.75 in a year, hypogonadism with PSA >=1.5, positive digital rectal exam (DRE) and/or positive Transrectal Ultrasonography (TRUS) finding. Each patient was then subjected to a TRUS-guided 10 core prostate biopsy. Results: 25% (3 out of 12) of the patients on TRT were found to have prostate cancer via biopsy and 32.1% (68 out of 212) of patients who did not receive TRT were found to have prostate cancer; insignificant with p = 0.757. Seventeen our of 76 (22.4%) of the patients on 5-ARI treatment were found to have prostate cancer and 36.5% (54 out of 148) of the patients who did not receive 5-ARI were found to have prostate cancer; significant with p = 0.03. There was no significant statistical difference in Gleason grades among patients who were on TRT, no TRT, on 5-ARI and no 5-ARI. Conclusions: Our data suggest that TRT is not associated with increased risk of prevalence or Gleason grade of prostate cancer. 5-ARI therapy is associated with lower prevalence of prostate cancer but with no relationship to Gleason grade.


2011 ◽  
Vol 24 (3) ◽  
pp. 298-306 ◽  
Author(s):  
Bobby C. Jacob

Erectile dysfunction (ED) is defined as the inability to achieve or maintain an erection sufficient for satisfactory sexual performance. Endogenous testosterone is critical for normal libido; however, studies have also demonstrated a potentially important role with respect to the erectile process. The prevalence of testosterone deficiency ranges from 1.7% to 35% in patients with ED, and age is a common factor linking ED and testosterone deficiency. By 2025, global estimates are that there will be 356 million men >65 years. Age-associated testosterone deficiency is characterized by symptoms such as ED, and low serum testosterone. Randomized, placebo controlled studies have established the utility of testosterone replacement therapy (TRT) for the restoration of serum testosterone levels to the normal range in hypogonadal males; however, well designed studies are limited with respect to specific evaluation of the role of TRT as monotherapy in improving erectile function. In addition, recent literature suggests a possible role for TRT in combination with phosphodiesterase-5 (PDE-5) inhibitors for men with ED. The following review describes the potential roles of testosterone in erectile physiology, examines the relationship between testosterone deficiency and ED, and reviews published literature evaluating the use of TRT in hypogonadal males with a diagnosis of ED.


2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
G. Hackett ◽  
M. Kirby ◽  
A. J. Sinclair

Low levels of testosterone are manifested by erectile dysfunction, reduced sexual desire, and loss of morning erections with increasing numbers of men are being diagnosed and require treatment. The prevalence rates of testosterone deficiency vary according to different studies but may be as high as 40% in populations of patients with type 2 diabetes. There is increasing evidence that testosterone deficiency is associated with increased cardiovascular and all-cause mortality. Screening for low testosterone is recommended in a number of high risk groups including those with type 2 diabetes and metabolic syndrome. There are recent data to suggest that testosterone replacement therapy may reduce cardiovascular mortality as well as improving multiple surrogate markers for cardiovascular events. Specific clinical trials of testosterone replacement therapy are needed in selected populations but in the meantime we must treat patients based on the best current evidence.


Sign in / Sign up

Export Citation Format

Share Document