madman
Super Moderator
* TD develops in 20-30% of men within 2-4 weeks of RP, with more profound TT suppression among those with higher-grade disease (e.g., Gleason 4+3). Mechanisms include retrograde venous shunting, DVC-induced intratesticular venous pressure elevation, and pneumoperitoneum-induced testicular ischemia. Symptom response post-RP is heterogeneous; some patients experience significant improvement in hypogonadal symptoms, while others do not and are prescribed exogenous testosterone.
* Approximately one-third of men develop transient or persistent TD after RP due to venous, ischemic, and hormonal disruptions; most recover spontaneously within a year.
Figure 1:
Etiology of Testosterone Deficiency After Radical Prostatectomy (2025)
Hammad, MAM1, Bandaru, D2, Furlan, V1, Hwang, Y1, Yafi, FA1, Daneshvar, M1, Lee, D1, Ahlering, T1, Shahait, M1
1 - UC Department of Urology, Irvine, CA, USA
2 - UC Riverside School of Medicine, Riverside, CA, USA
Introduction
Testosterone deficiency (TD) occurring after radical prostatectomy (RP) is clinically significant, as diminished androgen levels may hinder functional recovery and are associated with adverse oncologic outcomes. RP, a definitive treatment for localized prostate cancer, has been linked to acute alterations in sex steroid profiles. Observational data reveal that 37.5% of patients undergoing prostatectomy exhibit low total testosterone (TT) by postoperative day 90, with longitudinal studies noting a pattern of early postoperative hypergonadotropic hypogonadism.
Objective
To review the prevalence and underlying mechanisms of TD in the literature following RP.
Methods
A narrative synthesis of human studies measuring perioperative TT, luteinizing hormone (LH), follicle-stimulating hormone (FSH), and dihydrotestosterone levels was conducted. Mechanistic insights were drawn from translational and animal models assessing dorsal venous complex (DVC) ligation and pneumoperitoneum.
Results
TD develops in 20-30% of men within 2-4 weeks of RP, with more profound TT suppression among those with higher-grade disease (e.g., Gleason 4+3). Mechanisms include retrograde venous shunting, DVC-induced intratesticular venous pressure elevation, and pneumoperitoneum-induced testicular ischemia. Symptom response post-RP is heterogeneous; some patients experience significant improvement in hypogonadal symptoms, while others do not and are prescribed exogenous testosterone.
Conclusions
Approximately one-third of men develop transient or persistent TD after RP due to venous, ischemic, and hormonal disruptions; most recover spontaneously within a year. These findings support postoperative androgen monitoring and tailored testosterone replacement therapy if needed, while emphasizing the need for further prospective studies to clarify mechanisms and guide long-term management.
* Approximately one-third of men develop transient or persistent TD after RP due to venous, ischemic, and hormonal disruptions; most recover spontaneously within a year.
Figure 1:
Etiology of Testosterone Deficiency After Radical Prostatectomy (2025)
Hammad, MAM1, Bandaru, D2, Furlan, V1, Hwang, Y1, Yafi, FA1, Daneshvar, M1, Lee, D1, Ahlering, T1, Shahait, M1
1 - UC Department of Urology, Irvine, CA, USA
2 - UC Riverside School of Medicine, Riverside, CA, USA
Introduction
Testosterone deficiency (TD) occurring after radical prostatectomy (RP) is clinically significant, as diminished androgen levels may hinder functional recovery and are associated with adverse oncologic outcomes. RP, a definitive treatment for localized prostate cancer, has been linked to acute alterations in sex steroid profiles. Observational data reveal that 37.5% of patients undergoing prostatectomy exhibit low total testosterone (TT) by postoperative day 90, with longitudinal studies noting a pattern of early postoperative hypergonadotropic hypogonadism.
Objective
To review the prevalence and underlying mechanisms of TD in the literature following RP.
Methods
A narrative synthesis of human studies measuring perioperative TT, luteinizing hormone (LH), follicle-stimulating hormone (FSH), and dihydrotestosterone levels was conducted. Mechanistic insights were drawn from translational and animal models assessing dorsal venous complex (DVC) ligation and pneumoperitoneum.
Results
TD develops in 20-30% of men within 2-4 weeks of RP, with more profound TT suppression among those with higher-grade disease (e.g., Gleason 4+3). Mechanisms include retrograde venous shunting, DVC-induced intratesticular venous pressure elevation, and pneumoperitoneum-induced testicular ischemia. Symptom response post-RP is heterogeneous; some patients experience significant improvement in hypogonadal symptoms, while others do not and are prescribed exogenous testosterone.
Conclusions
Approximately one-third of men develop transient or persistent TD after RP due to venous, ischemic, and hormonal disruptions; most recover spontaneously within a year. These findings support postoperative androgen monitoring and tailored testosterone replacement therapy if needed, while emphasizing the need for further prospective studies to clarify mechanisms and guide long-term management.
