Testosterone Replacement Therapy on the Natural History of Prostate Disease

Moore, Aaron; Butcher, Michael; Köhler, Tobias

doi:10.1007/s11934-015-0526-6

Cited by 11 publications

(10 citation statements)

References 86 publications

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“…Benign Prostatic Hypertrophy/Lower Urinary Tract Symptoms Although a 2007 multinational physician survey revealed that up to 18% of providers considered benign prostatic hypertrophy (BPH) risk with T administration as very important, 112 no clinical trials demonstrate that TT worsens BPH/lower urinary tract symptoms. 113 No difference in prostatic androgens were found between men with and without BPH. 114 Placebo-controlled trials of exogenous administration of dihydrotestosterone (DHT) and T resulted in no changes in prostate DHT or T in blood sampling or prostate biopsy specimens.…”

Section: Prostate Cancermentioning

confidence: 93%

Adult-Onset Hypogonadism

Khera

Broderick

Carson

et al. 2016

Mayo Clinic Proceedings

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In August 2015, an expert colloquium commissioned by the Sexual Medicine Society of North America (SMSNA) convened in Washington, DC, to discuss the common clinical scenario of men who present with low testosterone (T) and associated signs and symptoms accompanied by low or normal gonadotropin levels. This syndrome is not classical primary (testicular failure) or secondary (pituitary or hypothalamic failure) hypogonadism because it may have elements of both presentations. The panel designated this syndrome adult-onset hypogonadism (AOH) because it occurs commonly in middle-age and older men. The SMSNA is a not-for-profit society established in 1994 to promote, encourage, and support the highest standards of practice, research, education, and ethics in the study of human sexual function and dysfunction. The panel consisted of 17 experts in men's health, sexual medicine, urology, endocrinology, and methodology. Participants declared potential conflicts of interest and were SMSNA members and nonmembers. The panel deliberated regarding a diagnostic process to document signs and symptoms of AOH, the rationale for T therapy, and a monitoring protocol for T-treated patients. The evaluation and management of hypogonadal syndromes have been addressed in recent publications (ie, the Endocrine Society, the American Urological Association, and the International Society for Sexual Medicine). The primary purpose of this document was to support health care professionals in the development of a deeper understanding of AOH, particularly in how it differs from classical primary and secondary hypogonadism, and to provide a conceptual framework to guide its diagnosis, treatment, and follow-up.

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Section: Prostate Cancermentioning

confidence: 93%

Adult-Onset Hypogonadism

Khera

Broderick

Carson

et al. 2016

Mayo Clinic Proceedings

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“…Androgens serve a critical role in prostate development, growth and pathogenesis. The use of 5ARIs and castration are effective therapies for BPH and prostate cancer, respectively ( 3 ). To investigate the variation of autophagy in human prostate epithelial cells under AD, a human prostate epithelial cell line, BPH-1, was used, which was cultured in a medium in which the androgens had been removed.…”

Section: Discussionmentioning

confidence: 99%

“…Nearly all males develop microscopic BPH by the age of 90 years ( 1 , 2 ). 5α-reductase inhibitors (5ARI) are able to reduce the concentration of dihydrotestosterone (DHT) in prostate tissue and thus shrink the prostate ( 3 ). Previous studies have revealed that normal prostatic epithelial cells responded to hormone deprivation by undergoing apoptosis ( 4 – 6 ).…”

Section: Introductionmentioning

confidence: 99%

Crosstalk between apoptosis and autophagy in prostate epithelial cells under androgen deprivation

Liu

Zhang

et al. 2018

Exp Ther Med

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The present study investigated the molecular mechanism of apoptosis and autophagy in prostate epithelial cells under androgen deprivation (AD). BPH-1 cells were divided into four groups as follows: Control (Cont), AD, autophagy inhibition (AI) and AD + AI groups. Cells in the four groups were treated accordingly, and the level of apoptosis was subsequently measured via flow cytometry. The expression of the microtubule-associated proteins 1A/1B light chain 3 (LC3), caspase-3, poly (ADP-ribose) polymerase 1 (PARP-1) and Beclin-1 proteins of BPH-1 cells was detected at different time points following culture in androgen-deprived medium. Western blotting revealed that the basal levels of the LC3-II protein were detected at 0 h. At 4 h, LC3-II was significantly increased compared with 0 h (P<0.05). Beginning at 20 h, the expression level of the LC3-II protein decreased significantly (P<0.05). Western blotting revealed that beginning at 24 h, the expression level of the PARP-1 protein decreased significantly (P<0.001) and the cleavage fragments of the PARP-1 protein appeared. These results further imply that autophagy serves a cell protective function by mutual inhibition with apoptosis in BPH-1 cells in the removal of androgen conditions. Furthermore, the fragments of the cleaved Beclin-1 protein appeared as 35 and 37 kDa bands. Flow cytometry analysis demonstrated that the rate of cell apoptosis in the AD, AI and AD + AI groups was significantly increased compared with the Cont group (P<0.01). Compared with the AD or the AI groups individually, the rate of cell apoptosis in the AD + AI group was significantly increased (P<0.001). These findings suggest that in the early stage of AD, autophagy has a compensatory function in the cell, whereas in the whole process, autophagy and apoptosis share a mutual antagonism. The Beclin-1-C protein fragment contributed positive feedback to the process of apoptosis, which may be a potential mechanism of AD therapy. Therefore, AD and AI exhibit a synergistic effect to further improve the level of apoptosis.

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“…Other potential confounders of interest included history of testosterone replacement therapy,28 29 history of vasectomy,30 31 history of prostate inflammation/prostatitis,32 33 history of BPH diagnosis, treatment or procedure,34 history of bladder cancer, other urological cancers and hematuria 3536…”

Section: Methodsmentioning

confidence: 99%

Evaluation of exposure to pioglitazone and risk of prostate cancer: a nested case–control study

Boxall¹,

Bennett

Hünger³

et al. 2016

BMJ Open Diab Res Care

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ObjectivesInvestigate potential association between pioglitazone exposure and risk of prostate cancer.Research design and methodsNested, matched case–control study. UK primary care data (Clinical Practice Research Datalink (CPRD) GOLD) linked to inpatient (Hospital Episode Statistics (HES)) and cancer registry (National Cancer Information Network (NCIN)) data. English men aged ≥40 years diagnosed with type 2 diabetes mellitus, January 1, 2001 to January 5, 2015. Cases, with prostate cancer diagnosis, matched with up to 4 controls by age, cohort entry date and region. ORs for association of exposure to pioglitazone to incident prostate cancer, adjusted for potential confounders.ResultsFrom a cohort of 47 772 men with 243 923 person-years follow-up, 756 definite cases of prostate cancer were identified. Incidence was 309.9/100 000 person-years (95% CI 288.6 to 332.8). Pioglitazone use was not associated with prostate cancer risk; adjusted OR 0.759, 95% CI 0.502 to 1.148. Analyses showed no difference when possible cases, prostate cancer in CPRD GOLD only, included (adjusted OR 0.726, 95% CI 0.510 to 1.034). No association when adjusted for channeling bias (OR 0.778, 95% CI 0.511 to 1.184) or limited to an index date prior to July 1, 2011 (adjusted OR 0.508, 95% CI 0.294 to 0.879), despite prostate-specific antigen screening occurring more frequently among cases than controls (81.6% of 756 definite cases cf. 24.2% of 2942 controls (p<0.01)). No association with duration of pioglitazone use, increasing pioglitazone dose or increasing time since initiation.ConclusionsIn this real-world, nested matched case–control study, exposure to pioglitazone was not associated with increased risk of prostate cancer.

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Testosterone Replacement Therapy on the Natural History of Prostate Disease

Cited by 11 publications

References 86 publications

Adult-Onset Hypogonadism

Adult-Onset Hypogonadism

Crosstalk between apoptosis and autophagy in prostate epithelial cells under androgen deprivation

Evaluation of exposure to pioglitazone and risk of prostate cancer: a nested case–control study

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