The document discusses testosterone replacement therapy (TRT) and prostate cancer. It notes that while traditional views held that high testosterone led to rapid cancer growth, recent evidence challenges this. Studies found no association between endogenous hormone levels and cancer risk. The saturation model suggests maximal cancer growth occurs at relatively low testosterone levels. Accumulating evidence also links low testosterone with higher-risk cancer features. TRT studies up to 3 years found similar cancer detection rates to screening. While long-term safety data is still needed, available evidence suggests TRT may be considered for selected prostate cancer patients with symptoms of hypogonadism after obtaining informed consent.
This presentation provides an overview of androgen deprivation therapy (ADT), also known as hormone therapy, for prostate cancer. It discusses the basic principles, including how prostate cancer cells rely on androgens like testosterone to grow. ADT aims to stop androgen production or block their effects. Methods include surgical removal of the testes, medications to reduce testosterone production, and anti-androgens to inhibit testosterone's action. Side effects from lowering testosterone levels can include hot flashes, fatigue, reduced libido and sexual dysfunction, as well as increased risks of osteoporosis, obesity, and cardiovascular issues over the long term.
This document discusses testosterone inactivating pharmaceuticals (TIP), also known as androgen deprivation therapy (ADT), for treating prostate cancer. It provides details on 6 types of anti-testosterone therapies with varying levels of potency. TIP is used as preliminary treatment before radiation to reduce prostate size, as ancillary treatment with radiation or surgery to improve cure rates, and as standalone therapy for intermediate-risk, high-risk, or advanced disease. TIP is also used after PSA relapse or for second-line treatment after other therapies stop working. Side effects of TIP include bone loss, metabolic effects, sexual dysfunction, and increased risk of fractures. Strategies are discussed to prevent bone complications like osteopor
This document discusses testosterone replacement therapy (TRT) and the potential side effect of polycythemia. It notes that longer-acting TRT formulations like intramuscular injections and pellet implants have a higher risk of causing polycythemia compared to shorter-acting options like transdermal gels and patches. The document also recommends screening patients for obstructive sleep apnea prior to starting TRT and managing polycythemia through dose adjustment or phlebotomy if hematocrit is elevated.
This document discusses emerging restorative therapies for erectile dysfunction including shockwave therapy, stem cells, and platelet-rich plasma injections. It provides an overview of the proposed mechanisms of action and current evidence from studies on each therapy. While initial studies show promise, the document concludes that more rigorous randomized controlled trials are still needed to establish efficacy and safety before these therapies can be considered non-experimental options for treating erectile dysfunction.
Tips on how to preven prostate cancer(1)Aaron Saund
The document discusses the controversy around PSA tests for prostate cancer screening. It notes that a US government panel recommends against PSA tests for healthy men, as studies show PSA tests can lead to overdiagnosis and unnecessary treatments without clear benefits. The document then outlines several dietary and lifestyle changes that may help prevent prostate cancer or slow its progression, including eating fatty fish and tomatoes, cruciferous vegetables, following a Mediterranean diet, drinking green tea, taking selenium supplements, getting vitamin D from sun exposure, and staying physically active.
Medical Therapy of Castration Resistance Prostate CancerEuropa Uomo EPAD
This document discusses treatment options for castration-resistant prostate cancer (CRPC). It provides background on CRPC and a history of medical treatments. Current standard treatments include chemotherapy with docetaxel or cabazitaxel, and hormonal therapies with abiraterone or enzalutamide. Radium-223 is an option for patients with bone metastases. Sipuleucel-T is an immunotherapy approved in the US. Future treatments may involve better understanding of molecular biology to personalize treatment selection and sequencing based on tumor and patient genetics and prior response.
This presentation provides an overview of androgen deprivation therapy (ADT), also known as hormone therapy, for prostate cancer. It discusses the basic principles, including how prostate cancer cells rely on androgens like testosterone to grow. ADT aims to stop androgen production or block their effects. Methods include surgical removal of the testes, medications to reduce testosterone production, and anti-androgens to inhibit testosterone's action. Side effects from lowering testosterone levels can include hot flashes, fatigue, reduced libido and sexual dysfunction, as well as increased risks of osteoporosis, obesity, and cardiovascular issues over the long term.
This document discusses testosterone inactivating pharmaceuticals (TIP), also known as androgen deprivation therapy (ADT), for treating prostate cancer. It provides details on 6 types of anti-testosterone therapies with varying levels of potency. TIP is used as preliminary treatment before radiation to reduce prostate size, as ancillary treatment with radiation or surgery to improve cure rates, and as standalone therapy for intermediate-risk, high-risk, or advanced disease. TIP is also used after PSA relapse or for second-line treatment after other therapies stop working. Side effects of TIP include bone loss, metabolic effects, sexual dysfunction, and increased risk of fractures. Strategies are discussed to prevent bone complications like osteopor
This document discusses testosterone replacement therapy (TRT) and the potential side effect of polycythemia. It notes that longer-acting TRT formulations like intramuscular injections and pellet implants have a higher risk of causing polycythemia compared to shorter-acting options like transdermal gels and patches. The document also recommends screening patients for obstructive sleep apnea prior to starting TRT and managing polycythemia through dose adjustment or phlebotomy if hematocrit is elevated.
This document discusses emerging restorative therapies for erectile dysfunction including shockwave therapy, stem cells, and platelet-rich plasma injections. It provides an overview of the proposed mechanisms of action and current evidence from studies on each therapy. While initial studies show promise, the document concludes that more rigorous randomized controlled trials are still needed to establish efficacy and safety before these therapies can be considered non-experimental options for treating erectile dysfunction.
Tips on how to preven prostate cancer(1)Aaron Saund
The document discusses the controversy around PSA tests for prostate cancer screening. It notes that a US government panel recommends against PSA tests for healthy men, as studies show PSA tests can lead to overdiagnosis and unnecessary treatments without clear benefits. The document then outlines several dietary and lifestyle changes that may help prevent prostate cancer or slow its progression, including eating fatty fish and tomatoes, cruciferous vegetables, following a Mediterranean diet, drinking green tea, taking selenium supplements, getting vitamin D from sun exposure, and staying physically active.
Medical Therapy of Castration Resistance Prostate CancerEuropa Uomo EPAD
This document discusses treatment options for castration-resistant prostate cancer (CRPC). It provides background on CRPC and a history of medical treatments. Current standard treatments include chemotherapy with docetaxel or cabazitaxel, and hormonal therapies with abiraterone or enzalutamide. Radium-223 is an option for patients with bone metastases. Sipuleucel-T is an immunotherapy approved in the US. Future treatments may involve better understanding of molecular biology to personalize treatment selection and sequencing based on tumor and patient genetics and prior response.
Hormonal therapy for prostate cancer involves reducing androgen levels or blocking the androgen receptor to inhibit tumor growth. There are several mechanisms for androgen axis blockade, including surgical castration to reduce testosterone by over 90%, antiandrogens that directly block the androgen receptor, and LH-RH agonists that shut down LH and testosterone production. Inhibition of androgen synthesis via drugs like ketoconazole that block testosterone production is another approach. General complications of long-term androgen deprivation include osteoporosis, hot flashes, sexual dysfunction, increased risks of diabetes and bone metastases.
1) Adding hormone therapy to radiotherapy improves outcomes for prostate cancer, including disease-specific mortality and distant metastases.
2) For high-risk or locally advanced prostate cancer, short-course neoadjuvant hormone therapy of 3-6 months improves local control when combined with radiotherapy.
3) Long-term hormone therapy of at least 2 years reduces the risk of metastases and improves survival more than short-term therapy, especially for high-grade disease.
Treatment of metastatic prostate cancer how urologists should sequence availa...فاضل الوائلي
This document discusses treatment options for metastatic prostate cancer. It begins by outlining first line hormonal therapies like androgen deprivation therapy using LHRH agonists or antagonists. It then discusses secondary hormonal manipulations for castration-resistant prostate cancer, including antiandrogens, CYP17A inhibitors, and estrogens. Novel agents targeting the androgen axis like abiraterone and MDV3100 are also reviewed. Chemotherapy options for metastatic CRPC including docetaxel and cabazitaxel are summarized. The timing of chemotherapy and immunotherapy agents like sipuleucel-T are also addressed.
1. Discuss normal vs. abnormal semen analysis
2. Evaluate different treatments of varicocele
3. Assess azoospermia and discuss micro dissection testicular sperm extraction
4. Diagnose Klinefelter syndrome and genetic abnormalities in men with infertility
Hormonal therapy in prostate cancer involves androgen deprivation therapy (ADT) to slow cancer growth by lowering testosterone levels or blocking its effects. ADT can be achieved through surgical castration via orchidectomy, medical castration using LHRH agonists or antagonists to inhibit testosterone production, or anti-androgens to block the effects of testosterone. While effective, ADT can cause adverse effects like hot flashes, loss of libido, and increased risks of bone loss, diabetes, and cardiovascular disease. Principles of ADT indicate that LHRH agonists and surgical castration are equally effective, and that combined androgen blockade provides no additional benefit over castration alone for
My Prostate Cancer Story by Paul SchellhammerTony Crispino
With permission of Dr. Schellhammer this slide deck should be interesting to any PCa patient. Dr. Schellhammer is a former president of the American Urological Association and a leading authority on prostate cancer. He has fought i long battle. He and his colleague, Paul Lange operated on each other and had vastly different results.
Anemia is common in cancer patients, occurring in 30-86% of cases depending on malignancy type and Hb level definition of anemia. Anemia can be caused by the disease itself through cytokine-mediated effects on erythropoiesis or nutritional deficiencies, or be treatment-related due to chemotherapy, radiotherapy or other drugs. Erythropoietin treatment is effective at reducing transfusion needs and improving quality of life by increasing Hb levels and reducing fatigue in the majority of anemic cancer patients. However, some patients do not respond due iron deficiency or other factors. Iron supplementation can help improve response rates to EPO treatment.
The document summarizes an analysis of DNA methylation patterns in blood samples from participants in a study investigating cardiovascular disease risk factors. The analysis compared changes in methylation levels between two time points: 3 hours after a high-fat meal and 3 weeks after treatment with a cholesterol-lowering drug. Larger variations in methylation levels were found at 3 weeks compared to 3 hours. Additionally, CpG sites that changed the most 3 hours after the meal were more likely to be associated with genes related to fat metabolism and heart health. This suggests DNA methylation is influenced by environmental factors in a time-sensitive manner.
The JUPITER trial was stopped early due to clear evidence of benefit from rosuvastatin treatment. The trial aimed to test whether rosuvastatin could reduce cardiovascular events in apparently healthy people with normal LDL cholesterol but high hsCRP. Over 17,000 participants were randomized to rosuvastatin 20mg or placebo. After almost 2 years, rosuvastatin showed a highly significant 44% reduction in the primary cardiovascular endpoint compared to placebo, demonstrating its benefit in primary prevention. This clear benefit led to the trial being stopped early.
This study assessed the prevalence of metabolic syndrome in men with normal and abnormal semen parameters. Of 526 men studied, 26.5% had metabolic syndrome, higher than the general population prevalence of 18%. However, the prevalence of metabolic syndrome was not significantly different between men with normal versus abnormal semen parameters. While obesity and metabolic syndrome may impact fertility in women, this study found metabolic syndrome did not appear to have a major effect on male fertility or semen parameters. Larger longitudinal studies are still needed to understand potential effects over time.
1) Women with coronary artery disease often experience delays in diagnosis and treatment compared to men. They are less likely to receive timely reperfusion therapy and invasive procedures.
2) Outcomes following procedures like PCI are generally similar for men and women now if treated aggressively and according to guidelines. However, women still face higher risks of vascular complications.
3) Presentation of acute coronary syndromes can differ between men and women. Women tend to be older with more comorbidities but may have less obstructive coronary disease. Outcomes improve when treatment is administered irrespective of gender according to clinical condition.
Donor Selection: Haploidentical donor. Dr. Wang Yuspa718
This document summarizes a study on donor selection for haploidentical hematopoietic stem cell transplantation. The study analyzed 678 transplant cases from 2002-2013 in China. The main findings were:
1) HLA disparity did not influence transplant outcomes, while donor age and family relationship did. Younger, unrelated donors and fathers had better outcomes than older donors and mothers.
2) Offspring donors had less GVHD and NRM than sibling donors.
3) Within siblings, NIMA (non-identical maternal aunt) donors had better outcomes than NIPA (non-identical paternal aunt) donors and maternal donors.
4) The mechanisms influencing outcomes between different donor types,
This document summarizes recent developments in treating advanced prostate cancer. It discusses advances in hormonal therapy including intermittent therapy and new agents like abiraterone and MDV3100. It also discusses chemotherapy options for castration-resistant prostate cancer including docetaxel, cabazitaxel, and the use of zoledronate or denosumab to prevent bone complications.
1) The document discusses endocrine therapy options for ER+ HER2- metastatic breast cancer (MBC), including first-line aromatase inhibitors versus tamoxifen, comparisons between different aromatase inhibitors, and the role of fulvestrant.
2) The FIRST trial found that fulvestrant 500 mg had significantly longer time to progression compared to anastrozole as first-line therapy for postmenopausal women.
3) For premenopausal women, combinations of luteinizing hormone-releasing hormone agonists with tamoxifen or aromatase inhibitors showed benefits, with no differences between the arms.
This document discusses metastatic castrate-resistant prostate cancer (CRPC) and its management at LASUTH Urology Unit. CRPC occurs when prostate cancer progresses despite testosterone suppression through androgen deprivation therapy. While initial responses to androgen deprivation are common, cancer inevitably becomes resistant. Mechanisms of resistance include hypersensitive androgen receptor pathways, outlaw pathways activated by other ligands, and bypass pathways not dependent on the androgen receptor. The epidemiology, criteria for defining progression, mechanisms of resistance, current management approaches, and LASUTH's experience with CRPC are outlined.
This document summarizes the risk of thrombosis/deep vein thrombosis (DVT) associated with multiple myeloma and its treatments. It finds that the risk of DVT is increased by certain drugs like thalidomide, lenalidomide, and dexamethasone, especially when combined with chemotherapy. Studies show aspirin, low molecular weight heparin, and warfarin can effectively prevent DVT when used as prophylaxis, with aspirin and heparin posing a lower bleeding risk than warfarin. A phase III trial compared aspirin, low dose warfarin, and low molecular weight heparin for DVT prevention in newly diagnosed multiple myeloma patients on thalidomide-containing regimens
Androgen Deprivation Therapy for Prostate CancerAlexander Small
This document summarizes a tumor board review on androgen deprivation therapy for prostate cancer. It begins with a case presentation of a patient with metastatic prostate cancer and then provides: 1) A brief history of the discovery of the connection between androgens and prostate cancer; 2) An overview of the androgen axis and various methods of androgen deprivation therapy including surgical castration, medical castration, anti-androgens, and GnRH agonists/antagonists; 3) A discussion of the adverse effects of androgen deprivation therapy including quality of life impacts, increased risks of osteoporosis and cardiovascular disease; 4) Considerations around treatment timing; and 5) Conclusions regarding optimal androgen deprivation therapy
This document summarizes information on prostate cancer, including risk factors, diagnosis, and treatment options. It also discusses the potential role of nutrition in prostate cancer. Key points include:
- Prostate cancer is the most common non-skin cancer in men and the second leading cause of cancer death. Risk increases with age and is higher in African-American men and those with a family history.
- Diagnosis involves a digital rectal exam, PSA test, biopsy. Treatment depends on cancer severity and includes surveillance, surgery, radiation, and hormone therapy.
- Nutritional factors like a low-fat, plant-based diet high in fiber and omega-3 fatty acids may reduce prostate cancer risk and slow progression by
1) A 46-year-old man with type 2 diabetes, hypertension, obesity, and dyslipidemia presented with erectile dysfunction. Laboratory tests confirmed metabolic syndrome and hypogonadism.
2) The patient meets criteria for metabolic syndrome according to NCEP-ATP III guidelines due to diabetes, hypertension, abdominal obesity, and low HDL. Hypogonadism was diagnosed based on low total testosterone, free testosterone, and bioavailable testosterone levels.
3) Guidelines recommend screening patients with diabetes and symptoms of hypogonadism for low testosterone. The patient should have been screened for erectile dysfunction due to his risk factors of diabetes and metabolic syndrome.
Hormonal therapy for prostate cancer involves reducing androgen levels or blocking the androgen receptor to inhibit tumor growth. There are several mechanisms for androgen axis blockade, including surgical castration to reduce testosterone by over 90%, antiandrogens that directly block the androgen receptor, and LH-RH agonists that shut down LH and testosterone production. Inhibition of androgen synthesis via drugs like ketoconazole that block testosterone production is another approach. General complications of long-term androgen deprivation include osteoporosis, hot flashes, sexual dysfunction, increased risks of diabetes and bone metastases.
1) Adding hormone therapy to radiotherapy improves outcomes for prostate cancer, including disease-specific mortality and distant metastases.
2) For high-risk or locally advanced prostate cancer, short-course neoadjuvant hormone therapy of 3-6 months improves local control when combined with radiotherapy.
3) Long-term hormone therapy of at least 2 years reduces the risk of metastases and improves survival more than short-term therapy, especially for high-grade disease.
Treatment of metastatic prostate cancer how urologists should sequence availa...فاضل الوائلي
This document discusses treatment options for metastatic prostate cancer. It begins by outlining first line hormonal therapies like androgen deprivation therapy using LHRH agonists or antagonists. It then discusses secondary hormonal manipulations for castration-resistant prostate cancer, including antiandrogens, CYP17A inhibitors, and estrogens. Novel agents targeting the androgen axis like abiraterone and MDV3100 are also reviewed. Chemotherapy options for metastatic CRPC including docetaxel and cabazitaxel are summarized. The timing of chemotherapy and immunotherapy agents like sipuleucel-T are also addressed.
1. Discuss normal vs. abnormal semen analysis
2. Evaluate different treatments of varicocele
3. Assess azoospermia and discuss micro dissection testicular sperm extraction
4. Diagnose Klinefelter syndrome and genetic abnormalities in men with infertility
Hormonal therapy in prostate cancer involves androgen deprivation therapy (ADT) to slow cancer growth by lowering testosterone levels or blocking its effects. ADT can be achieved through surgical castration via orchidectomy, medical castration using LHRH agonists or antagonists to inhibit testosterone production, or anti-androgens to block the effects of testosterone. While effective, ADT can cause adverse effects like hot flashes, loss of libido, and increased risks of bone loss, diabetes, and cardiovascular disease. Principles of ADT indicate that LHRH agonists and surgical castration are equally effective, and that combined androgen blockade provides no additional benefit over castration alone for
My Prostate Cancer Story by Paul SchellhammerTony Crispino
With permission of Dr. Schellhammer this slide deck should be interesting to any PCa patient. Dr. Schellhammer is a former president of the American Urological Association and a leading authority on prostate cancer. He has fought i long battle. He and his colleague, Paul Lange operated on each other and had vastly different results.
Anemia is common in cancer patients, occurring in 30-86% of cases depending on malignancy type and Hb level definition of anemia. Anemia can be caused by the disease itself through cytokine-mediated effects on erythropoiesis or nutritional deficiencies, or be treatment-related due to chemotherapy, radiotherapy or other drugs. Erythropoietin treatment is effective at reducing transfusion needs and improving quality of life by increasing Hb levels and reducing fatigue in the majority of anemic cancer patients. However, some patients do not respond due iron deficiency or other factors. Iron supplementation can help improve response rates to EPO treatment.
The document summarizes an analysis of DNA methylation patterns in blood samples from participants in a study investigating cardiovascular disease risk factors. The analysis compared changes in methylation levels between two time points: 3 hours after a high-fat meal and 3 weeks after treatment with a cholesterol-lowering drug. Larger variations in methylation levels were found at 3 weeks compared to 3 hours. Additionally, CpG sites that changed the most 3 hours after the meal were more likely to be associated with genes related to fat metabolism and heart health. This suggests DNA methylation is influenced by environmental factors in a time-sensitive manner.
The JUPITER trial was stopped early due to clear evidence of benefit from rosuvastatin treatment. The trial aimed to test whether rosuvastatin could reduce cardiovascular events in apparently healthy people with normal LDL cholesterol but high hsCRP. Over 17,000 participants were randomized to rosuvastatin 20mg or placebo. After almost 2 years, rosuvastatin showed a highly significant 44% reduction in the primary cardiovascular endpoint compared to placebo, demonstrating its benefit in primary prevention. This clear benefit led to the trial being stopped early.
This study assessed the prevalence of metabolic syndrome in men with normal and abnormal semen parameters. Of 526 men studied, 26.5% had metabolic syndrome, higher than the general population prevalence of 18%. However, the prevalence of metabolic syndrome was not significantly different between men with normal versus abnormal semen parameters. While obesity and metabolic syndrome may impact fertility in women, this study found metabolic syndrome did not appear to have a major effect on male fertility or semen parameters. Larger longitudinal studies are still needed to understand potential effects over time.
1) Women with coronary artery disease often experience delays in diagnosis and treatment compared to men. They are less likely to receive timely reperfusion therapy and invasive procedures.
2) Outcomes following procedures like PCI are generally similar for men and women now if treated aggressively and according to guidelines. However, women still face higher risks of vascular complications.
3) Presentation of acute coronary syndromes can differ between men and women. Women tend to be older with more comorbidities but may have less obstructive coronary disease. Outcomes improve when treatment is administered irrespective of gender according to clinical condition.
Donor Selection: Haploidentical donor. Dr. Wang Yuspa718
This document summarizes a study on donor selection for haploidentical hematopoietic stem cell transplantation. The study analyzed 678 transplant cases from 2002-2013 in China. The main findings were:
1) HLA disparity did not influence transplant outcomes, while donor age and family relationship did. Younger, unrelated donors and fathers had better outcomes than older donors and mothers.
2) Offspring donors had less GVHD and NRM than sibling donors.
3) Within siblings, NIMA (non-identical maternal aunt) donors had better outcomes than NIPA (non-identical paternal aunt) donors and maternal donors.
4) The mechanisms influencing outcomes between different donor types,
This document summarizes recent developments in treating advanced prostate cancer. It discusses advances in hormonal therapy including intermittent therapy and new agents like abiraterone and MDV3100. It also discusses chemotherapy options for castration-resistant prostate cancer including docetaxel, cabazitaxel, and the use of zoledronate or denosumab to prevent bone complications.
1) The document discusses endocrine therapy options for ER+ HER2- metastatic breast cancer (MBC), including first-line aromatase inhibitors versus tamoxifen, comparisons between different aromatase inhibitors, and the role of fulvestrant.
2) The FIRST trial found that fulvestrant 500 mg had significantly longer time to progression compared to anastrozole as first-line therapy for postmenopausal women.
3) For premenopausal women, combinations of luteinizing hormone-releasing hormone agonists with tamoxifen or aromatase inhibitors showed benefits, with no differences between the arms.
This document discusses metastatic castrate-resistant prostate cancer (CRPC) and its management at LASUTH Urology Unit. CRPC occurs when prostate cancer progresses despite testosterone suppression through androgen deprivation therapy. While initial responses to androgen deprivation are common, cancer inevitably becomes resistant. Mechanisms of resistance include hypersensitive androgen receptor pathways, outlaw pathways activated by other ligands, and bypass pathways not dependent on the androgen receptor. The epidemiology, criteria for defining progression, mechanisms of resistance, current management approaches, and LASUTH's experience with CRPC are outlined.
This document summarizes the risk of thrombosis/deep vein thrombosis (DVT) associated with multiple myeloma and its treatments. It finds that the risk of DVT is increased by certain drugs like thalidomide, lenalidomide, and dexamethasone, especially when combined with chemotherapy. Studies show aspirin, low molecular weight heparin, and warfarin can effectively prevent DVT when used as prophylaxis, with aspirin and heparin posing a lower bleeding risk than warfarin. A phase III trial compared aspirin, low dose warfarin, and low molecular weight heparin for DVT prevention in newly diagnosed multiple myeloma patients on thalidomide-containing regimens
Androgen Deprivation Therapy for Prostate CancerAlexander Small
This document summarizes a tumor board review on androgen deprivation therapy for prostate cancer. It begins with a case presentation of a patient with metastatic prostate cancer and then provides: 1) A brief history of the discovery of the connection between androgens and prostate cancer; 2) An overview of the androgen axis and various methods of androgen deprivation therapy including surgical castration, medical castration, anti-androgens, and GnRH agonists/antagonists; 3) A discussion of the adverse effects of androgen deprivation therapy including quality of life impacts, increased risks of osteoporosis and cardiovascular disease; 4) Considerations around treatment timing; and 5) Conclusions regarding optimal androgen deprivation therapy
This document summarizes information on prostate cancer, including risk factors, diagnosis, and treatment options. It also discusses the potential role of nutrition in prostate cancer. Key points include:
- Prostate cancer is the most common non-skin cancer in men and the second leading cause of cancer death. Risk increases with age and is higher in African-American men and those with a family history.
- Diagnosis involves a digital rectal exam, PSA test, biopsy. Treatment depends on cancer severity and includes surveillance, surgery, radiation, and hormone therapy.
- Nutritional factors like a low-fat, plant-based diet high in fiber and omega-3 fatty acids may reduce prostate cancer risk and slow progression by
1) A 46-year-old man with type 2 diabetes, hypertension, obesity, and dyslipidemia presented with erectile dysfunction. Laboratory tests confirmed metabolic syndrome and hypogonadism.
2) The patient meets criteria for metabolic syndrome according to NCEP-ATP III guidelines due to diabetes, hypertension, abdominal obesity, and low HDL. Hypogonadism was diagnosed based on low total testosterone, free testosterone, and bioavailable testosterone levels.
3) Guidelines recommend screening patients with diabetes and symptoms of hypogonadism for low testosterone. The patient should have been screened for erectile dysfunction due to his risk factors of diabetes and metabolic syndrome.
1. Vitaros is a topical cream containing alprostadil that is approved for the treatment of erectile dysfunction in multiple countries.
2. It is marketed as the first line treatment for erectile dysfunction, including for patients who cannot take oral PDE5 inhibitors due to health conditions or medications.
3. With over 7 million men in the Middle East potentially benefiting from Vitaros as it treats erectile dysfunction in patients who are non-responders to PDE5 inhibitors, it represents a significant market opportunity.
Il Vegacheck è una strumentazione medicale in grado di rilevare le alterazioni funzionali del nostro organismo, prima che compaiano le malattie. E' un esame innocuo, indolore, non invasivo che dura circa otto minuti. Il paziente è collegato all'apparecchio tramite sei elettrodi che analizzano le risposte bioelettriche del corpo.
I nutraceutici sono delle sostanze che possiedono effetti benefici sulla salute o sono in grado di prevenire le malattie cardiovascolari. I nutraceutici utilizzati per ridurre il colesterolo nel sangue sono fra i più venduti in Italia. Questa presentazione si interessa di passare in rassegna brevemente le sostanze nutraceutiche ipocolesterolemizzanti più impiegate in Italia.
Valutazione e gestione del rischio cardiovascolare in pazienti dai 45 ai 55 a...Sara Finollo
I fattori di rischio cardiovascolare sono condizioni statisticamente correlate all’insorgenza di una malattia cardiovascolare e sono derivanti da abitudini e stili di vita non corretti, da fattori ambientali e biologici, che, se presenti in un soggetto esente da manifestazioni cliniche di malattia, predicono la probabilità di andare incontro a patologia in un certo periodo di tempo. (Istituto Superiore Sanità, Progetto Cuore).
Sono indicatori di probabilità di sviluppare una malattia cardiovascolare e se in compresenza aumentano notevolmente il rischio di comparsa della patologia; la loro assenza come ovvio non esclude la malattia ma ne riduce drasticamente il rischio di sviluppo. Vennero identificati e valutati per la prima volta grazie allo studio osservazionale condotto nel 1948 dal cardiologo statunitense Thomas Royle Dawber che per le sue ricerche si basò sulla popolazione dell’intera cittadina di Framingham, nel Massachusetts. Dawber (ncbi.nlm.nih.gov) avviò dapprima lo studio tramite la “Division of Chronic Disease” della cittadina per poi far riferimento l’anno successivo al National Heart Institute degli Stati Uniti.
Lo studio Framingham fu il primo di una serie di ampi studi osservazionali che negli anni successivi vennero condotti su scala globale per valutare il rischio cardiovascolare.
I Mille volti della Nutrizione - Integratori alimentari: dal Mercato ai Consu...Digital for Academy
I Mille Volti della Nutrizione - Università degli Studi di Milano - Bicocca, 18 Settembre 2015.
Intervento del dott. Alessandro Colombo, Presidente gruppo Integratori e prod. salutistici - AIIPA Ass. Italiana Industrie Prod. Alimentari.
O documento apresenta o currículo de Samuel Rodrigues Lopes Sobrinho e discute a análise do comportamento dinâmico de um vagão submetido à excitação harmônica por meio de simulação multicorpos. O artigo descreve a modelagem do vagão e da via, identificando as frequências naturais de vibração do vagão e pontos críticos da interação vagão-via que podem causar riscos ao aumentar a velocidade.
Malattie cardiovascolari e infiammazione: un approccio nutraceuticoCarlo Maggio
Le malattie cardiovascolari rappresentano la prima causa di morte nei paesi industrializzati. La patologia di base che le accomuna è l'aterosclerosi. Tuttavia, negli ultimi anni si sta delineando il ruolo fondamentale dell'infiammazione cronica, sistemica di basso grado nel determinare l'insorgenza e la progressione dell'aterosclerosi. Le stesse statine, farmaci ampiamente utilizzati per la cura delle malattie cardiovascolari, presentano importanti effetti antinfiammatori. Nella nutraceutica numerosi principi già impiegati per la riduzione del colesterolo, come la berberina e la monacolina K, esplicano un'azione antinfiammatoria. La Medicina Funzionale spiega l'intreccio che esiste fra infiammazione, stress ossidativo, acidosi, disbiosi e alterazioni del sistema nervoso autonomo nella genesi delle malattie cardiovascolari.
This document summarizes information about androgen deficiency in aging men (ADAM syndrome). It discusses the physiology of androgens and how levels change with aging. ADAM syndrome, also called late-onset hypogonadism, describes the effects of declining testosterone in older men. Testosterone replacement therapy can improve sexual function, bone density, lean muscle mass, mood and cognition. However, risks include prostate issues and erythrocytosis. Guidelines recommend monitoring prostate-specific antigen and hematocrit for men undergoing testosterone replacement. More research is still needed to fully understand the risks and benefits of testosterone therapy in older men.
This document summarizes key information about prostate cancer including:
1. Risk factors such as age, ethnicity, family history, and diet.
2. Diagnostic tools like PSA testing which is imperfect but can be improved through measures of density and velocity.
3. Clinical stages from localized to metastatic disease and treatments available at each stage including androgen deprivation therapy and newer agents.
4. Ongoing research into better targeting the androgen receptor pathway which remains important even in advanced "castrate resistant" prostate cancer.
The document discusses the long-term side effects of androgen deprivation therapy (ADT) for prostate cancer, including increased risks of osteoporosis, cardiovascular events, sarcopenic obesity, and bone loss. It provides evidence that ADT increases standard cardiovascular risk factors and cardiovascular events. While the effect on cardiovascular mortality is disputed, age and pre-existing conditions are the main risk factors. Exercise and drugs like SERMs may help mitigate side effects, but do not reduce cardiovascular events. Careful management of known risk factors is important when treating with ADT.
The document summarizes key information about prostate cancer including incidence, mortality rates, clinical stages, risk groups for localized prostate cancer, treatment options for advanced disease including hormone therapy and chemotherapy, and results from clinical trials of chemotherapy agents like docetaxel and cabazitaxel.
- The document discusses various factors that may predict response and survival outcomes for men with metastatic prostate cancer receiving androgen deprivation therapy (ADT).
- Several studies have found that higher tumor levels of dihydrotestosterone (DHT) and androgen receptor content predicted better responses to ADT.
- Inherited genetic variants in hormone-related genes and the presence of certain gene fusions have also been linked to response to ADT.
- Lower PSA levels after 7 months of ADT induction, such as less than 0.2 ng/mL, are associated with longer survival. Bone pain, higher Gleason score, and other factors also predict poorer survival.
This document discusses several topics related to predicting response to hormonal therapy and survival in men with metastatic prostate cancer:
1) Androgen deprivation therapy (ADT) is standard treatment but not all patients respond equally well. Factors like surgical vs medical ADT and combined vs monotherapy have been studied.
2) Higher tumor levels of dihydrotestosterone (DHT) and androgen receptor content in tumors have been associated with better response to ADT and longer survival times.
3) Inherited genetic variants in hormone-related genes may also play a role in response to ADT, though more research is needed. The presence of certain gene fusions also appears to impact response.
4)
1) Endocrine therapy resistance in estrogen receptor positive breast cancer can occur through various mechanisms including loss of ER expression, crosstalk between ER and growth factor receptor pathways, and activation of the mTOR pathway.
2) Clinical trials have shown that combining endocrine therapies like aromatase inhibitors with targeted therapies against HER2 or mTOR can help overcome resistance, improving outcomes.
3) Further research is still needed to better understand resistance mechanisms and identify biomarkers to predict which combinations may help individual patients.
Localized prostate cancer is the most common cancer in men in Western countries. For patients with high risk localized prostate cancer, the current recommended treatment is androgen deprivation therapy combined with radiotherapy. Several large randomized controlled trials have shown this combination prolongs progression-free and overall survival compared to androgen deprivation alone. Additional treatment options for high risk localized prostate cancer currently being investigated include radical prostatectomy and chemotherapy with docetaxel. Erectile dysfunction is a common side effect of treatment that can be addressed with oral phosphodiesterase inhibitors or intracavernosal injections.
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This document provides an overview of metastatic prostate cancer management by Dr. Mohamed Abdulla of Cairo University. It discusses:
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For my 400 level class to my undergraduate degree, we were separated into research groups and choose a topic. The topic we researched all semester was sexual dysfunction. This topic incorporated prostate cancer and menopause. The following slide show is the result and conclusions of several papers read by our group.
We were able to conclude with an exercise prescription to slow the progression of prostate cancer. including: mode, duration, frequency, and intensity. Through collaborative analysis of other studies, we were also able to conclude sexual recommendations to slow the disease and lower risk.
Enjoy.
The document summarizes a study that aimed to predict clinical failure in patients with metastatic prostate cancer by identifying genes related to prostate cancer. Researchers analyzed gene expression levels of androgen receptor, estrogen receptor, and stem cell markers in cancer and stromal cells collected via laser capture microdissection from biopsy samples of 76 patients. Logistic regression analysis showed that expression of Sox2, Her2, and CRP in cancer cells and AR and ER in stromal cells highly predicted prostate-specific antigen recurrence. Ten factors were identified as prognostic for cancer-specific survival, including expression of Oct1, TRIM36, Sox2, c-Myc, AR, Klf4, ER, and clinical parameters. Patients were divided into risk
The document summarizes a study that aimed to predict clinical failure in patients with metastatic prostate cancer by identifying genes related to prostate cancer. Researchers analyzed gene expression levels of androgen receptor, estrogen receptor, and stem cell markers in cancer and stromal cells collected via laser capture microdissection from biopsy samples of 76 patients. Logistic regression analysis showed that expression of Sox2, Her2, and CRP in cancer cells and AR and ER in stromal cells highly predicted prostate-specific antigen recurrence. Ten factors were identified as prognostic for cancer-specific survival, including expression of Oct1, TRIM36, Sox2, c-Myc, AR, Klf4, ER, as well as PSA, Gleason score
Sequencing Agents in Metastatic Prostate Cancerflasco_org
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1. Testosterone e cancro alla prostata: è controindicata la
terapia sostitutiva con testosterone?
ALESSANDRO PIZZOCARO
U.O. Urologia
Servizio di Andrologia
Istituto Clinico Humanitas
Rozzano (MI)
2. Lack of sound evidence that TRT actually cause prostate cancer (PCA)
progression and/or recurrence in men with a history of PCA
• Key points
• The prostate saturation theory
• The association PCA-low testosterone levels
• The possible protective nature of TRT against the development of PCA
Moith Khera, Scott Dept Urol, Baylor College of Medicine, Houston, TX, USA; J. Sex Med, 2013
4. Traditional view
1. High T → rapid PCa growth
2. Low T → protective against PCa
3. T therapy contraindicated in men with PCa,
or even suspicion of PCa
5. Huggins and Hodges (1941)
1.Reduction of testosterone concentration by
castration or oestrogen treatment results in
regression of prostate cancer
2.Exogenous testosterone results in progression
of prostate cancer
6. Mental associations:
Risk of TRT – a survey among physicians in
Germany, Spain and England
Gooren LJ et al. Aging Male 2007; 10: 173–81.
7. Meta-analysis: Pooled data of 18 studies
No. of case patients/
Hormone Fifth No. of control subjects RR (95% Cl) RR & 95% Cl 2
1 for trend P
Testosterone 1 784/1302 1.00
2 761/1309 0.97 (0.85 to 1.11)
3 837/1287 1.08 (0.95 to 1.23) 0.17 .68
4 792/1281 1.03 (0.90 to 1.17)
5 712/1259 0.94 (0.82 to 1.07)
Free testosterone 1 691/1181 1.00
2 684/1165 1.01 (0.88 to 1.16)
3 750/1155 1.13 (0.98 to 1.29) 2.89 .09
4 707/1162 1.09 (0.95 to 1.25)
5 718/1152 1.11 (0.96 to 1.27)
DHT 1 240/298 1.00
2 192/284 0.83 (0.65 to 1.07)
3 188/282 0.82 (0.63 to 1.06) 1.19 .28
4 194/295 0.83 (0.64 to 1.08)
5 196/286 0.86 (0.66 to 1.11)
0.
5
0.7
5
1 1.
5
2.
0
3886 men with PCa and 6438 Controls
serum concentrations of sex hormones were not associated with
the risk of prostate cancer.
Endogenous Hormones and Prostate Cancer Collaborative Group J Natl Cancer Inst 2008; 100: 170–83.
8. PCa prevalence increases as
testosterone levels decline
40–49 50–59 60–69 70–79
% PCa
Total T
Age (years)
9. Androgens are essential for normal
development of the prostate
• Secretory functions
• Cellular differentiation
• Normal proliferation
10. Eugonadal man
Prostate volume 19 mL
PSA 0.9 ng/mL
Untreated
hypogonadal man
Prostate volume 8 mL
PSA 0.4 ng/mL
11. Prostate volume (mL)
Prostate volume measured by
transrectal ultrasonography
Hypogonadal patient without therapy
Normal men
Age (years)
50
40
30
20
10
0
20 30 40 50 60 70 80
Behre HM et al. Clin Endocrinol 1994; 40: 341–9.
12. Prostate volume (mL)
Prostate volume measured by
transrectal ultrasonography
Hypog. pat. without therapy Hypog. pat. with therapy Normal men
Age (years)
50
40
30
20
10
0
20 30 40 50 60 70 80
Behre HM et al. Clin Endocrinol 1994; 40: 341–9.
13. Prostate size in 334 hypogonadal men after a total of
6,596 injections of TU (maximal treatment duration 15 years)
Zitzmann M and Saad F
Endocrine Reviews 2010 (Abstract Book)
14. PSA in 334 hypogonadal men after a total of
6,596 injections of TU (maximal treatment duration 15 years)
Zitzmann M and Saad F
Endocrine Reviews 2010 (Abstract Book)
15. Testosterone and the prostate
Treatment with testosterone
• Incidence of cancer in testosterone treatment
studies up to 3 years: 1%
• Risk similar to detection in screening
programmes
Rhoden E & Morgentaler A. New Engl J Med 2004; 350: 482–92.
16. Can very high doses of testosterone
induce adverse events in the prostate?
17. Serum testosterone and PSA in young men treated with
escalating doses of testosterone
Bhasin S et al. Am J Physiol Endocrinol Metab 2001; 281: e1172–81.
10
8
6
4
2
0
Serum PSA at Week 20
18. Serum testosterone and PSA in older men treated with
escalating doses of testosterone
Bhasin S et al. J Clin Endocrinol Metab 2005; 90: 678–88.
14
10
8
6
4
2
0
Serum PSA at Week 20
12
24. Testosterone levels and Gleason scores in 47 men
with prostate cancer before radical prostatectomy
p<0.05
Madersbacher S et al. Urology 2002; 60: 869–74.
25. Testosterone levels and prostate cancer cases
among 345 hypogonadal men
(TT <300 or FT <1.5 ng/dL) with PSA ≤4 ng/mL
p=0.04 p=0.04
Morgentaler A & Rhoden EL. Urology 2006; 68: 1263–7.
26. Kaplan-Meier PSA failure-free survival curves according to
preoperative testosterone levels
Yamamoto S et al. Eur Urol 2007; 52: 696–701.
27. DHT levels and prostate cancer survival
Prostate cancer-specific survival for the 65 prostate cancer patients divided into two groups
with dihydrotestosterone (DHT) level above and below the median. There is a significant
improved survival in the group with DHT above the median (log rank p=0.0075).
Kjellman A et al. Eur Urol 2008; 53: 106–11.
28. Seattle-Veterans Study
1031 hypogonadal men
Treated n=398, age 61 yrs
Shores et al JCEM 2012
baseline T=5.6 nmol/L
incident PCa 1.6%
Untreated n=633, age 63 yrs
baseline T=6.7 nmol/L
incident PCa 2.0%
Log Rank p=0.029
Shores M et al. J Clin
Endocrinol Metab 2012; 97:
30. Testosterone Replacement Therapy Following the Diagnosis ofProstate
Cancer: Outcomes and Utilization Trends
Alan L. Kaplan AL et Al, J Sex Med 2014;11:1063–1070
31. Testosterone Replacement Therapy Following the Diagnosis ofProstate
Cancer: Outcomes and Utilization Trends
Alan L. Kaplan AL et Al, J Sex Med 2014;11:1063–1070
Conclusion
TRT was not associated with worse overall or cancer-specific mortality nor was it
associated with the use of salvage hormone therapy (ADT).
Although our findings suggest TRT may be safe in the setting of prostate cancer
diagnosis and treatment, confirmatory prospective studies are needed.
32. A New Era of Testosterone and Prostate Cancer:
From Physiology to Clinical Implications
Mohit Khera , David Crawford, Alvaro Morales, Andrea Salonia, Abraham Morgentaler
European Urology 65, 2014; 115–123
33. A New Era of Testosterone and Prostate Cancer:
From Physiology to Clinical Implications
Khera M , Crawford D, Morales A, Salonia A, Morgentaler A, EUROPEAN UROLOGY
65 (2014) 115–123
The small size and limited duration of these case series make it impossible to assess the overall safety of
testosterone therapy after definitive treatment for PCa, but so far, these results are reassuring.
Large, randomized prospective studies will be needed to provide reliable safety information.
35. Urinary flow rate in untreated hypogonadal men (n=47),
TRT – treated hypogonadal men (n=78)
and matched controls (n=75)
Max flow (mL/s)
untreated treated controls
40
35
30
25
20
15
10
5
0
Behre HM et al. Clin Endocrinol 1994; 40: 341–9.
36. TRT with intramuscular TU over 26 weeks
International Prostate Symptom Score and PSA in 20
patients with pre-diagnosed LOH and LUTS
p<0.00001
p<0.00001
NS
Kalinchenko SY et al. Aging Male 2008; 11: 57–61.
37. CONCLUSIONS
The long-held belief that PCa risk is related to high serum androgen
concentrations can no longer be supported.
Current evidence indicates that maximal androgen-stimulated PCa growth is
achieved at relatively low serum testosterone concentrations (Saturation
model)
Accumulating data indicate an important association between low
testosterone concentrations and worrisome aspects of PCa
It may therefore be reasonable to consider testosterone therapy in selected
men with PCa and symptomatic hypogonadism, despite the limited safety
information in this population
38. *
TRT in PCa pts
*TRT only after
- obtaining informed consent and
- beginning with the lowest- risk individuals (such as those with undetectable PSA >1
yr following RP).
Informed consent should include the information that no long-term safety data are
available and there is therefore an unknown degree of risk that PCa may recur or
progress.
Khera M. 2014
39. Odds Ratio for Major Adverse Cardiovascular Events (MACE) According
to Baseline Characteristics in Subjects Treated with Testosterone or Placebo
MACE: cardiovascular death, non-fatal myocardial infarction, stroke, acute coronary syndromes, and/or heart failure
CVD: Cardiovascular diseases; LL: Lower limit; UL: Upper limit;
MH-OR: Mantel-Haenszel odds ratio; TT: Total testosterone
100
Odds ratio for MACE
Source # Trials MH-OR LL p TRT Placebo
#Events # Patients #Events # Patients
Placebo TS
Associated diseases
Elderly men 10 1,22 0,49 3,03 0,67
Men with CVD 2 2,48 0,35 17,45 0,36
Frail men 5 2,25 0,72 7,08 0,17
Men with metabolic diseases 4 0,19 0,04 0,85 0,03
Hypogonadism status
Mixed population 14 1,26 0,58 2,73 0,56
TT < 12 nM 12 0,84 0,32 2,23 0,73
Type of support
Drug company not supported 12 0,94 0,39 2,24 0,88
Drug company supported 14 1,07 0,51 2,24 0,86
Trial duration
≤ 12 weeks 4 1,02 0,20 5,29 0,98
>12 weeks 22 1,01 0,55 1,84 0,98
13 954 6 549
3 62 1 64
13 401 4 355
1 303 5 203
15 1066 11 865
16 829 9 476
10 437 8 332
21 1458 12
2 147 2 145
29 1746 18 1196
0.01 0.1 1 10
UL
1009
Corona G et al. Expert Opin Drug Saf, published online August 19, 2014
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Editor's Notes
hohes Testosteron = hohes PCa-Risiko / schlechter Verlauf
niedriges Testosteron = niedriges PCa-Risiko / günstiger Verlauf
Verhältnis von T zum PCa = Benzin ins Feuer gießen
Data on serum concentrations of sex hormones from 18 prospective studies that included 3886 men with incident prostate cancer and 6438 control subjects
The androgen hypothesis has therefore been replaced by
the saturation model [10] to accommodate the dual
observations that PCa is (1) exquisitely sensitive to
variations in androgens at low concentrations and (2)
indifferent to variations at normal and high concentrations.
The simple yet profound paradigm change is that
androgens appear to have a finite ability to stimulate PCa
growth. This creates opportunities for new clinical uses of
testosterone therapy
Indications for testosterone
therapy in men include low testosterone levels in
combination with signs and symptoms of testosterone
deficiency, such as fatigue, erectile dysfunction, depression,
decreased libido, and decreased muscle mass. Although any
history of PCa has been a longstanding contraindication for
testosterone therapy, there may now be circumstances
where this is a reasonable therapeutic choice, as we discuss
below.
The saturation model explains the paradoxical observations
that prostate tissue is exquisitely sensitive to changes in
serum testosterone at low concentrations but becomes
indifferent to changes at higher testosterone concentrations.
A threshold effect occurs in which increasing androgen
concentrations reach a limit (the saturation point) beyond
which there is no further ability to induce androgen-driven
changes in prostate tissue growth
This explains why
dramatic changes in PSA are notedwhen serum testosterone
is manipulated into or out of the castration range, whereas
minimal or absent PSA changes occurwhen supraphysiologic
testosterone doses are administered to normal men.
One important mechanism contributing to the saturation
model is the finite ability of androgen to bind AR.
Maximal androgen–AR binding (ie, saturation) occurs atfairly low
androgenconcentrations inratandhumanprostate
tissue, reported in human prostate in vitro at approximately
4 nmol/l (approximately 125 ng/dl). In clinical practice,
the saturation point appears to be approximately 8 nmol/l
or 250 ng/dl, subject to interindividual variation.
Morgentaler A, Rhoden EL. Prevalence of prostate cancer amonghypogonadal men with prostate-specific antigen levels of 4.0 ng/mLor less. Urology 2006;68:1263–7.
In a larger study of 345 men with testosterone
deficiency and PSA levels <4.0 ng/ml, men with the lowest
tertile of serum testosterone had double the risk of PCa
compared withmenwith less severe testosterone deficiency.
The cancer rate was 30% for these men with a PSA value of
2.0–4.0 ng/ml [25].
FU ergänzt
PCA-> PSA
Population-based observational study of testosterone replacement therapy in men with a history
of prostate cancer (149,354 subjects)
Age 65 years or older, diagnosed with prostate cancer between 1991 and 2007
The cohort was divided into those that received TRT (n = 1,181) following prostate cancer diagnosis and those that did not (n = 148,173).
Utilization was associated with younger age (P = 0.001) and higher education (P < 0.0001) status (Table 1).
Median follow-up after prostate cancer diagnosis was 6 years (IQR 3–8) for the no TRT and 8 years (IQR 5–11) for the TRT groups (P < 0.001).
RESULTS:
First: TRT was not associated with increased overall or cancer-specific mortality. In fact, mortality events were significantly lower in the TRT group than in the men who did not receive TRT. The reason for lowered mortality rates among men receiving TRT is not clear
Second: the use of TRT in men with prostate cancer was exceedingly low, and usage declined over time. Less than 1% of men in
the cohort received testosterone therapy. The prevalence of hypogonadism ranges from 2.1 to 25% in the general population, depending on the
strictness of the criteria
Third: use of TRT was directly related to income and educational status and inversely related to age.
Finally, TRT was not associated with later use of salvage ADT, which may be considered a proxy for clinically significant disease recurrence following treatment. Within the median follow-up of 6 years, men who underwent TRT were no more likely to be treated with salvage ADT than men not receiving TRT. Thus, by this measure, progressive disease was not associated with use of TRT in men with a history of prostate cancer.
The small size and limited duration of these case series make it impossible to assess the overall safety of testosterone therapy after definitive treatment for PCa, but so far, these results are reassuring.
Large, randomized prospective
studies will be needed to provide reliable safety information.
We are aware of a single controlled prospective study
to date following RP (Baylor College of Medicine, Clinical-
Trials.gov identifier NCT00848497).
One possible explanation for the lack of PCa recurrence
noted in the previous studies is that these men may not have
had any residual PCa cells to be stimulated by androgens.
Amore provocative study, therefore, is to assess the response
to testosterone therapy in men with untreated PCa.
Morgentaler et al. treated 13 men on active surveillance
with testosterone therapy for a median of 2.5 yr (range:
1.0–8.1) [8]. All men underwent follow-up prostate biopsies,
with a mean of two sets of biopsies per patient. At initial
biopsy, 12 men had Gleason score 6 and one had Gleason
7 (3 + 4). Mean serum testosterone increased from 238 to
664 ng/dl. Mean PSA and prostate volume did not change
with testosterone therapy. No definite PCa progression was
noted in any man, and no cancer was found in 54% of followup
biopsies. These were the first results to directly assess the
effect of raising testosterone in men with untreated PCa.
These results inmenwith untreated PCamust be regarded
cautiously given the severely limited global experience, and a
report by Morales of erratic PSA responses to testosterone
therapy in several men on active surveillance [45].