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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypogonadism is highly prevalent in older men and men who have prostate cancer. The symptoms of hypogonadism, such as depression, decreased libido, erectile dysfunction, and decreased bone mineral density, can significantly impair a man's quality of life. Moreover, we know that testosterone plays an important role in erectile preservation and in the growth and function of cavernosal and penile nerves. There are compelling data to suggest that testosterone replacement therapy (TRT) in normal and high-risk men does not increase the risk for prostate cancer. In the few studies of men treated with TRT after a radical prostatectomy, there have been no biochemical recurrences. Based on these data, it is difficult to justify withholding TRT following a radical prostatectomy. If we do not lower the testosterone levels of eugonadal men after a radical prostatectomy, how can we justify not replacing testosterone levels in hypogonadal men to make them eugonadal following a radical prostatectomy?
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PMID:The role of testosterone replacement therapy following radical prostatectomy. 1798 94

Age-related decline in serum testosterone and dehydroepiandrosterone sulfate concentrations occur in men. Low concentrations of these endogenous androgens have been linked with insulin resistance, which is an important upstream driver for metabolic abnormalities such as hyperglycemia, hypertension, or hyperlipidemia, and increased cardiovascular risk. Moreover, men with diabetes have significantly less circulating androgen than nondiabetic men. Here, we summarize how androgen affects insulin resistance and atherosclerosis in men with type 2 diabetes. Low serum concentrations of endogenous androgens are associated with visceral fat accumulation. Androgen deprivation by castration to treat prostate cancer increases insulin resistance, while testosterone administration in type 2 diabetic men with androgen deficiency improves glucose homeostasis and decreases visceral fat, in addition to alleviating symptoms of androgen deficiency including erectile dysfunction. Androgen correlates inversely with severity of atherosclerosis and has beneficial effects upon vascular reactivity, inflammatory cytokine, adhesion molecules, insulin resistance, serum lipids, and hemostatic factors. Because men with type 2 diabetes have relative hypogonadism, testosterone supplementation could decrease both insulin resistance and atherosclerosis.
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PMID:Role of endogenous androgen against insulin resistance and athero- sclerosis in men with type 2 diabetes. 1822 Jun 53

Testosterone is more than a "male sex hormone". It is an important contributor to the robust metabolic functioning of multiple bodily systems. The abuse of anabolic steroids by athletes over the years has been one of the major detractors from the investigation and treatment of clinical states that could be caused by or related to male hypogonadism. The unwarranted fear that testosterone therapy would induce prostate cancer has also deterred physicians form pursuing more aggressively the possibility of hypogonadism in symptomatic male patients. In addition to these two mythologies, many physicians believe that testosterone is bad for the male heart. The classical anabolic agents, 17-alkylated steroids, are, indeed, potentially harmful to the liver, to insulin action to lipid metabolism. These substances, however, are not testosterone, which has none of these adverse effects. The current evidence, in fact, strongly suggests that testosterone may be cardioprotective. There is virtually no evidence to implicate testosterone as a cause of prostate cancer. It may exacerbate an existing prostate cancer, although the evidence is flimsy, but it does not likely cause the cancer in the first place. Testosterone has stimulatory effects on bones, muscles, erythropoietin, libido, mood and cognition centres in the brain, penile erection. It is reduced in metabolic syndrome and diabetes and therapy with testosterone in these conditions may provide amelioration by lowering LDL cholesterol, blood sugar, glycated hemoglobin and insulin resistance. The best measure is bio-available testosterone which is the fraction of testosterone not bound to sex hormone binding globulin. Several forms of testosterone administration are available making compliance much less of an issue with testosterone replacement therapy.
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PMID:The many faces of testosterone. 1822 57

Safety of testosterone undecanoate in relation to initiation of cancer and prostatic adenoma (PA) in patients with androgenic deficiency and erectile dysfunction (ED) was studied for 12 months in 49 patients aged 57 to 73 years treated with intramuscular testosteron injections. The size of the prostate in patients with adenoma was 46.34 +/- 21.12 cm3 while in adenoma-free patients--19.11 +/- 6.57 sm3. Diabetes mellitus of type 2 (DM-2) was diagnosed in 46.9% patients. All the patients had documented hypogonadism and ED. Tests for PSA and transrectal ultrasound investigation was made in all the patients. 12 month testosterone therapy produced normalization of a mean level of testosterone in both groups, index of erectile function increased. In one patient PSA rose higher than normal value. None of the patients developed obstruction of the urinary tract. Body mass index, lipid spectrum and carbohydrate metabolism also improved. Thus, long-term therapy with testosterone undecanoate has no effect on PSA level, does not induce urinary obstruction with enlarged prostate. The presence of DM-2 is not a contraindication for androgen therapy in adenoma patients. By reducing body mass index, total cholesterol, triglycerides and LDLP, testosterone therapy lowers the risk of prostatic cancer.
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PMID:[Safety of long-term replacement hormonal therapy in patients with erectile dysfunction and androgen deficiency]. 1825 26

It is well known that testosterone enhances sexual interest leading to an increased frequency of sexual acts and an increase in the frequency of sleep-related erections. However, it has little effect on fantasy- or visually induced erections. Exact contribution to erection from testosterone in men remains unclear. Animal studies have well demonstrated that testosterone plays critical physiological (activity of nitric oxide synthases and phosphodiesterases), biochemical (through an endothelial-independent pathway and adrenergic tonicity) and structural (change of fibroelasticity and hollow cell accumulation) roles in erectile function. The supplementation of testosterone to castrated animals can restore erectile function. Clinically, reports of patients with erectile dysfunction (ED) combined with hypogonadism who receive testosterone therapy have inconsistent results. However, testosterone may ameliorate the expression of the phosphodiesterase-5 (PDE5) inhibitor, and the use of testosterone in conjunction with the PDE5 inhibitor revealed convincing results. Because of potential risks in clinical use, testosterone therapy should be individualized, carefully considered and closely monitored, especially, in patients with possible occult prostate cancer, and large benign prostatic hyperplasia. Lower urinary tract symptoms might be worsened by this treatment, since the prostate is an androgen-dependent tissue.
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PMID:The relationship between hypogonadism and erectile dysfunction. 1830 86

This paper provides a systematic review of the literature about prostate cancer risk associated with testosterone therapy for hypogonadism. A comprehensive search of MEDLINE, EMBASE and other resources was conducted to identify articles that highlight occurrences of prostate cancer in men receiving testosterone therapy for hypogonadism treatment. Articles that met study inclusion criteria were assessed for causality between testosterone treatment and prostate cancer, increased prostate-specific antigen or abnormal digital rectal examination findings. Of 197 articles relating to testosterone therapy, 44 met inclusion criteria: 11 placebo-controlled, randomized studies; 29 non-placebo-controlled studies of men with no prostate cancer history; and 4 studies of hypogonadal men with history of prostate cancer. Of studies that met inclusion criteria, none demonstrated that testosterone therapy for hypogonadism increased prostate cancer risk or increased Gleason grade of cancer detected in treated vs untreated men. Testosterone therapy did not have a consistent effect on prostate-specific antigen levels.
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PMID:Testosterone therapy in hypogonadal men and potential prostate cancer risk: a systematic review. 1863 57

Advances in the understanding of the pathophysiology of a variety of urological disorders have resulted in the development of novel medications to manage these diseases. While many disorders such as erectile dysfunction, overactive bladder, hypogonadism and benign prostatic hypertrophy have traditionally been managed primarily by urologists, the use of these newer medications has become commonplace in the primary care setting. For example, symptomatic benign prostatic hyperplasia therapy, while historically treated with primary surgical intervention, is now commonly initially managed with medical therapy. Prostate cancer patients are being treated with newer formulations of long term hormone therapy that range from monthly to yearly administration. Additionally, the open dialogue about erectile dysfunction can be directly traced to the development of oral therapy for this condition. Testosterone replacement therapy can be administered using a variety of oral, transdermal and intramuscular therapies in order to minimize side effects and provide a more consistent dosing pattern. Finally, overactive bladder, which is a significant problem socially, has many new medications available for its treatment. This article will review some of the newer classes of urological medications, provide an understanding of basic uropharmacology that may guide treatment recommendations, and provide insight into the potential adverse side effects and interactions of these useful medications.
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PMID:Uropharmacology for the primary care physician. 1870 69

Prostate cancer is the most common gender-specific malignancy in men in the USA. Androgen-deprivation therapy (ADT) is commonly used in the treatment of metastatic or recurrent prostate cancer. The use of ADT is increasing with the advocacy of adjuvant and neoadjuvant ADT for treating asymptomatic patients with locally advanced prostate cancer. Although the use of ADT has resulted in improved survival in men with advanced prostate cancer, ADT, with its resulting severe hypogonadism, causes profound metabolic side-effects. We comprehensively reviewed previous reports using Medline searches of English-language literature (1950 to the present), with the keywords 'hypogonadism', 'testosterone', 'androgen deprivation therapy', 'hormonal treatment', 'prostate cancer', 'diabetes', 'metabolic syndrome', and 'cardiovascular disease'. Men with prostate cancer who undergo long-term ADT are at greater risk of developing dyslipidaemia, insulin resistance, hyperglycaemia and metabolic syndrome. These metabolic and physiological changes are a direct result of the induced severe hypogonadism and might predispose patients to a greater risk of cardiovascular morbidity and mortality. There is a need for prospective studies aimed and designed to investigate the metabolic and cardiovascular adverse effects of ADT, and assess the benefit/risk ratio, especially in special populations such as diabetics.
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PMID:Metabolic and cardiovascular effects of androgen deprivation therapy. 1872 14

Hypogonadism is a common condition, especially among older men, but often goes undiagnosed and untreated. It can be associated with a number of signs and symptoms that affect health and quality of life, including feelings of low energy and fatigue; decreased sex drive and performance; decreased muscle mass and strength; decreased bone mineral density; and increased body fat, particularly abdominal fat, a putative risk factor for metabolic syndrome and type 2 diabetes mellitus. The evidence supporting testosterone replacement therapy (TRT) in improving these and related conditions is strong and consistent for body composition and sexual function; moderately consistent for bone mineral density; inconsistent for insulin sensitivity, glycemic control, and lipid profiles; and weak and inconsistent for mood and cognitive function. The concern of some physicians about the potential for TRT to stimulate prostate cancer is not supported by decades of data accumulated to date, though studies of longer duration (eg, 10 years or more) would be even more convincing. Other research needs are discussed. As the front line of health care delivery, primary care physicians need to be vigilant in diagnosing and treating symptomatic hypogonadism. Based on current guidelines, we recommend assessing testosterone levels when an adult man exhibits signs of hypogonadism, and as part of normal medical screening in men starting at age 40 to 50 years, to establish a baseline. A physician should discuss the possibility of TRT with symptomatic patients who have a serum total testosterone level < 300 ng/dL. If TRT is initiated, a patient's response and adverse events should be assessed every 3 to 6 months, and therapy adjusted accordingly.
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PMID:Testosterone replacement therapy in hypogonadal men: assessing benefits, risks, and best practices. 1882 32

Late-onset hypogonadism (LOH) and testosterone replacement therapy (TRT) are subjects of much recent research. Because aging men are at risk for benign prostatic hyperplasia (BPH) and prostate cancer, elucidating the relationship between testosterone and these diseases is crucial to ensure its safe administration. It is known that testosterone supplementation may worsen active prostate cancer and that its blockade or removal slows the disease's progression. However, recent studies have attempted to show that, in individuals in whom prostate cancer has been ruled out, TRT may simply restore serum testosterone levels to within normal limits without significant adverse affects on the prostate. Patients undergoing TRT should be monitored carefully for any evidence of prostatic disease.
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PMID:Testosterone and the prostate: implications for the treatment of hypogonadal men. 1894 16


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