Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypogonadism from long-term androgen deprivation therapy (ADT), either by bilateral orchiectomy or administration of gonadotropin-releasing hormone (GnRH) agonists, causes significant and accelerated bone loss that may increase the risk of bone fractures in men with prostate cancer. Recent reports, as well as new data from our institution, have shown a high prevalence of pre-existing osteopenia and osteoporosis in men with prostate cancer before receiving ADT, and this is of great concern because of the risk of further bone loss during ADT. Data from these studies suggest the urgent need for clinical guidelines for screening, prevention, and treatment of these cases. This article reviews the prevalence and risk factors associated with osteoporosis in men and addresses risk factors in men with prostate cancer not receiving ADT. Considerations for the patient selection and timing of bone densitometry will also be discussed.
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PMID:Risk factors for male osteoporosis. 1467 May 49

To determine if bone mineral density (BMD) substantially influences health-related behaviors in men at risk for osteoporosis, we surveyed 102 men who were participating in a study of prostate cancer and bone loss. Subjects included 68 men with prostate cancer, 44 of whom were hypogonadal on androgen deprivation therapy, and 34 healthy age-matched controls without prostate cancer. At least 6 mo after an initial evaluation, assessment of BMD, and osteoporosis information session, men were administered a questionnaire regarding their healthrelated behaviors. We found that men with osteopenia were 4 times as likely (13%) and men with osteoporosis were more than 10 times as likely (41%) to start taking bisphosphonates compared to men with a normal bone mass (3%, p < 0.0001). Men with low bone mass were more likely to begin taking calcium (p < 0.05) and vitamin D supplements (p < 0.05). Hypogonadal men were 10 times as likely to begin using bisphosphonates (34%) compared to the control group (3%, p < 0.0001) and twice as likely to begin using calcium supplements (57% vs 24%, p < 0.05). Caffeine consumption, alcohol consumption, dietary calcium intake, exercise, and smoking habits were not different in men with osteoporosis or those who were hypogonadal compared to controls. We conclude that men with low bone mass and hypogonadism were more likely to start using bisphosphonates, calcium supplements, and vitamin D supplements after having a bone density test. However, they were not more likely to make significant health-related lifestyle changes after obtaining the results of their bone mass.
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PMID:Does bone mineral density and knowledge influence health-related behaviors of elderly men at risk for osteoporosis? 1471 44

Primary and secondary osteoporosis are prevalent in more than 2 million American men. One of the main causes of this is hypogonadism, in turn brought upon by early androgen deprivation therapy used in prostate cancer treatment. Androgen deprivation therapy produces a host of adverse effects on the skeleton, including an increase in bone turnover, a decrease in bone mineral density, and an increase in fracture risk. In addition, based on observations in preclinical models, these adverse effects on the skeletal integrity may promote the development of or progression of metastasis to bone. Loss of bone due to androgen deprivation therapy is an important clinical issue for many men with prostate cancer, but osteoporosis is not an inevitable consequence of androgen deprivation therapy. Because of interpatient variations in peak bone mass as well as differences in rates of treatment-related bone loss, not all men with prostate cancer require treatment for osteoporosis. All men on androgen deprivation therapy should receive calcium and multivitamin supplements and should be considered for bisphosphonate therapy; this is particularly so for men with either a low baseline BMD or observed high rates of bone loss during androgen deprivation therapy.
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PMID:The role of bisphosphonates in men with prostate cancer receiving androgen deprivation therapy. 1520 84

A prior comparison of 750 mg flutamide daily to 500 mg daily with an LHRH analog or orchiectomy showed no difference in effect on prostate specific antigen (PSA). However, any difference was likely masked by hypogonadism from concomitant LHRH analog or orchiectomy. We sought to evaluate different flutamide dosing schedules without this confounding factor. We recruited 50 men with advanced prostate cancer who elected to receive hormonal therapy to be randomized to 1 of 3 flutamide treatment groups: 1) 250 mg once daily, 2) 250 mg twice daily, or 3) 250 mg 3 times daily for 3 months, after which the therapy of their choice was instituted. Serum samples at the initiation of therapy and at the 1- and 3-month time point were assessed for PSA, testosterone, liver function tests, hematology, and renal function. Prostate volume, androgen deficiency symptoms, and a compliance diary were also recorded. Testosterone and PSA levels show a dose-dependent response to flutamide monotherapy. Loss of libido and erectile dysfunction occurred in all 3 treatment groups, with a trend toward worsening sexual function with higher flutamide dosing, but this trend did not reach statistical significance. Prostate volumes decreased by an average of 34.3% in the patients receiving 250 mg flutamide 3 times daily, 27.8% in patients receiving 250 mg flutamide twice daily, and 19.2% in those receiving a once daily dose of 250 mg flutamide. There was a significant difference between the once daily group and the 3 times daily group (P =.047). Flutamide at 500 mg did not result in significant changes in testosterone, PSA, prostate volume, or androgen deficiency symptoms compared to 750 mg daily after 3 months.
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PMID:Flutamide administration at 500 mg daily has similar effects on serum testosterone to 750 mg daily. 1522 52

The endocrine system of aging males reveals changes of more or less unknown significance for estrogens, dehydroepiandrosterone (DHEA), melatonin and growth hormone. The difference between physiological changes and clear hormone deficiency is not really understood and the clinical relevance of the observed changes needs to be investigated. Estrogens do not show any changes, but DHEA, melatonin or growth hormone show several changes in their concentrations concomitant with increasing age, without validated clinical significance. According to the guidelines of the ISSAM, the significance of changes in DHEA, DHEAS, melatonin, growth hormone and IGF-1 are not well enough understood to justify routine examination when investigating late-onset hypogonadism in aging men. There is no indication for treatment with these hormones (with the exception of, e.g., estrogens in prostate cancer or male-to-female-transsexualism), as the assumed positive effects as well as negative side effects are not clearly understood and need further investigation.
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PMID:[Hormone therapy in the aging male. Estrogen, DHEA, melatonin, somatotropin]. 1530 6

Testosterone has been available to practitioners for several decades. However, testosterone prescriptions have increased in recent years partly because of the introduction of newer delivery systems that are topical and have good bioavailability. In the US alone, approximately 2 million prescriptions for testosterone were written in 2002. This represents a 30% increase from 2001 and a 170% increase from 1999. There has also been a 500% increase in prescription sales in the past 10 years. The rise in prescriptions may be in part due to the increasing recognition of hypogonadism in ageing males or andropause. Treatment relating to hypogonadism has relieved symptoms and improved the quality of life of many individuals. Epidemiological studies point toward an association with increased morbidity and mortality, with low testosterone states in ageing males. For example, there is a higher prevalence of depression, coronary heart disease, osteoporosis, fracture rates, frailty and even dementia with low testosterone states. Recently, there have been some concerns raised regarding the long-term safety of testosterone replacement therapy (TRT) from the Institute of Medicine. Current evidence suggests no causal relationship between prostate cancer and physiological dosing of testosterone, especially with careful selection and monitoring of patients. Cardiovascular risks have, overall, been neutral, although suggestions have been made that there are positive vasodilatory properties with testosterone. Mild eythrocytosis can be a common side effect of TRT, but thromboembolic events have rarely been reported in the literature. This paper addresses the evidence to date regarding the safety aspects of TRT. The medical-legal implications of TRT for men at this point in time is also discussed.
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PMID:Risks of testosterone replacement therapy in ageing men. 1550 Apr 18

The concerns about testosterone therapy in ageing men with late-onset hypogonadism mainly address the risk of prostatic disease, i.e. either benign prostatic hyperplasia (BPH) or prostate cancer (PCa). Both conditions are highly dependent on androgen action and recent clinical data on the cancer-preventive effect of the 5alpha-reductase inhibitor finasteride have supported the possible role of androgens in PCa. However, the clinical data especially on the long-term effects of exogenous androgen substitution in regard to prostate safety are nonconclusive in many respects. As sufficient clinical studies on these risks will not be available in the near future, the approach of testosterone therapy towards prostate complications should be kept on a safe but practical basis. This review includes some recommendations in regard to testosterone therapy and prostate monitoring in patients with BPH and bladder outlet obstruction, with previous history of curative treatment for PCa or with prostatic intraepithelial neoplasia.
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PMID:Testosterone therapy in the ageing male: what about the prostate? 1554 Oct 51

For over 50 years, testosterone therapy has been used for the treatment of hypogonadism. In recent years, there has been an increase in the use of testosterone therapy for men with late-onset hypogonadism, as more convenient and effective modes of application are developed. Testosterone therapy in these men can significantly improve their sense of well-being, and lead to increases in muscle and bone mass, upper body strength, virility and libido [Gruenewald, Matsumoto. J Am Geriatr Soc 2003;51:101; Morales. Aging Male 2004; in press]. However, ensuring that optimal testosterone therapy is achieved in men with hypogonadism remains challenging. Oral delivery of unmodified testosterone is not possible, due to rapid first-pass metabolism and its short half-life. Therefore, different derivatives and formulations of testosterone have been developed to enhance potency, prolong duration of action or improve bioavailability. In addition, several different routes of administration have now been evaluated, including intramuscular injections, oral formulations, transdermal patches, transbuccal systems and transdermal testosterone gel. Despite the broad range of testosterone therapy on offer, each form has its benefits and limitations, and some will suit one patient more than another. An important concern among clinicians is that testosterone therapy may cause or promote prostate cancer. While current evidence supports the safety of testosterone therapy, androgens are growth factors for pre-existing prostate cancer. Therefore, before therapy is initiated, careful digital rectal examination and determination of prostate-specific antigen (PSA) in serum should be performed, in order to exclude evident or suspected prostate cancer. The first 3-6 months after initiating testosterone therapy is the most critical time for monitoring effects on the prostate. Therefore, it is important to monitor PSA levels every 3 months for the first year of treatment; thereafter, regular monitoring (mostly for prostate safety but also for cardiovascular and haematological safety) during therapy is mandatory.
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PMID:The current status of therapy for symptomatic late-onset hypogonadism with transdermal testosterone gel. 1596 69

Due to a decrease in Leydig cell function, a considerable proportion of men over 50 years of age will develop hypogonadism. Consequently, loss of libido and several other testosterone-dependent symptoms may become evident. When decreased levels of biologically available testosterone are found, and corresponding symptoms are present, these men could be eligible for testosterone substitution therapy. Testosterone treatment in testosterone-deprived men has been shown to improve general well-being, osteoporosis, muscle atrophy, libido and--if present--anemia. Despite these positive effects, testosterone treatment has to be performed with caution. Although it has not been proven that elevation of the serum testosterone level to the normal range results in a greater risk of developing prostate cancer, the effects of testosterone on a prostate cancer already present are well established. Several studies have demonstrated that testosterone treatment does not result in a significant increase in serum levels of prostate-specific antigen (PSA) or prostate volume. The long-term effects, however, are currently unknown. For these reasons, testosterone treatment should be performed only when the presence of prostate cancer is unlikely; i.e. when PSA levels are within normal limits and digital rectal examination does not reveal any suspicious findings. These examinations may still miss some small prostate cancers that could be promoted by testosterone treatment. The determination of PSA levels under testosterone treatment is necessary every 3 months, at least for the first year. Steadily rising PSA levels require immediate cessation of testosterone administration and the initiation of further diagnostic procedures (prostate biopsy), to rule out prostate cancer.
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PMID:Clinical experiences with testosterone therapy: prostate safety. 1579 26

Bone is a major target tissue for sex hormones and hypogonadism is a known cause of male osteoporosis. Androgen-deprivation therapy (ADT) for prostate cancer yields hypogonadotropic status and accelerates age-related decrease in bone mineral density. The risk for osteoporotic fractures is also increased which may lead to a shorter life expectancy for prostatic cancer patients. Baseline and follow up bone density measurement is desired for all men beginning ADT and it is advisable to take calcium and vitamin D as well as maintain a moderate exercise. Bisphosphonate is a possible treatment for those in whom osteoporosis develops. More data are desirable to make a guideline to prevent and treat male osteoporosis under ADT.
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PMID:[Bone loss in men under androgen-deprivation therapy for prostate cancer]. 1582 42


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