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

Sex hormones appear to play a pivotal role in determining cardiovascular risk. Androgen deprivation therapy for males with prostate cancer results in a hypogonadal state that may have important, but as yet undetermined, effects on the vasculature. We studied the effects of androgen deprivation therapy on large artery stiffness in 22 prostate cancer patients (mean age, 67 +/- 8 yr) over a 6-month period. Arterial stiffness was assessed using pulse-wave analysis, a technique that measures peripheral arterial pressure waveforms and generates corresponding central aortic waveforms. This allows determination of the augmentation of central pressure resulting from wave reflection and the augmentation index, a measure of large artery stiffness. Body compositional changes were assessed using bioelectrical impedance analysis. Fasting lipids, glucose, insulin, testosterone, and estradiol were measured. After a 3-month treatment period, the augmentation index increased from 24 +/- 6% (mean +/- SD) at baseline to 29 +/- 9% (P = 0.003) despite no change in peripheral blood pressure. Timing of wave reflection was reduced from 137 +/- 7 to 129 +/- 10 msec (P = 0.003). Fat mass increased from 20.2 +/- 9.4 to 21.9 +/- 9.6 kg (P = 0.008), whereas lean body mass decreased from 63.2 +/- 6.8 to 61.5 +/- 6.0 kg (P = 0.016). There were no changes in lipids or glucose during treatment. Median serum insulin rose from 11.8 (range, 5.6-49.1) to 15.1 (range, 7.3-83.2) mU/liter at 1 month (P = 0.021) and to 19.3 (range, 0-85.0 mU/liter by 3 months (P = 0.020). There was a correlation between the changes in fat mass and insulin concentration over the 3-month period (r = 0.56; P = 0.013). In a subgroup of patients whose treatment was discontinued after 3 months, the augmentation index decreased from 31 +/- 7% at 3 months to 29 +/- 5% by 6 months, in contrast to patients receiving continuing treatment in whom the augmentation index remained elevated at 6 months compared with baseline (P = 0.043). These data indicate that induced hypogonadism in males with prostate cancer results in a rise in the augmentation of central arterial pressure, suggesting large artery stiffening. Adverse body compositional changes associated with rising insulin concentrations suggest reduced insulin sensitivity. These adverse hemodynamic and metabolic effects may increase cardiovascular risk in this patient group.
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PMID:The effects of induced hypogonadism on arterial stiffness, body composition, and metabolic parameters in males with prostate cancer. 1154 59

Androgen substitution has been intensively debated due to major concerns with respect to unknown interactions with prostate cancer initiation and progression. Certainly, androgen substitution should be considered in men with symptomatic hypogonadism (< 1% of men) in whom prostate cancer has been excluded. Serum PSA values should not exceed the currently employed age specific reference values (40-50 years: 2.5 ng/ml, 50-60 years: 3.5 ng/ml, 60-70 years: 4.5 ng/ml and over 70 years: 6.5 ng/ml). A family history of prostate cancer and/or prostatic intraepithelial neoplasia (PIN) should be considered as relative contraindications. If androgen substitution is to be initiated, serum PSA should be monitored at 3 month intervals including digital rectal examinations (DRE). In case of abnormal results (PSA and/or DRE) substitution therapy should be terminated and random prostate biopsies performed. In addition, major issues regarding the optimal substitution pathway (transdermal versus intramuscular versus implants versus oral) remain unclarified and require further investigation. Furthermore, little is known about the precise type and dosage of androgens to be substituted. Lastly, only 10%-18% of men with hypogonadism are symptomatic, reducing the number of patients in whom substitution therapy may be an option significantly. Although substitution therapy is valuable in selected men, unclear issues related to prostate cancer initiation and progression, timing, type and dosage of androgen substitution raise major concerns and need further investigation. Meanwhile patients need to be counselled and advantages balanced against disadvantages, side effects and potential risks.
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PMID:[Androgen substitution in men from the urologic point of view]. 1205 Sep 44

It is known that bone mineral density (BMD) is low in men who are hypogonadal. However, the rate and sites of bone loss following testosterone deficiency are not known. The resulting hypogonadism after GnRH analog therapy for the treatment of prostate cancer allows us to examine bone loss and bone resorption immediately after testosterone withdrawal. Therefore, we examined the effects of GnRH analog treatment on bone loss and bone resorption in men with prostate cancer. BMD and serum and urine concentrations of markers of bone turnover were determined in men with prostate cancer and in age-matched controls. Measurements were taken before GnRH therapy and 6 and 12 months after instituting therapy. After 12 months of GnRH therapy, the BMD of the total hip and ultra distal radius decreased significantly (P < 0.001) in men with prostate cancer compared with the controls. The mean bone loss was 3.3% and 5.3%, respectively. The observed reduction in BMD in the spine (2.8%) and the femoral neck (2.3%) did not reach statistical significance. No significant bone loss was observed in the control subjects. The concentration of the urine marker of bone resorption, N-telopeptide, was significantly increased from baseline and from controls at both 6 and 12 months in patients treated with GnRH analog therapy compared with control subjects (P < 0.05). The concentration of a serum marker of bone formation, bone-specific alkaline phosphatase, was not significantly different from baseline or from controls at 6 and 12 months. Thus, the decreased total hip and ultra distal radius BMD and increased urinary N-telopeptide concentration after testosterone withdrawal demonstrate an increase in trabecular bone loss and enhanced bone resorption. These findings demonstrate a significant loss of bone in men with prostate cancer after receiving GnRH therapy and suggest that the total hip and radius are the preferred sites for monitoring bone loss in older men. In addition, markers of bone resorption may be helpful.
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PMID:Bone loss following hypogonadism in men with prostate cancer treated with GnRH analogs. 1216 91

Hypogonadal men share a variety of signs and symptoms such as decreased muscle mass, osteopoenia, increased fat mass, fatigue, decreased libido and cognitive dysfunctions. Controlled trials have demonstrated favourable effects of androgen substitution therapy on these signs and symptoms in men with severe primary or secondary hypogonadism. Thus, androgen substitution therapy is warranted in men with true hypogonadism at all ages. Symptoms experienced by otherwise healthy ageing males are non-specific and vague, although some may be similar to symptoms of hypogonadism. Therefore, the term 'andropause' has been suggested. However, testosterone levels show no or only modest variation with age in men; with large prospective studies suggesting a maximal decline of total testosterone of 1.6% per year. Thus, in contrast to the sudden arrest of gonadal activity in females around menopause, men do not have an andropause. As large placebo-controlled studies of androgen treatment in elderly males are lacking, proper risk assessment of adverse effects such as prostate cancer following testosterone treatment in elderly males is completely lacking. In the future, testosterone therapy may prove beneficial in some elderly males with low-normal testosterone levels. However, at this point in time, widespread use of testosterone in an elderly male population outside controlled clinical trials seems inappropriate.
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PMID:Androgens and the ageing male. 1239 23

Testosterone supplementation is commonly used as a treatment for hypogonadal men with or without erectile dysfunction. The effect of parenteral testosterone replacement therapy on the development or growth of prostate cancer is unclear. We assessed the effect of this treatment on serum prostate-specific antigen (PSA) levels and risk of prostate cancer in hypogonadal men with erectile dysfunction. Criteria for inclusion were a normal pre-treatment PSA (<4.0 ng/mL) in conjunction with a normal digital rectal examination (DRE) or a negative pretreatment prostate biopsy for men with either an abnormal DRE or an elevated PSA. Patients received intramuscular injections every 2 to 4 weeks, allowing for dose titration. In this retrospective analysis, 54 hypogonadal men with erectile dysfunction were included, with a mean age of 60.4 years (range 42.0-76.0) and a mean follow-up of 30.2 months (range 2.0-82.0) on testosterone therapy. Mean pretreatment total testosterone level was 1.89 ng/mL (range 0.2-2.92), which increased during treatment to a mean of 9.74 ng/mL (range 1.50-26.30, P <.001). Mean pretreatment PSA was 1.86 ng/mL (median 1.01 ng/mL, range 0.0-15.80), which increased to a mean PSA level of 2.82 ng/mL (median 1.56 ng/mL, range 0.0-32.36, P <.01) with testosterone treatment. Of the 54 men included in this study, 6 (11.1%) required prostate biopsy while on testosterone therapy because of a rise in serum PSA above 4.0 ng/mL. One patient (1.9%) was diagnosed with prostate cancer. In conclusion, testosterone replacement therapy in men with erectile dysfunction and hypogonadism is associated with a minor PSA elevation, but there does not appear to be a short-term increase in risk for the development of prostate cancer.
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PMID:Prostate-specific antigen changes in hypogonadal men treated with testosterone replacement. 1239 40

Hypogonadism is a recognised cause of osteoporosis in men. When patients with advanced prostate cancer are treated with luteinising hormone releasing hormone (LHRH) agonist analogues their circulating testosterone levels decline and these patients may develop fractures.We have undertaken a cross-sectional study on a cohort of patients treated with goserelin (n=41) and compared their bone density and bone turnover with patients with prostate cancer not on goserelin and elderly patients living in the community.There was no difference in bone density between the patients on treatment and those living in the community and there was a similar incidence of osteoporosis (50 and 42%, respectively). The bone marker measurements were higher in the treated patients: urine N-telopeptide (NTX) 80.1 (9) (mean (s.e.)) BCE/mmol, compared to 30.1 (2.9), P<0.001 in elderly patients; and bone alkaline phosphatase 41.9 (6.1) u/l in treated patients and 20.7 (1.5) in untreated prostate cancer patients, P<0.002. Patients on treatment with radionuclide scan evidence of metastases did not have higher bone marker values than those with negative scans.As increased bone turnover and low bone density are associated with enhanced risk of osteoporotic fractures, we suggest that patients on LHRH agonist analogues should receive advice and possibly anti-bone resorptive treatment with bisphosphonates to prevent further bone loss and fractures.Prostate Cancer and Prostatic Diseases (2001) 4, 161-166.
Prostate Cancer Prostatic Dis 2001
PMID:Bone loss associated with the use of LHRH agonists in prostate cancer. 1249 35

The endocrine system has a major role in erections in normal men and it can also be a cause of significant morbidity. The relationship between serum testosterone measurement and erectile function is complex. Androgen treatment should certainly be considered in patients without prostate cancer but with a clinical picture that suggests a relevant contribution of hypogonadism to the ED. Other, nondiabetic, endocrine abnormalities may need to be considered in the management or the patient with ED.
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PMID:Endocrine causes of impotence (nondiabetes). 1258 May 59

Hansen's disease causes testicular failure secondarily, and because of this, it has been considered that prostate cancer would not be found in association. Three of 14 patients with chronic leprosy in Suruga National Sanatorium Hansen's Disease Hospital were found to have prostate cancer. A 72-year-old with lepromatous leprosy was diagnosed with stage T3a prostate cancer and treated with radical prostatectomy after hormonal therapy, plus irradiation. An 80-year-old with lepromatous leprosy was diagnosed with stage T2 prostate cancer and treated with irradiation and follow up only without hormone therapy and surgery because of his low testosterone level and old age. An 82-year-old with borderline leprosy was diagnosed with stage T1c prostate cancer and because of the pathological finding of low Gleason score and his old age, he was treated with hormonal therapy only. Two of the three cases had elevated concentrations of follicle-stimulating hormone and luteinizing hormone, which suggests that their prostatic cancers might have been equivalent to be under the influence of hormone therapy. Therefore, in aged male patients with Hansen's disease, the follicle-stimulating hormone, luteinizing hormone and testosterone concentrations should be measured, as well as that of prostate-specific antigen, and a prostate biopsy should be also considered if the prostate-specific antigen concentration is increased, even with hypogonadism.
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PMID:Prostate cancer in patients with Hansen's disease. 1262 16

There is now convincing evidence that in a subset of aging men, increasing with age, plasma testosterone levels fall below a critical level resulting in hypogonadism. This state of testosterone deficiency has an impact on bone, muscle and brain function and is maybe a factor in the accumulation of visceral fat which again has a significant impact on the cardiovascular risk profile. From the above it follows that androgen replacement to selected men with proven androgen deficiency will have beneficial effects. There is, however a concern that androgen administration to aging men may be harmful in view of effects on prostate disease. Benign prostate hyperplasia (BPH) and prostate cancer are typically diseases of the aging male, steeply increasing with age. But epidemiological studies provide no clues that the levels of circulating androgen are correlated with or predict prostate disease. Similarly, androgen replacement studies in men do not suggest that these men suffer in a higher degree from prostate disease than control subjects. It seems a defensible practice to treat aging men with androgens if and when they are testosterone-deficient, but long-term studies including sufficient numbers of men are needed.
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PMID:Androgen deficiency in the aging male: benefits and risks of androgen supplementation. 1294 21

Prostate cancer detection is a rare occurrence in patients with Klinefelter syndrome, in whom chronically low circulating androgen levels are common findings. Administration of exogenous testosterone has increasingly been used to treat young adolescents diagnosed with Klinefelter syndrome and documented androgen deficiency. Although testosterone replacement in adult patients has been associated with prostatic enlargement, it remains unknown whether chronic supplementation of exogenous testosterone to pubescent males with hypogonadism results in early prostate carcinogenesis. We report a first case of prostate cancer in a patient with Klinefelter syndrome who had undergone long-term testosterone replacement therapy since childhood for chronically depressed levels of testosterone.
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PMID:Prostate cancer in Klinefelter syndrome during hormonal replacement therapy. 1462 28


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