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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to test the hypothesis of a causal relationship between high insulin levels and the development of benign prostatic hyperplasia (BPH) and to determine the clinical, anthropometric, metabolic and insulin profile in men with fast-growing BPH compared with men with slow-growing BPH. The present study was designed as a risk factor analysis of BPH in which the estimated annual BPH growth rate was related to components of the metabolic syndrome. Two hundred and fifty patients referred to the Urological Section, Department of Surgery, Central Hospital, Varberg, Sweden, with lower urinary tract symptoms with or without manifestations of the metabolic syndrome were consecutively included. The prevalences of atherosclerotic disease manifestations, non-insulin-dependent diabetes mellitus (NIDDM) and treated hypertension were obtained. Data on blood pressure, waist and hip measurement, body height and weight were collected and body mass index (BMI) and waist/hip ratio (WHR) were calculated. Blood samples were drawn from fasting patients to determine insulin, total cholesterol, triglycerides, HDL and LDL cholesterol, uric acid, alanine aminotransferase (ALAT) and prostate-specific antigen (PSA). The prostate gland volume was determined using ultrasound. The median annual BPH growth rate was 1.04 ml/year. Men with fast-growing BPH had a higher prevalence of NIDDM (p = 0.023) and treated hypertension (p = 0.049). These patients were also taller (p=0.004) and more obese as measured by body weight (p<0.001), BMI (p=0.026), waist measurement (p <0.001), hip measurement (p = 0.006) and WHR (p=0.029). Moreover, they had elevated fasting plasma insulin levels (p = 0.018) and lower HDL cholesterol levels (p = 0.021) than men with slow-growing BPH. The annual BPH growth rate correlated positively with diastolic blood pressure (rs = 0.14; p = 0.009), BMI (rs = 0.24; p < 0.001) and four other expressions of obesity and fasting plasma insulin level (rs = 0.18; p = 0.008), and negatively with the HDL cholesterol level (rs = -0.22; p = 0.001). In conclusion, the data suggest that NIDDM, hypertension, tallness, obesity, high insulin and low HDL cholesterol levels constitute risk factors for the development of BPH. The results also suggest that BPH is a component of the metabolic syndrome and that BPH patients may share the same metabolic abnormality of a defective insulin-mediated glucose uptake and secondary hyperinsulinaemia, as patients with the metabolic syndrome. The findings support the hypothesis of a causal relationship between high insulin levels and the development of BPH, and give rise to a hypothesis of increased sympathetic nerve activity in men with BPH.
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PMID:Clinical, anthropometric, metabolic and insulin profile of men with fast annual growth rates of benign prostatic hyperplasia. 1041 80

Prostate cancer is one of the most common cancers in men, therefore has become recently an essential problem of public health. The factors influencing cancer include: androgens metabolism disorders, diabetes mellitus, overweight and obesity, smoking, alcohol and black coffee intake, diet rich in saturated fats and poor in unsaturated, lack of physical activity, geographical zone, race, such carcinogenic substances as: cadmium, materials used in rubber, painting, printing, ship industry etc., contagious factors and also older age and a positive family history of the disease. To diagnose prostate cancer in its early stage such screening procedures as physical examination--digital rectal exam (DRE) and determination of prostate-specific antigen (PSA) level in blood serum are used. The aim of the study was to assess prostate cancer risk factors occurrence in the examined 193 men, aged 50-70 years, who reported to urology outpatient department at Clinical Hospital in Lublin, measure the PSA level in blood serum and examine the correlation between them. Respondents filled in a questionnaire about the presence of prostate cancer risk factors and urogenital symptoms. The questionnaire was completed with DRE and PSA measurement. The results led us to the following conclusions: 1/ in the studied population elevated PSA level is determined in 3.1% of 193 examined men, 2/ increased PSA occurs mainly in men from rural areas, with elementary education, divorced, older (>60 years), using fat-rich diet, smokers, black coffee drinkers, with overweight or obesity and non diabetic, 3/ a combination of PSA test with DRE seems to be useful and rather cheap for the detection of prostate cancer in the early stage of its development.
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PMID:Increasing level of prostate-specific antigen and prostate cancer risk factors among 193 men examined in screening procedure. 1532 67

Increasing prostate volume contributes to urinary tract symptoms and may obscure prostate cancer detection. We investigated the association between obesity and prostate volume, prostate-specific antigen (PSA) and PSA density among 753 men referred for prostate biopsy. Among men with a negative biopsy, prostate volume significantly increased approximately 25% from the lowest to highest body mass index (BMI), waist or hip circumference or height categories. PSA was 0.7 ng/ml lower with a high waist-to-hip ratio. These associations were less consistent among subjects diagnosed with high-grade prostatic intraepithelial neoplasia or cancer. Our data suggest that obesity and height are independently associated with prostate volume..
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PMID:The association between body size, prostate volume and prostate-specific antigen. 1717 79

Many investigators suggested that obesity predisposes to adverse prostate cancer characteristics and outcomes. We tested the effect of obesity on the rate of aggressive prostate cancer at either prostate biopsy or radical prostatectomy (RP). Clinical and pathological data were available for 1,814 men. Univariable and multivariable logistic regression models addressed the rate of high grade prostate cancer (HGPCa) at either biopsy or final pathology. Clinical stage, prostate-specific antigen (PSA), percentage of free PSA and prostate volume were the base predictors. All models were fitted with and without body mass index (BMI), which quantified obesity. BMI and its reciprocal (InvBMI) were coded as cubic splines to allow nonlinear effects. Predictive accuracy (PA) was quantified with area under curve estimates, which were subjected to 200 bootstrap re-samples to reduce overfit bias. Gains in PA related to the inclusion of BMI were compared using the Mantel-Haenszel test. HGPCa at biopsy was detected in 562 (31%) and HGPCa at RP pathology was present in 931 (51.3%) men. In either univariable or multivariable models predicting HGPCa at biopsy, BMI or InvBMI failed to respectively reach statistical significance or add to multivariable PA (BMI gain = 0%, p = 1.0; InvBMI gain = -0.2%, p = 0.9). Conversely, in models predicting HGPCa at RP, BMI and InvBMI represented independent predictors but failed to increase PA (BMI gain = 0.7%, p = 0.6; InvBMI gain = 0.5, p = 0.7%). Obesity does not predispose to more aggressive prostate cancer at biopsy. Similarly, obesity does not change the ability to identify those who may harbor HGPCa at RP.
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PMID:Obesity does not predispose to more aggressive prostate cancer either at biopsy or radical prostatectomy in European men. 1745 51

Both obesity and prostate cancer are epidemic in Western society. Although initial epidemiologic data appeared conflicting, recent studies, especially large prospective studies published in the past 6-12 months, have clarified the association between obesity and prostate cancer. The aim of this paper is to review the epidemiologic data linking obesity and prostate cancer, with an emphasis on new data published since 2005. A PubMed search was done on the keywords, "prostate cancer" and "obesity." Relevant articles and their references were reviewed for data on the association between obesity and prostate cancer. Recent data suggest that obesity is associated with reduced risk of nonaggressive disease but increased risk of aggressive disease. This may in part be explained by an inherent bias in our ability to detect prostate cancer in obese men (lower prostate-specific antigen values and larger sized prostates making biopsy less accurate for finding an existing cancer). Ultimately, this leads to increased risk of cancer recurrence after primary therapy and increased risk of prostate cancer mortality. The biologic causes of these associations are likely multifactorial, although the lower testosterone levels among obese men appear to be one of the most promising explanations. The association between obesity and prostate cancer is complex. Emerging data suggest a differential effect of obesity by disease aggressiveness: obesity may reduce the risk of nonaggressive disease while it may promote aggressive disease.
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PMID:Obesity and prostate cancer: making sense out of apparently conflicting data. 1747 39

Recent studies have suggested that obesity is associated with lower serum prostate-specific antigen levels, perhaps influencing the recommendation for prostate biopsy and potentially explaining part of the observed poorer prognosis among obese men. African-American men have the greatest rates of prostate cancer and are more likely to die of the disease, making early detection a priority in this group. We present findings from the Flint Men's Health Study, a study of African-American men, that are consistent with most studies suggesting that overweight men have prostate-specific antigen levels that are 0.15 to 0.30 ng/mL lower than those who are not overweight. We have coupled our results with a systematic review of publications in this area.
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PMID:Body composition and serum prostate-specific antigen: review and findings from Flint Men's Health Study. 1830 73

The purpose of this study was to evaluate the relationship of baseline body mass index (BMI) and serum testosterone level with prostate cancer outcomes in men with castration-resistant metastatic prostate cancer (CRPC). BMI and testosterone levels were evaluated for their ability to predict overall survival (OS) and prostate-specific antigen (PSA) declines in the TAX327 clinical trial, an international phase III randomized trial of one of the two schedules of docetaxel and prednisone compared with mitoxantrone and prednisone. In this study of 1006 men with CRPC, the median serum testosterone level was 14.5 ng per 100 ml (range 0-270), the median BMI was 27 kg m(-2) (range 15.7-46.5), and 26% of men were obese or morbidly obese (BMI>or=30). Obesity was associated with younger age, lower PSA and alkaline phosphatase levels, and higher performance status, primary Gleason sum, testosterone and hemoglobin compared to absence of obesity. In multivariate analysis, neither BMI, presence of obesity, nor baseline testosterone was significantly associated with OS or PSA declines. Higher testosterone levels among obese men suggest incomplete gonadal suppression with current therapies, but these differences may not be clinically relevant in men with CRPC. There was evidence of potential hemodilution of PSA and alkaline phosphatase levels in obese men.
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PMID:The relationship of body mass index and serum testosterone with disease outcomes in men with castration-resistant metastatic prostate cancer. 1857 90

Studies suggest inverse associations between obesity and prostate-specific antigen (PSA). However, there is little evidence whether factors related to obesity, including lifestyle (diet and physical activity) and physiologic factors (insulin resistance and metabolic syndrome), influence PSA. We used dietary, physical activity, and serum PSA, insulin, glucose, and lipid data for men >40 years from the National Health and Nutrition Examination Survey (2001-2004; N = 2,548). Energy, fat, and carbohydrate intakes were estimated from a 24-hour dietary recall. Men were considered as having metabolic syndrome based on the Adult Treatment Panel III criteria. Leisure-time physical activity and doctor-diagnosed hypertension were self-reported. Body mass index was calculated from measured weight and height. We computed the geometric mean PSA (ng/mL), adjusted for age, race, and body mass index, by tertile of energy, fat, and carbohydrate intake and level of physical activity, and among men with and without insulin resistance and metabolic syndrome in the whole population and by race. The geometric mean PSA (95% confidence interval) among men in the lowest tertile of energy was 1.05 (0.97-1.1) relative to 0.85 (0.8-0.9) in the highest tertile (P = 0.0002) in the whole population. The PSA concentrations were lower among overweight men with higher versus lower energy intake (P = 0.001). The PSA concentrations in men with insulin resistance was lower [0.87 (0.8-0.9)] relative to men without insulin resistance [0.98 (0.9-1.1)] at P = 0.04. All associations were in similar directions within racial subgroups. No associations were observed between the other lifestyle and physiologic factors. Additional studies are required to confirm these results and to investigate the potential mechanisms that may explain these relationships.
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PMID:Associations of lifestyle and physiologic factors with prostate-specific antigen concentrations: evidence from the National Health and Nutrition Examination Survey (2001-2004). 1876 17

The advent of prostate-specific antigen screening has changed the global epidemiology of prostate cancer, with men being diagnosed with organ-confined cancer at a younger age. Radical prostatectomy with curative intent for these patients, while delivering excellent long-term survival outcomes, still has significant side effects, chiefly postprostatectomy incontinence. Increasing age, shorter pre- and post-operative membranous urethral length, anastomotic strictures, obesity, low surgeon volume, variations of surgical technique and previous prostate surgery have been reported as negative risk factors for delayed continence recovery and/or permanent incontinence following radical prostatectomy. Significant progress in elucidating the functional anatomy and physiology of the male continence mechanism from cadaveric and videourodynamic studies have enabled surgeons to propose innovative surgical techniques during radical prostatectomy for augmenting continence preservation and early return. These have included optimizing the preservation of urethral rhabdosphincter length; avoiding rhabdosphincter injury; posterior reconstruction of Denonvilliers' musculofascial plate; preservation of the bladder neck and internal sphincter; bladder neck intussusception; bladder neck mucosal eversion; preservation of the puboprostatic ligaments and arcus tendineus; and preservation of putative nerves supplying the continence mechanism. We review the scientific and technical advances in continence recovery following radical prostatectomy, identify the key principles undergirding early return of continence, highlight various treatment strategies for early and refractory postprostatectomy incontinence and describe our experience with a paradigm of these unified key principles. Increasing application of these principles in computer-aided (robotic), minimally invasive and minimal-access (i.e., single-port or natural orifice transluminal) approaches will hopefully enable patients to derive maximal benefit from curative prostatectomy while experiencing early return of continence in the not too distant future.
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PMID:Scientific and technical advances in continence recovery following radical prostatectomy. 1957 98

The purpose of this article is to review the pertinent literature and compare the outcomes after radical prostatectomy (RP) and radiotherapy (RT). The probability of cure is similar after either RP or RT. The likelihood of significant treatment complications is probably higher after RP compared with RT. Preservation of erectile function is at least as good or better with RT compared with RP. Urinary continence is more likely to be preserved after RT compared with RP. Each treatment results in distinct patterns of adverse changes in quality of life that are worsened by factors including obesity, large prostate size, high prostate-specific antigen (PSA), and older age.
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PMID:Is radical prostatectomy the "gold standard" for localized prostate cancer? 2001 78


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