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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 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

Previous studies have suggested that hyperinsulinaemia and other components of metabolic syndrome are risk factors for clinical prostate cancer. This prospective study tested the hypothesis that hyperinsulinaemia and other components of metabolic syndrome are risk factors for lethal clinical prostate cancer. The clinical, haemodynamic, anthropometric, metabolic and insulin profile at baseline in men who had died from clinical prostate cancer during follow-up was compared with the profile of men who were still alive at follow-up. If the hypothesis is true, men with an unfavourable prognosis would have a higher profile at baseline than those with a favourable prognosis. A total of 320 patients in whom clinical prostate cancer, stages T2-3, had been diagnosed were consecutively included in the study during 1995-2003. Height, body weight, waist measurement, hip measurement and blood pressure were determined. Body mass index and waist/hip ratio (WHR) were calculated. Blood samples were collected to determine triglycerides, total cholesterol, high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol, uric acid, alanine aminotransferase and fasting plasma insulin level. The prostate gland volume was measured using transrectal ultrasound. The annual benign prostatic hyperplasia (BPH) growth rate was calculated. The diagnosis of prostate cancer was established using transrectal ultrasound-guided automatic needle biopsy of the prostate gland. All patients with clinical prostate cancer were followed up until their death or until the study was terminated on 31 December 2003. At follow-up, 54 patients had died from prostate cancer and 219 were still alive. The results showed that the men who died of clinical prostate cancer during the follow-up period were older (P < 0.001), had a larger prostate gland volume (P < 0.001), a faster BPH growth rate (P < 0.001), a higher prevalence of type 2 diabetes (P < 0.035) and treated hypertension (P < 0.023), a higher stage (P < 0.001) and grade (P = 0.028) of clinical prostate cancer, a higher prostate-specific antigen (PSA) level (P < 0.001) and a higher PSA density (P < 0.001) at baseline than men still alive with clinical prostate cancer at follow-up. These men also had a lower HDL-cholesterol level (P = 0.027), a higher fasting plasma insulin level (P = 0.004), a higher WHR (P = 0.097) of borderline significance and a higher uric acid level (P = 0.079) of borderline significance. Eliminating the effect on mortality of higher stage and grade of the clinical prostate cancer and PSA at baseline, the following statistically significant correlations remained: a higher fasting plasma insulin level (P = 0.010) and a lower HDL-cholesterol level of borderline significance (P = 0.065). In conclusion, hyperinsulinaemia and five other previously established components of metabolic syndrome are shown to be prospective risk factors for deaths that can be ascribed to prostate cancer. These findings confirm previous study, which indicate that prostate cancer is a component of metabolic syndrome. Moreover, these data indicate that hyperinsulinaemia and other metabolic disorders precede deaths caused by prostate cancer. Thus, our data support the hypothesis that hyperinsulinaemia is a promoter of clinical prostate cancer. Furthermore, our data suggest that the insulin level could be used as a marker of prostate cancer prognosis and tumour aggressiveness, regardless of the patient's prostate cancer stage, cancer grade and PSA level.
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PMID:Hyperinsulinaemia: a prospective risk factor for lethal clinical prostate cancer. 1624 13

As the primary prevention of disease has been emphasized, there may be a growing need for well-conditioned development and spread of OTC test equipment, OTC test reagent and remote healthcare. Some typical examples of "simple and rapid examination items, which can be done at home by established technology" are explained in this paper and may be required in the near future by the whole Japanese population with a view to the current status of OTC test and the coming relaxation of governmental regulation. The reasons why these examination items should be commercialized as Switch OTC and the epidemiological background are further discussed. In relation to metabolic syndrome derived from super spreader-like visceral mature adipocyte: SSVMAC, visceral fat rate measurement by bioelectrical impedance technology, postprandial blood glucose determination/urinary glucose determination, and urinary microalbumin detection, are explained with an example, together with the importance of early morning blood pressure recording. In the field of cancer and infectious diseases, immunological fecal occult blood determination as a marker of distal colorectal cancer, in which both higher survival rate and recovery rate by early detection have been established, Helicobacter pylori IgG antibodies or antigen examination including an examination of gastroduodenal disorder, prostate-specific antigen (PSA) and genital chlamydia are emphasized.
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PMID:[Future outlook for OTC examination (test)]. 1644 86

Hypogonadism in men has a complex and varied pathogenesis. In addition to multiple established causes of the disease, low testosterone levels are associated with various comorbidities, including metabolic syndrome and type 2 diabetes. Symptoms associated with hypogonadism include reduced sex drive, fatigue, and mood disturbances, but accurate diagnosis requires biochemical testing. Total testosterone is considered the appropriate testosterone measurement in most situations in primary care, although free testosterone is a more accurate marker and is indicated in some situations. Testosterone replacement therapy is a valid treatment option for men with testosterone deficiency accompanied by symptoms of hypogonadism. The goals of therapy are to restore physiologic testosterone levels and alleviate symptoms. A potential association of testosterone replacement therapy with prostate cancer is the biggest safety concern, so patient monitoring should include regular digital rectal examination and prostate-specific antigen tests.
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PMID:Evolving issues in male hypogonadism: evaluation, management, and related comorbidities. 1754 24

Prior studies report slightly lower prostate-specific antigen (PSA) levels among obese men. To understand this effect, we investigated the association between PSA and blood HbA1c, C-peptide, leptin and adiponectin levels in African-American (AA) (n=121) and Caucasian (CA) (n=121) men. Among AA men, PSA levels decreased with increasing C-peptide levels (PSA=0.99, 0.93, 0.75 and 0.53 ng ml(-1) across quartiles of C-peptide, respectively; P(trend)=0.005). Among CA men, PSA levels decreased with increasing HbA1c (PSA=0.84, 0.73, 0.77 and 0.45 ng ml(-1) across quartiles of HbA1c, respectively; P(trend)=0.005). This may suggest that metabolic disturbances related to metabolic syndrome or diabetes affect the ability to detect early-stage prostate cancer.
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PMID:Association between prostate-specific antigen and leptin, adiponectin, HbA1c or C-peptide among African-American and Caucasian men. 1793 44

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

Central obesity in adulthood, the metabolic syndrome, erectile failure and lower urinary tract symptoms (LUTS) are all associated with lower-than-normal testosterone levels, although the relationship between testosterone and LUTS appears weak. The metabolic syndrome is associated with an overactivity of the autonomic nervous system. Alternatively, the metabolic syndrome is associated with markers of inflammation, such as C-reactive protein (CRP), maybe signalling intraprostatic inflammation. A large cohort of 95 middle-aged to elderly hypogonadal men (T levels 5.9-12.1 nmol l(-1)) were treated with parenteral testosterone undecanoate and its effects on the metabolic syndrome {waist circumference, cholesterol, CRP and LUTS [residual bladder volume (RBV), International Prostate Symptoms Score (IPSS), prostate volume, prostate-specific antigen (PSA)]} were evaluated. Along with the improvements of the metabolic syndrome, there was a significant decline of the values of the IPSS, RBV and CRP. There was a (low) level of correlation between the decline of waist circumference and residual volume of urine but not with IPSS and prostate size. Along with the improvement of the metabolic syndrome upon testosterone administration, there was also an improvement of the IPSS and of RBV of urine and CRP. The mechanism remains to be elucidated.
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PMID:Concurrent improvement of the metabolic syndrome and lower urinary tract symptoms upon normalisation of plasma testosterone levels in hypogonadal elderly men. 1914 23

Prostate cancer is the most frequently diagnosed malignancy among UK men and accounts for 12% of male deaths. Androgen deprivation therapy (ADT) is commonly used as part of the treatment for prostate cancer. It is effective at suppressing prostate-specific antigen, stabilizing disease, alleviating symptoms in advanced disease, and potentially prolonging survival. However ADT, presumably at least in part owing to low testosterone levels is associated with insulin resistance, the development of metabolic syndrome plus increased overall and cardiovascular disease mortality. We have reviewed the relationship between prostate cancer, ADT, metabolic syndrome, type 2 diabetes, and cardiovascular disease. We have not reviewed other potential medical problems such as osteoporosis. We suggest that there should be a baseline assessment of patients' risk for cardiovascular disease before starting ADT. Consideration should be given to starting appropriate therapies including lifestyle advice, antihypertensive and lipid-lowering agents, insulin sensitizer, plus possibly aspirin. Having started ADT, the patients should have a regular (possibly annual) assessment of their cardiovascular risk factors.
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PMID:Prostate cancer, androgen deprivation therapy, obesity, the metabolic syndrome, type 2 diabetes, and cardiovascular disease: a review. 2129 30

Androgen-dependent pathways regulate maintenance and growth of normal and malignant prostate tissues. Androgen deprivation therapy (ADT) exploits this dependence and is used to treat metastatic prostate cancer; however, regression initially seen with ADT gives way to development of incurable castration-resistant prostate cancer (CRPC). Although ADT generates a therapeutic response, it is also associated with a pattern of metabolic alterations consistent with metabolic syndrome including elevated circulating insulin. Because CRPC cells are capable of synthesizing androgens de novo, we hypothesized that insulin may also influence steroidogenesis in CRPC. In this study, we examined this hypothesis by evaluating the effect of insulin on steroid synthesis in prostate cancer cell lines. Treatment with 10 nmol/L insulin increased mRNA and protein expression of steroidogenesis enzymes and upregulated the insulin receptor substrate insulin receptor substrate 2 (IRS-2). Similarly, insulin treatment upregulated intracellular testosterone levels and secreted androgens, with the concentrations of steroids observed similar to the levels reported in prostate cancer patients. With similar potency to dihydrotestosterone, insulin treatment resulted in increased mRNA expression of prostate-specific antigen. CRPC progression also correlated with increased expression of IRS-2 and insulin receptor in vivo. Taken together, our findings support the hypothesis that the elevated insulin levels associated with therapeutic castration may exacerbate progression of prostate cancer to incurable CRPC in part by enhancing steroidogenesis.
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PMID:Insulin increases de novo steroidogenesis in prostate cancer cells. 2174 18

Among men treated with prostatectomy or radiation therapy for localized prostate cancer, the state of an increasing prostate-specific antigen (PSA) level is known as biochemical recurrence (BCR). BCR can be predictive of the development of subsequent distant metastases and ultimately death, but BCR often predates other signs of clinical progression by several years. Although patients may be concerned about their rising PSA levels, physicians attempting to address patient anxiety must inform them that BCR is not typically associated with imminent death from disease, and that the natural history of biochemical progression may be prolonged. Misinterpretation of the significance of early changes in PSA may cause patients to receive androgen deprivation therapy (ADT) prematurely, especially in settings where the disease is unlikely to impact survival. In addition, knowledge of the morbidities associated with ADT (hot flashes, impotence, sarcopenia, metabolic syndrome, bone loss, and increased risk of vascular disease) has accelerated the search for alternative treatment options for these patients. Clinical trials investigating when and how to best use and supplement hormonal therapies in this patient population are under way, as are trials of novel nonhormonal targeted agents, immunotherapies, natural products, and other pharmaceuticals that have been approved by the US Food and Drug Administration (FDA) for other indications. This review will summarize the acceptable standards of care for the management of biochemically recurrent prostate cancer, and will also outline some novel experimental approaches for the treatment of this disease state.
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PMID:Management of biochemically recurrent prostate cancer after local therapy: evolving standards of care and new directions. 2341 59


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