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Metabolic syndrome is associated with increased cancer risk and progression at almost all sites, including the prostate in high-stage prostate cancer. However, several reports have described an inverse relationship between metabolic syndrome and its components and low-stage incident prostate cancer. Such anomalies in cancer research hamper efforts to fight cancer. Evidence suggests that metabolic syndrome and its components have two distinct effects in prostate cancer, concealing prostate cancer in low-stage disease and promoting progression to high-stage incident, nonlocalized, and lethal prostate cancer. The concealment of prostate cancer by metabolic syndrome and its components might be related to bias mechanisms that reduce PSA level and lead to a delayed diagnosis of low-stage prostate cancer, meaning that fewer men with metabolic syndrome are diagnosed with low-stage disease. The inverse link between metabolic syndrome and its components and low-stage incident prostate cancer might simply be the result of such bias and the shortcomings of the diagnostic procedure rather than being related to prostate cancer biology itself. The evidence summarized here supports the hypothesis that the link between metabolic syndrome and its components and incident prostate cancer is a two-way and stage-dependent one, a theory that requires further research.

The metabolic syndrome is common in countries with Western lifestyles. It comprises a number of disorders-including insulin resistance, hypertension and obesity-that all act as risk factors for cardiovascular diseases. Urological diseases have also been linked to the metabolic syndrome. Most established aspects of the metabolic syndrome are linked to benign prostatic hyperplasia (BPH) and prostate cancer. Fasting plasma insulin, in particular, has been linked to BPH and incident, aggressive and lethal prostate cancer. The metabolic syndrome has also been shown to be associated with nonprostatic urological conditions such as male hypogonadism, nephrolithiasis, overactive bladder and erectile dysfunction, although data on these conditions are still sparse. Overall, the results of studies on urological aspects of the metabolic syndrome seem to indicate that BPH and prostate cancer could be regarded as two new aspects of the metabolic syndrome, and that an increased insulin level is a common underlying aberration that promotes both BPH and clinical prostate cancer. Urologists need to be aware of the effect that the metabolic syndrome has on urological disorders and should transfer this knowledge to their patients.

A higher insulin level has been linked to the risk of prostate cancer promotion. However, several reports claim that there is no association between a higher insulin level and the risk of incident prostate cancer. In the present report, the insulin hypothesis was tested once more prospectively in men with a benign prostatic disorder. Three hundred and eighty-nine consecutive patients referred with lower urinary tract symptoms without clinical prostate cancer were included during 1994-2002. Follow-up was performed in 2006. Data were obtained from the Swedish National Cancer Register and the Regional Cancer Register, Oncological Centre, Göteborg, Sweden. At this follow-up, 44 of the patients included had developed prostate cancer. Men with prostate cancer diagnosis had a higher systolic (P0.001) and diastolic blood pressure (P0.000), were more obese as measured by BMI (P=0.010), waist (P=0.007) and hip measurements (P=0.041) than men who did not have prostate cancer diagnosis at follow-up. These men also had a higher uric acid level (P=0.040), and a higher fasting serum insulin level (P=0.023) than men who did not have prostate cancer diagnosis at follow-up. Following exclusion of T1a/b prostate cancer cases, the difference of the fasting serum insulin level between the groups was still significant (P=0.038). Our data support the hypothesis that a higher insulin level is a promoter of prostate cancer. Moreover, our data suggest that the insulin level could be used as a marker of the risk of developing prostate cancer. The present findings also seem to confirm that prostate cancer is a component of the metabolic syndrome. Finally, our data generate the hypothesis that the metabolic syndrome conceals early prostate cancer.

The aetiology of benign prostatic hyperplasia (BPH) remains unclear. The objective of the present study was to test the insulin, oestradiol and metabolic syndrome hypotheses as promoters of BPH. The design was a risk factor analysis of BPH in which the total prostate gland volume was related to endocrine and anthropometric factors. The participants studied were 184 representative men, aged 72-76 years, residing in Göteborg, Sweden. Using a multivariate analysis, BPH as measured by the total prostate gland volume correlated statistically significantly with fasting serum insulin (beta=0.200, P=0.028), free oestradiol (beta=0.233, P=0.008) and lean body mass (beta=0.257, P=0.034). Insulin and free oestradiol appear to be independent risk factors for BPH, confirming both the insulin and the oestradiol hypotheses. Our findings also seem to confirm the metabolic syndrome hypothesis. The metabolic syndrome and its major endocrine aberration, hyperinsulinaemia, are possible primary events in BPH.

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.

Previous studies have shown that non-insulin-dependent diabetes mellitus (NIDDM), hypertension, atherosclerotic disease manifestations, tallness, obesity, dyslipidaemia, hyperuricaemia, hyperinsulinaemia and high alanine aminotransferase (ALAT) levels are risk factors for development of benign prostatic hyperplasia (BPH). This indicates that BPH is a component of the metabolic syndrome. In a subsequent study, we found that there was an association between the BPH growth rate and the development of clinical prostate cancer. These findings generated a hypothesis that clinical prostate cancer also was a component of the metabolic syndrome. In the present study, this hypothesis was tested on 299 patients with recently diagnosed clinical prostate cancer. If this hypothesis is true, patients with clinical prostate cancer of high stage and grade would have a larger prostate gland volume, a faster BPH growth rate and a more pronounced clinical, haemodynamic, anthropometric, metabolic and insulin profile than patients with clinical prostate cancer of low stage and grade have.Two hundred and ninety-nine patients in whom clinical prostate cancer was diagnosed were consecutively included. The prevalence of NIDDM, treated hypertension and atherosclerotic manifestations was provided by the respective patient's medical history. Body length, body weight, waist measurement, hip measurement and blood pressure were determined. Body mass index (BMI) and waist/hip ratio (WHR) were calculated. Blood samples were drawn to determine triglycerides, total cholesterol, high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol, uric acid, ALAT and the fasting plasma insulin level. The prostate gland volume was measured using transrectal ultrasound. The annual BPH growth rate was calculated. The prostate cancer diagnosis was established.Patients with clinical prostate cancer, prostate-specific antigen (PSA)50 ng/ml, stage T3, had a bigger prostate gland volume (p0.001), a faster BPH growth rate (p0.001), were more obese, as measured by body weight (p = 0.062), BMI (p = 0.003), waist measurement (p = 0.011) and hip measurement (p = 0.051) and showed a higher systolic blood pressure (p0.070) than patients with T2 clinical prostate cancer. When patients with clinical prostate cancer, PSA50 ng/ml, were included at the comparison, T3 tumour patients showed a higher prevalence of treated hypertension (p = 0.026) than patients with T2 tumours. Patients with clinical prostate cancer, PSA50 ng/ml, G3, had a greater prostate gland volume (p = 0.004), a faster BPH growth rate (p = 0.005) and were more obese as determined by waist measurement (p = 0.044) and WHR (p = 0.073). Moreover, subjects with a G3 tumour were more dyslipidaemic, as shown by a higher triglyceride level (p = 0.019) and a lower HDL-cholesterol level (p = 0.005), and were more hyperuricaemic (p = 0.023), showed a higher plasma insulin level (p = 0.019) and a higher ALAT level (p = 0.061) than those with a G1 tumour. When patients with clinical prostate cancer, PSA50 ng/ml, were included at the comparison, G3 patients had a greater prostate gland volume (p = 0.002) and a faster BPH growth rate (p = 0.003) than patients with G1 tumours.The results of the present study suggest that the prostate gland volume, the BPH growth rate, hypertension, obesity, dyslipidaemia, hyperuricaemia, hyperinsulinaemia and high ALAT levels are risk factors for the development of clinical prostate cancer. Thus, our results support the hypothesis that clinical prostate cancer is a component of the metabolic syndrome. Patients with clinical prostate cancer may have the same metabolic abnormality of a defective insulin-stimulated glucose uptake and secondary hyperinsulinaemia as patients with the metabolic syndrome. Our data also support the hypothesis that hyperinsulinaemia is a promoter of clinical prostate cancer.

Postoperative skin complications increase health care costs and cause patient suffering. In the OR, patients are exposed to materials with adhesive substances that have the potential to cause allergic or toxic effects on the skin. Intraoperatively and postoperatively, these reactions can result in skin complications. The objective of this study was to investigate the incidence of skin reactions in connection with the application of different materials. Skin reactions after preoperative skin testing occurred in 3% to 50% of patients with atopic or contact eczema, allergy, or asthma in their medical history. AORN J 77 (April 2003) 762–771.

Objective. The aim of this study was to test whether lower urinary tract symptoms (LUTS) and urinary incontinence are associated with the metabolic syndrome (MetS). The association between LUTS and benign prostatic enlargement (BPE) was also investigated. Material and methods. A cross-sectional, representative risk factor analysis of LUTS, as measured by the International Prostate Symptom Score (IPSS), and urinary incontinence was conducted. Among 950 representative individuals, aged 69–81 years, the association between clinical, anthropometric, endocrine, metabolic and inflammatory factors on the one hand, as both major and minor aspects of MetS, and LUTS and urinary incontinence, on the other hand, was analysed. The prostate gland volume was measured in a subgroup of 155 randomly selected individuals and the association between LUTS and BPE was estimated. Results. No significant association was found between LUTS or urinary incontinence and the major aspects of the MetS. However, in a multivariate analysis, serum serotonin showed an independent negative correlation with LUTS and with urinary incontinence while fasting serum glucose and serum adiponectin showed a positive correlation with LUTS. Furthermore, in a subgroup of 155 individuals, the prostate gland volume correlated positively with LUTS. Conclusions. The study did not show an association between LUTS or urinary incontinence and the major components of the MetS. However, serum serotonin showed an independent negative correlation with LUTS and with urinary incontinence while fasting serum glucose and serum adiponectin showed a positive correlation with LUTS. The data confirm the general knowledge that BPE may be one of the causative factors of LUTS.

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

Purpose: We tested the hypothesis that low vitamin D is associated with benign prostatic hyperplasia. We also studied whether body composition, sex hormones, serum sex hormone-binding globulin, albumin corrected serum calcium, adiponectin and lipid status are associated with benign prostatic hyperplasia. Materials and Methods: We investigated 184 representative, randomly selected men 72 to 76 years old enrolled in the Gothenburg arm of the Osteoporotic Fractures in Men Study (MrOS). Men with a history of prostate cancer, prostate operation or medication for benign prostatic hyperplasia were excluded from study, leaving 155 available for analysis. A cross-sectional study was performed in which benign prostatic hyperplasia measured by total prostate volume was related to clinical, anthropometric, endocrine and metabolic factors on univariate and multivariate analyses with regression models. Results: Median prostate volume was 40 ml. In multivariate models only 25-OH vitamin D, albumin corrected serum calcium, serum sex hormone-binding globulin and high density lipoprotein cholesterol were significantly and inversely associated with large prostate glands. Conclusions: The current report adds 4 independent factors associated with benign prostatic hyperplasia, including low 25-OH vitamin D, serum calcium, sex hormone-binding globulin and high density lipoprotein cholesterol.

Background. Theoretical considerations have raised the suspicion that transurethral resection of the prostate (TURP) may increase the risk of developing prostate cancer in clinically benign prostate glands. Previous studies have not shown an increased risk among men who had undergone TURP for benign prostatic hyperplasia compared with the risk in age-matched control subjects. However, in all of these studies, all men with stage T1 prostate cancer in the TURP-group were excluded, possibly creating a bias, because no similar exclusion could be made for the controls. Methods. The incidence and mortality of clinical prostate cancer were studied in 198 patients who had TURP and in 203 age-matched male control subjects. In both groups, all patients with known prostate cancer and patients with suspected cancer by digital rectal examination were excluded from the study. However, patients with stage T1 cancer found by the TURP were included in the comparison between the groups. Results. The mean age in the two groups was 67 ± 6 years. The patients were followed for an average of 10.2 ± 1.2 years and 10.4 ± 1.8 years in the TURP group and the control group, respectively. Clinical prostate cancer developed in six patients who had TURP and subsequently in five control (odds ratio, 0.8 [0.2-3.11; P < 0.97]. Before follow-up, three men in each group died because of prostate cancer (odds ratio, 1.3 (0.24-7.45); P < 0.97). Conclusions. The results of this study suggest that neither benign prostatic hyperplasia nor TURP increased the risk of developing clinical prostate cancer over the next 10 years in patients with a benign prostate gland determined by rectal examination before TURP.

To investigate the prevalence of and restrictions in various parts of daily life due to lower urinary tract symptoms (LUTS) in an unselected Swedish male population.A random selection of 3345 men throughout Sweden, aged between 41 and 80, was contacted by telephone and evaluated according to International Prostate Symptom Score (IPSS). The responders were then sent two different questionnaires based on degree of LUTS, IPSS8 or7.2106 men (66%) answered the questionnaire. Of these, 33.4% had an IPSS7 and the IPSS increased with age. Of the men with IPSS7 only 41% had consulted health services for their symptoms and 23% had received treatment. Thirty-seven per cent claimed that their problems had a great negative effect on their quality of life and 77% that they had affected their relationship with their spouse negatively to a great extent. Forty per cent did not consult health services despite their symptoms. In men with an IPSS8 as many as 33% believed that LUTS would limit them in at least some part of their daily life.LUTS is a common condition among Swedish men with a severe impact on quality of life and everyday life. Despite readily available medical assistance, two out of five men with LUTS still do not try to obtain a remedy. The data presented here identify a need for improved education regarding LUTS, to increase awareness of the condition and the treatment options that are available.

An open, prospective, randomized study was performed to investigate the effect of norfloxacin prophylaxis on stricture formation and operative outcome after transurethral resection of the prostate. After resection, the 359 patients studied were randomly divided into 2 groups: 1) those given norfloxacin as prophylaxis for 15 days following removal of the catheter (norfloxacin group) and 2) those given no antimicrobial prophylaxis during the same period (control group). Of the patients 94 were excluded. At followup 6 to 12 months postoperatively, the number of strictures in the anterior urethra was 2 of 135 in the norfloxacin group and 22 of 130 in the control group (p0.01). Strictures in the bladder neck developed in 3 of 135 and 4 of 130 patients, respectively (not significant). As a consequence of a lower structure incidence in the anterior urethra in the norfloxacin group, fewer patients in that group were dissatisfied with the operative outcome. The results suggest that norfloxacin provides effective prophylaxis against stricture formation after transurethral resection of the prostate.

To determine the validity coefficient of the total prostate gland volume as an expression of the transition zone (TZ) volume. To test the hypothesis of hyperinsulinaemia as a causal factor for the development of benign prostatic hyperplasia (BPH).Three hundred and seven consecutive patients with lower urinary tract symptoms were studied. A subgroup of 114 patients were tested with regard to the validity coefficient between the total prostate gland volume and the TZ volume. In the total material of 307 men, a BPH risk factor analysis was performed in which groups of men with the following conditions were related to the annual BPH growth rate: men without or with metabolic disease; men with different components of the metabolic syndrome, and men with low or high fasting plasma insulin values. The prostate gland volume and the TZ volume were determined using ultrasound. The presence of non-insulin-dependent diabetes mellitus (NIDDM) and treated hypertension was obtained from the patients' medical records. Data on blood pressure, waist and hip measurement, body height and weight were collected and body mass index and waist/hip ratio were calculated. Blood samples were drawn from fasting patients to determine the insulin and HDL-cholesterol values.In the subgroup of men subjected to measurement of both the total prostate gland volume and the TZ volume, the correlation coefficient between total prostate gland volume and the TZ volume was r.s. = 0.97 (p0.0001) which, thus, constituted the validity coefficient. The median annual BPH growth rate in the total group was 1.03 ml/year. The median annual BPH growth rate was faster in men with metabolic disease (p0.0001), NIDDM (p0.0001), treated hypertension (p0.0001), obesity (p0.0001) and dyslipidaemia (p0.0001) than in men without metabolic disease. Moreover, the annual BPH growth rate correlated positively with the diastolic blood pressure (r.s. = 0.27; p0.001), the BMI (r.s. = 0.22; p0.001) and four other expressions of obesity, and negatively with the HDL-cholesterol level (r.s. = -0.15; p0.001). The median annual BPH growth rate was faster in men with a high than in men with a low fasting plasma insulin level (p = 0.019). When the patients were divided into quartiles, the median annual BPH growth rate increased statistically significantly with increasing fasting plasma insulin levels. The fasting plasma insulin values correlated with the annual BPH growth rates (p = 0.009). When performing a multivariate analysis using the total prostate gland volume as dependent variable, fasting plasma insulin (p = 0.001) and age (p0.001) became statistically significant.The results of the present report suggest that the total prostate gland volume constitutes a valid expression of BPH. The findings support the hypothesis that hyperinsulinaemia is causally related to the development of BPH and generate the hypothesis of an increased sympathetic nerve activity in men with BPH.

A prospective, randomized study was done to investigate the role of transurethral catheters in stricture formation after transurethral resection of the prostate. The operative outcome after using transurethral catheters made of 2 different materials compared with suprapubic catheters was also investigated. We studied 344 patients who underwent transurethral resection of the prostate. After resection the patients were randomly divided into 3 groups: 1) those drained by a transurethral polytetrafluoroethylene (Teflon)-coated latex catheter, 2) those drained by a transurethral polyvinylchloride catheter and 3) those drained by a suprapubic polyvinylchloride catheter. At 6 to 24 months the numbers of strictures in the anterior urethra were 10 of 102 and 11 of 102 in the transurethral drainage groups, respectively. The corresponding number of strictures in the suprapubic drainage group was 1 of 94 (p less than 0.01). Strictures in the bladder neck had developed in 5 of 102, 3 of 103 and 3 of 94 patients, respectively (not significant). As a consequence of a lower incidence of strictures in the anterior urethra in the suprapubic drainage group, more patients in that group were satisfied with the results of the operation.

A flow-cytometric (FCM) and fluorescence in situ hybridization (FISH) study was performed in 153 patients with clinically localised prostate cancer (PC) to evaluate retrospectively the prognostic significance of DNA ploidy, S-phase fraction (SPF) and chromosome 7 copy number. Deletions in 7q31.1 were analysed in a subset of 26 tumours. The mean follow-up time was 6 years (range 4–16 years). Twelve cases of benign prostatic hyperplasia (BPH) were studied as a control. Chromosome 7 enumeration and deletion studies were conducted using the α-satellite D7Z1 probe and a cosmid probe specific for the marker D7S522 on 7q31.1. Higher SPF was associated with shorter overall survival and shorter time to local progression and metastasis. Near diploid (DNA index 1.05–1.20) cases had a lower frequency of metastases and lower Gleason scores than aneuploid cases. Increased absolute chromosome 7 copy number (centromere count) was associated with higher Gleason score, higher SPF and shorter local progression-free and prostate cancer survival. Absolute chromosome 7 copy number was concordant with FCM DNA ploidy in the majority (75%) of cases. Relative gain or loss of chromosome 7 (centromere counts compared to ploidy) was infrequent, and no correlation was found with clinical parameters. Deletions in 7q31.1 were infrequent. Our results indicate that in localised PC (i) SPF is a prognostic factor, (ii) absolute chromosome 7 copy number is concordant with the ploidy status of the tumour (relative gain or loss of chromosome 7 is infrequent and has no independent prognostic value) and (iii) the frequency of deletions in 7q31.1 is low and not correlated with clinical outcome. Int. J. Cancer (Pred. Oncol.) 79:553–559, 1998. © 1998 Wiley-Liss, Inc.

The purpose of the present study was to perform a BPH risk factor analysis in men, relating the prostate gland volume to components of the metabolic syndrome and to identify clues to the etiology of BPH. Our material comprised a consecutive series of 158 patients with lower urinary tract symptoms with or without manifestations of the metabolic syndrome. In this group, the measured volume of the prostate was related consecutively to potential risk factors. The diagnoses atherosclerosis, non-insulin-dependent diabetes mellitus (NIDDM) and treated hypertension were obtained from the patient's medical history. Data on blood pressure, waist and hip measure, 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, cholesterol, triglycerides, HDL and LDL-cholesterol, uric acid and ALAT. The prostate gland volume was determined using ultrasound. Our results show that there was a larger prostate gland in men with NIDDM (P=0.0058), treated hypertension (P=0.0317), obesity (P0.0001), low HDL-cholesterol levels (P=0.0132) and high insulin levels (P0.0001) than in men without these conditions. The prostate gland volume correlated positively with the systolic blood pressure (r(s)=0.17; P=0.03), obesity (r(s)=0.34; P0.0001) and fasting insulin (r(s)=0.38; P0.0001) and negatively with HDL-cholesterol (r(s)=-0.22; P=0.009). On the basis of our findings, we concluded that NIDDM, treated hypertension, obesity, low HDL-cholesterol levels and high insulin levels constitute risk factors for the development of BPH. The results suggest that BPH is a facet of the metabolic syndrome and that BPH patients may share the same metabolic abnormality of a defective insulin-mediated glucose uptake and secondary hyperinsulinemia as patients with the metabolic syndrome. The findings generate a hypothesis of a causal relationship between high insulin levels and the development of BPH. In a clinical setting, the findings of the present report suggest that, in any patient presenting with BPH, the possible presence of NIDDM, hypertension, obesity, high insulin and low HDL-cholesterol levels should be considered. Conversely, in patients suffering from these conditions, the possibility of a clinically important BPH should be kept in mind.

In a retrospective study, the frequency of atrial arrhythmias of types known to cause systemic embolisation and the effect of anticoagulant treatment were studied in 106 patients with arterial embolism. Such embolising arrhythimas were found in 84 patients (79%). Permanent atrial fibrillation was documented in 53 patients (50%) and episodic atrial arrhythmia was encountered in 28 patients (26%). In 21 of 28 patients with sinus rhythm on admission, an embolising arrhythmia could be identified in previous ECG recordings. Patients with atrial arrhythmias had a significantly higher rate of prior embolic episodes and embolic events during follow-up (53 events in 84 patients) compared to the patients without arrhythmia (6 events in 22 patients) (P less than 0.05). In patients with atrial arrhythmias postoperative treatment with peroral anticoagulation was associated with a lower mortality (P less than 0.003) and a lower rate of reembolisation and stroke (P less than 0.0005). It is concluded that every fourth patient presenting with arterial embolism had an atrial arrhythmia of episodic nature. Most of these patients had normal sinus rhythm on admission but could be identified in previous ECG recordings. This study suggests that patients with arterial embolism and atrial arrhythmia have a higher risk of further embolisation with an ensuing risk of morbidity and death, compared to patients without arrhythmia. A positive effect of anticoagulation seemed to be present in patients with atrial arrhythmia whereas such a positive effect could not be identified in patients without arrhythmia.

Urethral stricture is the most common late complication of transurethral prostatectomy (TURP). The cause is unknown. A prospective, randomised study was undertaken to investigate the role of the transurethral catheter in stricture formation. A total of 205 patients subjected to TURP were studied. Following resection, they were randomly divided into 2 groups: those drained by a transurethral siliconised latex catheter and those drained by a suprapubic siliconised latex catheter. At follow-up, 6 to 24 months later, 17% of the patients in the transurethral group had developed urethral stricture; the corresponding figure in the suprapubic group was 4%. As a consequence of the higher incidence of stricture in the transurethrally drained group, more patients in that group were dissatisfied with the results of the operation. It was concluded that the post-operative transurethral catheter was an important factor in stricture formation following TURP and that transurethral drainage with a siliconised latex catheter resulted in a higher incidence of stricture. This led to a greater number of patients being dissatisfied with the results of the operation, but the catheter did not affect the results in any other way.