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 (P`0.0001), low HDLcholesterol levels (P 0.0132) and high insulin levels (P`0.0001) 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; P`0.0001) and fasting insulin (r s 0.38; P`0.0001) and negatively with HDL-cholesterol (r s À0.22; P 0.009).On the basis of our ®ndings, 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 ®ndings generate a hypothesis of a causal relationship between high insulin levels and the development of BPH. In a clinical setting, the ®ndings 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.

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In order to assess the association between atopy and cancer risk, a cohort of 6593 skin-prick-tested patients was established. Among atopic subjects, no overall increased cancer risk was found, but the incidence of both breast cancer (standardized incidence ratio (SIR) 2.50, 95% CI 1.01-5.16) and malignant lymphomas (SIR 4.40, 95% CI 1.20-11.3) was significantly enhanced. Atopic subjects with asthma showed a decreased overall cancer risk (SIR 0.73, 95% CI 0.27-1.60), as compared with the other asthmatic subjects (SIR 1.46, 95% CI 1.03-2.04). The cancer risk for subjects with rhinitis was near unity (SIR 1.11), irrespective of whether the subjects were atopic or not. An almost significant risk increase for cancer was observed among subjects with urticaria (SIR 1.70, 95% CI 0.99-2.80). Our results support neither the original hypothesis of an overall cancer protective effect of atopy, nor that of an opposite effect; rather, they strengthen the view that the association between atopic diseases and cancer is complex.

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.