Biomedical subjects

Jan Hammarsten

Publications and source records attributed to Jan Hammarsten.

4 recordsLinked to original sources

PubMed2005

Hyperinsulinaemia: a prospective risk factor for lethal clinical prostate cancer.

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.

Aged↗

PubMed2004

Clinical, haemodynamic, anthropometric, metabolic and insulin profile of men with high-stage and high-grade clinical prostate cancer.

AIMS: 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. METHODS: 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. RESULTS: Patients with clinical prostate cancer, prostate-specific antigen (PSA) < 50 ng/ml, stage T3, had a bigger prostate gland volume (p < 0.001), a faster BPH growth rate (p < 0.001), 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 (p < 0.070) than patients with T2 clinical prostate cancer. When patients with clinical prostate cancer, PSA > 50 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, PSA < 50 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, PSA > 50 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. CONCLUSIONS: 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.

Adenocarcinoma↗

PubMed2003

Preoperative skin testing of materials used in surgical procedures.

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.

Adhesives↗

PubMed2002

Calculated fast-growing benign prostatic hyperplasia--a risk factor for developing clinical prostate cancer.

OBJECTIVE: Whether there is an association between the development of benign prostatic hyperplasia (BPH) and clinical prostate cancer is controversial. The present report tests the hypothesis of an association between BPH growth and the development of clinical prostate cancer by examining stage, grade and PSA-level in men with recently discovered clinical prostate cancer with slow or fast-growing BPH. If the hypothesis is true, men with fast-growing BPH would have a more advanced clinical prostate cancer. MATERIAL AND METHODS: Two hundred and twenty patients in whom a clinical prostate cancer was diagnosed were consecutively included. The prevalence of atherosclerotic disease, non-insulin-dependent diabetes mellitus (NIDDM) or treated hypertension was provided by the respective patient's medical history. Tallness, body weight, waist measurement, hip measurement and blood pressure were determined. The body mass index (BMI) and waist/hip ratio (WHR) were calculated. Blood samples were drawn to determine triglycerides, total cholesterol, HDL-cholesterol, 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, assuming that the total prostate gland volume was 20 mL at the patient age of forty. The prostate cancer diagnosis was established using the technique of transrectal ultrasound-guided automatic needle biopsy of the prostate. RESULTS: Men with clinical prostate cancer, PSA <50 ng/mL, and with fast-growing BPH had a higher systolic (p = 0.009) and diastolic (p = 0.020) blood pressure, were taller (p < 0.001) and more obese, as determined by body weight (p < 0.001), BMI (p = 0.005), waist measurement (p < 0.001) and hip measurement (p = 0.003). They also had a higher fasting plasma insulin level (p = 0.014) and a lower HDL-cholesterol level (p = 0.067) than men with slow-growing BPH. Moreover, men with clinical prostate cancer, PSA <50 ng/mL, and fast-growing BPH had more pronounced clinical prostate cancer, as measured by grade (p = 0.029) and PSA-level (p = 0.016), than men with slow-growing BPH. In the total material, including men with clinical prostate cancer, PSA >/=50 ng/mL, men with fast-growing BPH also had a higher prevalence of NIDDM (p = 0.039) and a borderline statistical significance for higher stage (p = 0.09) than men with slow-growing BPH. The BPH growth rate was significantly associated with the clinical prostate cancer grade (p = 0.018) and PSA-level (p = 0.002) but not with the clinical cancer stage in a multivariate statistical analysis. CONCLUSIONS: This report confirms findings in previous studies that fast-growing BPH is a risk factor for NIDDM, hypertension, tallness, obesity, dyslipidaemia and hyperinsulinaemia. The present report extends this list of risk factors to include atherosclerotic disease manifestations, hyperuricaemia and higher ALAT levels. The study suggests that fast-growing BPH is a risk factor for developing clinical prostate cancer and, thus, supports the hypothesis of an association between the development of BPH and clinical prostate cancer. The study generates the hypothesis that clinical prostate cancer is a component of the metabolic syndrome and that insulin is a promoter of clinical prostate cancer.

Age Distribution↗