Metabolic Syndrome and Benign Prostatic Hyperplasia/What Component of Metabolic Syndrome Is Related to Benign Prostatic Hyperplasia?

Objective:Our objective was to evaluate the association of benign prostatic hyperplasia (BPH) with each component of metabolic syndrome (MS), and determine which component plays the major risk for developing BPH.Materials and Methods:This cross-sectional observational study was performed on 203 male patients aged over 50, who came to the internal medicine outpatient clinics just for a check-up with/without any known disease. Forty-three of them were healthy control patients and the rest had only 1 criterion of MS. They were searched for the presence of BPH.Results:BPH prevalence ranged between 45.5-65.6% in the subgroups, there was no statistically significant difference in the presence of BPH between these groups. There was a slight positive correlation between glucose level and prostate volume. Triglyceride levels were positively correlated with Qmax and negatively correlated with the grade of hypertrophy. There was also a slight positive correlation between systolic blood pressure and prostate volumes, grade of hypertrophy, and IPSS scores.Conclusion:BPH prevalence was not different between MS components. We concluded that none of the MS components increase the occurrence of BPH by itself but when those metabolic disorders come together and form a syndrome, the prevalence of BPH increases

Invasion Mechanisms of Bladder Cancer: A Molecular Review

Bladder cancer (BC) is a very common cancer and it has high mortality rates, especially in late stages. BC is considered as a different disease in various stages and grades. Non-muscle-invasive BC and muscle-invasive BC have different properties. There are some prognostic factors for progression and recurrence rates of BC and we have some risk assessment methods. These factors are based on clinical findings and histopathological properties. We do not know which factors and molecular processes are effective in the invasion mechanism. In this review, we summarized possible invasion mechanisms of BC

Invasion Mechanisms of Bladder Cancer: A Molecular Review

Bladder cancer (BC) is a very common cancer and it has high mortality rates, especially in late stages. BC is considered as a different disease in various stages and grades. Non-muscle-invasive BC and muscle-invasive BC have different properties. There are some prognostic factors for progression and recurrence rates of BC and we have some risk assessment methods. These factors are based on clinical findings and histopathological properties. We do not know which factors and molecular processes are effective in the invasion mechanism. In this review, we summarized possible invasion mechanisms of BC

Cough-Induced Spontaneous Rupture of the Kidney Secondary to Anticoagulant Therapy: Wunderlich’s Syndrome

Spontaneous renal or other organ ruptures secondary to anticoagulants have rarely been reported. The clinical features of renal rupture include acute flank/abdominal pain, haematuria, hypotension and shock. It can occur due to increased intraabdominal pressure during coughing. Rupture is most commonly caused by renal tumors such as angiomyolipomas. In the literature, other known causes are long-term haemodialysis, arteriosclerosis or arteritis. Wunderlich’s syndrome is an extremely dangerous complication that may cause death if not treated intensively. If the haemorrhage is self-limiting and the patient is responsive to fluid replacement, the patient can be managed conservatively. Selective angiographic embolization and emergency nephrectomy (partial or total) are the treatment options. In the literature, we found only one case that was presented as spontaneous non-traumatic renal rupture associated with coughing. In our case, total nephrectomy had to be performed, but it was not adequate

Bladder Cancer and Polymorphisms of DNA Repair Genes (XRCC1, XRCC3, XPD, XPG, APE1, hOGG1)

Carcinogenic molecules from cigarettes are known to cause DNA damage to bladder epithelial cells, but such damage can be corrected by some DNA repair mechanisms such as base and nucleotide excision repair, double-strand repair and mismatch repair. Various gene products play a role in these DNA repair systems. The aim of this study was to investigate six of these genes (XRCC1, XRCC3, XPD, XPG, APE1, hOGG1) each of which has a separate role in these repair mechanisms. The study was performed on 83 bladder cancer patients and 45 health), controls. The genes were amplified by polymerase chain reaction (PCR) and restriction fragment polymorphism determinations were used to elucidate the specific changes in the gene region. There was no difference in smoking status between patient and control groups. It was found that there was a statistical significance in XRCC3 T carriers between patient and control groups and so there was a 4.87-fold protective role by the XRCC3 T allele against bladder cancer. The AA genotype and A allele carriers of the APE gene were more frequent in the transitional epithelial carcinoma group than in the adenocarcinoma group. The genotype distribution for the APE gene was determined to be significantly different between local and invasive cases; G allele carriers for this gene were significantly higher in invasive cancer types

Bladder cancer and polymorphisms of DNA repair genes (XRCC1, XRCC3, XPD, XPG, APE1, hOGGl)

Carcinogenic molecules from cigarettes are known to cause DNA damage to bladder epithelial cells, but such damage can be corrected by some DNA repair mechanisms such as base and nucleotide excision repair, double-strand repair and mismatch repair. Various gene products play a role in these DNA repair systems. The aim of this study was to investigate six of these genes (XRCC1, XRCC3, XPD, XPG, APE1, hOGG1) each of which has a separate role in these repair mechanisms. The study was performed on 83 bladder cancer patients and 45 health), controls. The genes were amplified by polymerase chain reaction (PCR) and restriction fragment polymorphism determinations were used to elucidate the specific changes in the gene region. There was no difference in smoking status between patient and control groups. It was found that there was a statistical significance in XRCC3 T carriers between patient and control groups and so there was a 4.87-fold protective role by the XRCC3 T allele against bladder cancer. The AA genotype and A allele carriers of the APE gene were more frequent in the transitional epithelial carcinoma group than in the adenocarcinoma group. The genotype distribution for the APE gene was determined to be significantly different between local and invasive cases; G allele carriers for this gene were significantly higher in invasive cancer types