Subanalysis was done for stricture etiology by patient age and stricture site.
Results: The most important causes were idiopathy, transurethral resection, urethral catheterization, pelvic fracture and hypospadias surgery. Overall iatrogenic causes (transurethral resection, urethral catheterization, cystoscopy, prostatectomy, brachytherapy and hypospadias surgery) were the etiology in 45.5% of stricture cases. In patients younger than 45 years the main causes were idiopathy, hypospadias surgery and pelvic fracture. In patients older than 45 years the main causes were transurethral resection and idiopathy.
In cases of penile urethra hypospadias surgery idiopathic stricture, urethral catheterization and lichen sclerosus were the main causes, selleck chemicals while in the bulbar urethra idiopathic BAY 63-2521 mouse strictures were most prevalent, followed by strictures due to transurethral resection. The main cause of multifocal/panurethral anterior stricture disease was urethral catheterization, while
pelvic fracture was the main cause of posterior urethral strictures.
Conclusions: Of strictures treated with urethroplasty today iatrogenic causes account for about half of the urethral stricture cases in the developed world. In about I of 3 cases no obvious cause could be identified. The etiology is significantly different in younger vs older patients and among stricture sites.”
“Several studies have reported that brain-derived neurotrophic factor (BDNF) might be associated with nicotine dependence. However, there are few click here studies on BDNF levels in humans with nicotine dependence. In the present study, we compared the differences in plasma BDNF levels in patients with nicotine dependence and in healthy nonsmokers, and we investigated serial changes in plasma BDNF levels in patients with nicotine dependence following smoking cessation. Forty-five voluntary smokers and 66 nonsmokers were recruited in this study. Of the 45
smokers, 12 were taking varenicline, 21 were using a nicotine patch, and 12 were unaided in their cessation effort by their own choice. Plasma BDNF levels were measured at baseline using an enzyme-linked immunosorbent assay (both smokers and nonsmokers) and at weeks 4 and 12 after smoking cessation (abstinent smokers only). A total of 19 smokers were able to remain abstinent during the entire study period. Baseline plasma BDNF levels were significantly lower in smokers compared to nonsmokers (F = 4.410, p = 0.002). The plasma BDNF levels in the abstinent smokers significantly increased from baseline after 4 weeks of smoking cessation (z = -2.86, p = 0.004) but had a tendency of decrease in the period between weeks 4 and 12. We could not find differences in the plasma BDNF levels among the three smoker subgroups at week 12 following cessation. Changes in plasma BDNF levels might be related to the process of abstinence and the pathophysiology of nicotine dependence. (C) 2009 Elsevier Ireland Ltd.