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Ureteropelvic stenosis, also known as ureteropelvic junction obstruction, is an obstruction in the region of the pyeloureteral junction resulting in a urinary discharge disorder of the renal pelvis, which requires treatment.Since the first description of pyeloplasty by Trendelenburg in 1886 and the successful establishment of open pyeloplasty by Anderson and Hynes in 1949, the treatment strategies for ureteropelvic junction obstruction have developed considerably, especially in the last two decades. Although open pyeloplasty is still considered to be the gold standard, this concept is supplemented by modern minimally-invasive techniques today. These include laparoscopic pyeloplasty, laparoscopic single-site pyeloplasty, robot-assisted pyeloplasty, robot-assisted single-site pyeloplasty, and endopyelotomy. This article provides an overview of the different treatment strategies for ureteropelvic junction obstruction as well as the complication management of pyeloplasty in adult age., Competing Interests: Interessenkonflikt: Die Autoren geben an, dass keine Interessenkonflikte bestehen., (© Georg Thieme Verlag KG Stuttgart · New York.)

Purpose: Obesity is considered to be a risk factor for prostate cancer. Mitogenic actions of leptin, an adipocyte-derived hormone in a variety of cancer cell types have been identified. We have investigated the proliferative effects of leptin on human prostate cancer cells and assessed the role of tyrosine kinase signalling in mediating these actions., Materials and Methods: Two human androgen-resistant prostate cancer cell lines and one androgen-sensitive human prostate adenocarcinoma cell line were treated with leptin (5-100 ng / mL) for up to 48 hours. Under serum-free conditions, cell proliferation was measured using an enzyme-linked colorimetric assay. Furthermore, phosphorylation of a downstream component of MAPK (ERK1 / 2) was detected by Western blotting and a specific inhibitor of MAPK (PD98059; 40 microM) was used to evaluate the role of this signalling pathway., Results: Leptin dose-dependently increased the cell number in both androgen-resistant cell lines after 24 h and 48 h of incubation (percent of control: DU145 = 194.6 +/- 5.9 %, PC-3 = 177.9 +/- 6.8 %; 100 ng / mL leptin; 48 h; p < 0.001). Conversely, leptin's proliferative effect on the androgen-sensitive cell line was less pronounced (percent of control: LNCaP = 112.3 +/- 6.1 %; 100 ng / mL leptin; 48 h). Leptin also caused dose-dependent ERK1 / 2 phosphorylation in both androgen-resistant cell lines. In addition, pre-treatment with PD98059 inhibited these responses and attenuated leptin's mitogenic action., Conclusions: Data from this in vitro study suggest an association between obesity-associated hyperleptinemia and an increased risk for prostate cancer. Further investigations are necessary to clarify whether these data have clinical relevance regarding the use as a prognostic marker for predicting the timing of the occurrence of androgen resistency., (Copyright Georg Thieme Verlag Stuttgart . New York.)

Currently, radical retropubic prostatectomy is the standard procedure for clinically localized prostate cancer. The surgical technique has been continuously refined for decades, resulting in reduced morbidity and improved functional and oncologic results. Since the late 90s, radical prostatectomy has been increasingly performed laparoscopically. A search of the available data has found that the articles published so far have proven the feasibility of the laparoscopic procedure but never confirmed its less invasiveness. In accordance with previous studies that have evaluated the invasiveness of various open and laparoscopic procedures, our clinic, which has routinely performed both techniques for several years, addressed the question whether laparoscopic prostatovesiculectomy indeed induces less severe surgical trauma. This prospective nonrandomized comparison study of the University Clinic of Urology at the Martin-Luther University at Halle-Wittenberg recruited a total of 64 patients, who underwent laparoscopic radical prostatectomy (n = 32) or open retropubic prostatectomy (n = 32) from January 2003 to April 2004. Both patient groups were comparable as to preoperative staging, PSA value and Gleason score. Besides perioperative parameters, such as surgical time, intra- and postoperative complications, blood loss and transfusion rate, need for analgetics and length of hospital stay, the comparison included oncologic data, such as Gleason score, pathologic stage and numbers of positive specimen margins. To get objectively reproducible data, the range of the systemic answers concerning the surgically induced tissue trauma was recorded as laboratory data. In all patients, pre-, intra-, and postsurgical markers of the acute-phase C-reactive protein, serum amyloid A (SAA), interleukin-6 (IL-6) and interleukin-10 (IL-10) were measured. The transfusion rate was 6 % for laparoscopic prostatectomies and 12 % for open prostatectomies. A rectal tear had to be intraoperatively repaired in one laparoscopically operated patient. The postoperative use of analgetics was comparable in both groups. The median hospital stay was 12.4 days for the laparoscopic and 11.2 days for the open surgical group. For T2 tumors, positive specimen margins were found in 6 cases (17 %) of the laparoscopic and in 4 cases (12 %) of the open surgical group. As to the indicators of any systemic reaction, no significant difference could be found during the entire clinical course between both surgical methods. In comparison with patients who underwent conventional open prostatectomy, patients with laparoscopically radical prostatectomy had identical to slightly higher serum levels of the acute-phase parameters, as evidence of an equal or a discretely manifested systemic response to the surgical trauma. The so far assumed less invasiveness of laparoscopic radical prostatectomy is not objectively supported by the data from this study. Thus, surgical trauma and its linked invasiveness must be considered equal for both methods, at least for the time being.

Purpose: Hematogenous spread of BCG after intravesical instillation against bladder cancer is rare, but may result in systemic infection and hypersensitivity reaction. We investigated fluoroquinolones and steroids in an animal model to improve the therapeutic options in local and systemic BCG infection. Furthermore, we tested the antitumor effectiveness of intravesical BCG with simultaneous application of fluoroquinolones and/or steroids., Methods: After systemic BCG infection, experiments were performed with quinolones as antimicrobial agent. Trimethoprim/sulfamethoxazole (TMS) was also tested in comparison to quinolones as a non-specific antimicrobial agent. To evaluate the hyperergic reaction after repeated BCG infection (hypersensitivity model), re-infection was performed seven days after primary infection with accompanying oral antimicrobial therapy with and without steroids. Intravesical tumor therapy was carried out with BCG in orthotopic murine bladder tumor model MB 49 together with simultaneous antimicrobial therapy., Results: After primary infection, quinolones led to a significant prolonged survival independent of steroid administration. Steroids alone after primary BCG infection reduced the survival. In contrast to these experiments, only steroid-treated mice had a significant improvement in survival after a second challenge with BCG. Therapeutic efficacy of BCG was not affected by antibacterial therapy with quinolones. Steroids alone induced a significantly increased death rate during intravesical BCG therapy., Conclusion: Quinolones have a positive effect on survival in acute systemic BCG infection in mice. Re-infection with BCG led to severe hyperergic reaction that can only be influenced by steroids. Thus, quinolones can be used in primary systemic BCG infection after topical application as a sufficient alternative to common tuberculostatics. Repeated BCG instillation may lead to hyperergic reaction, making additional administration of steroids essential. In this animal model, therapeutic efficacy of BCG obviously was not affected by additional administration of antimicrobials.

The early detection of prostate cancer and the aggressive treatment is the only chance for a cure. The use of PSA-related screening techniques brings forward the diagnosis of the disease by 5-10 years. While such early detection regimens shift the stage at the time of detection towards locally confined disease, and while there is no doubt that early treatment is the only way of curing prostate cancer, the application of screening in practice and healthcare policy remains controversial. This is because there are uncertainties about the degree of "over-diagnosis" which most probably results from screening, and from uncertainties about the risk-benefit balance. Randomized studies will show whether early detection of prostate cancer can reduce cancer-specific mortality. Conclusive data will not be available before 2005 respectively 2008. At that time, only the validated complied information about the risks and benefits of screening and about the possible therapeutic consequences may provide a way out of this current dilemma. A synopsis of the (European Randomized Study of Screening for Prostate Cancer) was given by F. H. Schröder in the British Journal of Urology International, December 2003.