Preliminary results of a new tool to evaluate cavernous body fibrosis following radical prostatectomy: penile elastography.

Development of cavernous tissue fibrosis due to neurovascular bundle damage during radical prostatectomy has been shown in many trials with invasive methods. In this study, we evaluated the changes in cavernous tissue elasticity by elastography in patients who underwent radical prostatectomy with or without neurovascular bundle preservation. Data from 65 patients underwent open retropubic radical prostatectomy between April 2014 and December 2015 was collected prospectively. Patients were grouped with respect to nerve-sparing status (non-, unilateral, and bilateral nerve sparing). International Index of Erectile Function scores, penile lengths, and elasticity scores were recorded at preoperative and postoperative follow-up visits (at 3rd and 6th months). The primary endpoint of the study was to evaluate the changes of the elasticity scores in all groups. Elasticity scores were measured with real-time elastography by a single experienced radiologist. Mean age, baseline total testosterone level, IIEF-5 score, elasticity scores of the cavernous body, and penile length were comparable in all groups. At postoperative 3rd and 6th months, statistically significant higher (in favor for fibrosis) mean cavernous body elasticity scores (p = 0.0001), lower mean IIEF-5 scores (p = 0.0001), and shorter penile lengths (p < 0.05) were observed in non-nerve-sparing group compared to other groups while there were no statistically significant differences between unilateral and bilateral nerve-sparing groups. Very strong negative correlation was detected between IIEF-5 and elasticity scores (p = 0.0001). According to our results, preservation of the neurovascular bundle in at least one side mediates lower elasticity scores, better International Index of Erectile Function scores, and penile lengths. Preliminary results of the penile elastography studies are promising for prediction of erectile functions and cavernous tissue fibrosis.

Is active surveillance a suitable option for African American men with prostate cancer? A systemic literature review.

BACKGROUND: Certain patients presenting with either low or very-low-risk prostate cancer (PCa) can represent a therapeutic dilemma for physicians. The oncologic outcomes of active surveillance (AS) for men with very-low-risk PCa are overall excellent. However, there are concerns about AS related to the potential for upgrading or upstaging. The African American (AA) population is under-represented in studies evaluating AS outcomes and this is particularly important because of the unique epidemiology of PCa in AA men. METHODS: A literature review through the Medline database published from 1990 until August 2015 was performed to identify studies reporting outcomes of the AA population with low-risk PCa that underwent either AS or treatment. An additional search for studies on genetic mechanisms involved in development of PCa in AA men was also performed. RESULTS: Eleven studies on pathologic results of AA men who would qualify for AS were identified and in eight of these studies AA race was found to be associated with adverse pathological outcomes such as positive surgical margins, upgrading or upstaging. The other three studies reported no significance in these parameters with respect to race. Five more studies reported outcomes of AS in AA men with different study end points. AA men were mainly found to have a higher rate of disease reclassification subsequent to active treatment. The studies on genetic mechanisms also identified different genetic alterations in the AA population. CONCLUSIONS: AA men with clinically defined low-risk PCa may have either a higher grade or volume of cancer that was not detected on routine evaluation. Therefore, AS among such patients should be approached with caution. We recommend discussing such risks with AA patients with an acknowledgement that existing favorable outcomes noted in largely Caucasian populations may not be applicable to AA patients. We propose a modified evaluation plan for AA patients that includes an early confirmatory biopsy preceded by an magnetic resonance imaging to optimally detect occult cancer foci.

Effects of transforming growth factor on the developing embryonic ureter: An in-vitro megaureter model in mice.

INTRODUCTION: It is generally agreed that the cause of a megaureter is narrowing at the vesicoureteral junction, with a functional obstruction arising from an aperistaltic, juxtavesical segment that is unable to transport urine at an acceptable rate. Histological examinations of megaureter specimens have reported several histological analyses, and the pathogenic role of transforming growth factor is still a matter of speculation. OBJECTIVE: To evaluate whether transforming growth factor-beta (TGF-ß) and its receptors (TGFRs) are expressed during ureterovesical junction (UVJ) and lower ureter development in mice, and whether exogenous TGF-ß might postpone the maturation of smooth muscle cells, in the pathogenesis of megaureter using an embryonic organ-culture model. METHODS: Expression of TGF-ß and TGFRs on the lower ureter and UVJ were determined at different embryonic days (E) (E16, 18, 20 and postnatal day 1). The functional studies were performed by harvesting ureters from wild-type mice at embryonic day 16 (E16), which were grown in serum-free organ-culture; some cultures were supplemented with TGF-ß (2 and 20 ng/ml) and/or with soluble TGFR, which blocks bioactivity. Organs were harvested after 6 days and the expression of CD31 and Ki67 were assessed using immunohistochemistry. The muscle content of the UVJ and ureter were analyzed by flowcytometry. RESULTS: The TGF-ß and TGFR positive cells were immune detected in embryonic ureters. The TGF-ß expression was highest on E18 and decreased postnatally. Exogenous TGF-ß decreased ureterovesical (UV) muscle differentiation and proliferation. The longitudinal muscle fibers were significantly less in TGF-ß explants. The TGF-ß also decreased the proportions of cells expressing α smooth muscle actin (α-SMA). Soluble TGFR blocked the effects of exogenous TGF-ß. CONCLUSIONS: In organ culture, exogenous TGF-ß postpones the UV smooth muscle proliferation and affects the muscular structure. Whether the effects of TGF-ß are direct or indirect, these form an in-vitro megaureter model. The finding that TGF-ß is highest in embryonic ureters in vivo and decreased postnatally suggests that a pathological persistence might potentially explain the pathogenesis of primary megaureters.