BACKGROUND: Sperm DNA damage (fragmentation) is a recently discovered cause of male infertility for which no efficient treatment has yet been found. Previous findings have suggested that clinically relevant sperm DNA damage may occur at the post-testicular level. This study was undertaken to assess the clinical usefulness of ICSI with testicular spermatozoa in this indication. METHODS: The percentage of spermatozoa with fragmented DNA, assessed by terminal deoxyribonucleotidyl transferase-mediated dUTP nick-end labelling assay, and ICSI outcomes were compared in two sequential attempts performed, respectively, with ejaculated and testicular spermatozoa in 18 men with increased sperm DNA fragmentation. RESULTS: The incidence of DNA fragmentation was markedly lower in testicular spermatozoa as compared with ejaculated spermatozoa. No differences in fertilization and cleavage rates and in embryo morphological grade were found between the ICSI attempts performed with ejaculated and with testicular spermatozoa. However, eight ongoing clinical pregnancies (four singleton and four twin) were achieved by ICSI with testicular spermatozoa (44.4% pregnancy rate; 20.7% implantation rate), whereas ICSI with ejaculated spermatozoa led to only one pregnancy which was spontaneously aborted. CONCLUSIONS: These data show that ICSI with testicular spermatozoa provides the first efficient assisted reproduction treatment option for men with high levels of sperm DNA damage.

To evaluate the diagnostic accuracy of unenhanced and quantitative contrast-enhanced ultrasonography (US) in the differential diagnosis of small nonpalpable testicular lesions. The local review board approved the protocol, and all patients provided written informed consent. One hundred fifteen patients (median age, 34 years; age range, 14-61 years) with nonpalpable testicular lesions were consecutively enrolled between 2006 and 2012 and underwent unenhanced scrotal US, contrast-enhanced US, surgical enucleation, and at least 18 months of follow-up. Clinical and histologic features were recorded, and qualitative and quantitative analysis of contrast-enhanced US time-intensity curves were performed. Logistic regression analysis was performed to explore features of malignancy. Receiver operating characteristic ( ROC receiver operating characteristic ) curves were developed for cumulative unenhanced and contrast-enhanced US scores. All lesions were 1.5 cm or smaller. Forty-four of the 115 patients (38%) had malignant tumors, 42 had benign tumors (37%), and 29 (25%) had nonneoplastic lesions. The features at unenhanced US that enabled the best differentiation of tumors versus nonneoplastic lesions and benign versus malignant tumors were parenchymal microlithiasis (26 of 86 patients with tumors vs five of 29 patients with nonneoplastic lesions [P = .178]; four of 42 patients with benign lesions vs 22 of 44 patients with malignant tumors [P < .001]), irregular margins (26 of 86 patients with tumors vs three of 29 patients with nonneoplastic lesions [P < .001]; eight of 42 patients with benign lesions vs 18 of 44 patients with malignant tumors [P < .001]), and internal vascularization (70 of 86 patients with tumors vs seven of 29 patients with nonneoplastic lesions [P < .001]; 28 of 42 patients with benign lesions vs 42 of 44 patients with malignant tumors [P < .001]). For contrast-enhanced US, the rapidity of wash-in (34 of 44 patients vs 15 of 42 patients, P < .001) and washout (33 of 44 patients vs five of 42 patients, P < .001) were the parameters that best differentiated malignant from benign tumors, with a typical prolonged washout observed in Leydig cell tumors (12 of 21 patients, P < .001 when compared with seminomas). Overall, the combination of unenhanced and contrast-enhanced US achieved a high accuracy in the diagnosis of small testicular malignancies (area under the ROC receiver operating characteristic curve performance: 0.927; 95% confidence interval: 0.872, 0.981). Benign testicular tumors are frequent incidental findings. Quantitative scrotal contrast-enhanced US is a noninvasive diagnostic tool that could improve the differential diagnosis and individualized management of small testicular lesions.

We evaluated the accuracy of detrusor wall thickness and intravesical prostatic protrusion, and the association of each test to diagnose bladder prostatic obstruction in patients with lower urinary tract symptoms. We enrolled in the study 100 consecutive patients with lower urinary tract symptoms due to benign prostatic hyperplasia. Baseline parameters were International Prostate Symptom Score, prostate volume, urinary flow rate, intravesical prostatic protrusion, detrusor wall thickness, Schaefer obstruction class, minimal urethral opening pressure and the urethral resistance algorithm bladder outlet obstruction index. A ROC curve was produced to calculate AUC and evaluate the diagnostic performance of intravesical prostatic protrusion, detrusor wall thickness and prostate volume for bladder prostatic obstruction. We noted a highly significant correlation between intravesical prostatic protrusion and the bladder outlet obstruction index (Spearman's rho = 0.49, p = 0.001), and Schaefer obstruction class (Spearman's rho = 0.51, p = 0.001). A highly significant correlation was also observed for detrusor wall thickness and the bladder outlet obstruction index (Spearman's rho = 0.57, p = 0.001), detrusor wall thickness and Schaefer obstruction class (Spearman's rho = 0.432, p = 0.02). On multivariate analysis intravesical prostatic protrusion and detrusor wall thickness were the only parameters associated with bladder prostatic obstruction (p = 0.015). The AUC for intravesical prostatic protrusion was 0.835 (95% CI 0.756-0.915) and for detrusor wall thickness it was 0.845 (95% CI 0.78-0.91). The association of intravesical prostatic protrusion and detrusor wall thickness produced the best diagnostic accuracy (87%) when the 2 tests were done consecutively. Suprapubic ultrasound of detrusor wall thickness and intravesical prostatic protrusion is a simple, noninvasive, accurate system to assess bladder prostatic obstruction in patients with lower urinary tract symptoms due to benign prostatic hyperplasia.

Cito G, et al. World J Mens Health. 2019 Jan;37:e25. https://doi.org/10.5534/wjmh.190057

FSH, identified as an endogenous product of the prostate, is a glycoprotein with proliferative activity. Increasing evidence of autocrine/paracrine activities of gonadotropins at extragonadal sites led us to investigate the gene expression and cellular localization of FSH-R in normal and diseased human prostates. Prostate specimens, including normal gland, BPH, PCa and human androgen refractory (PC3) and androgen dependent (LNCaP) prostate cancer cell lines (European Collection of Cell Cultures, Salisbury, United Kingdom), were analyzed for FSH-R expression by semiquantitative and real-time reverse transcriptase-polymerase chain reaction and immunohistochemistry. We also evaluated cyclic adenosine monophosphate production by cultured PC3 and LNCaP stimulated with human FSH. Little FSH-R expression was seen in 9 of 13 normal and 8 of 15 BPH specimens. Of 30 PCa samples 21 were FSH-R positive with generally higher expression compared to normal prostate and BPH samples. Real-time reverse transcriptase-polymerase chain reaction of matched normal/tumor pairs confirmed higher FSH-R mRNA expression in PCa. PC3 cells expressed FSH-R, while LNCaP cells were FSH-R negative. FSH-R protein was mainly localized in the glandular epithelium and in some stromal cells in normal prostate, BPH and PCa specimens. PC3 cells expressed FSH-R protein and their treatment with FSH induced a significant increase in cyclic adenosine monophosphate production. These results indicate that a subset of PCa expresses FSH-R mRNA and protein at levels higher than those of normal and hyperplastic tissues that express FSH-R. This suggests that FSH might contribute to some cases of PCa via a receptor mediated mechanism.