[Does diagnostic ureterorenoscopy increase the risk of bladder recurrence after total nephroureterectomy? A review of the literature]. / L'urétérorénoscopie diagnostique augmente-t-elle le risque de récidive vésicale après néphro-urétérectomie totale ? Une revue de la littérature.

OBJECTIVE: The objective of our study was to evaluate, in a review of the literature, the impact of diagnostic ureteroscopy before total nephroureterectomy (NUT) on the risk of bladder recurrence. METHODS: We conducted a literature review in the Pubmed database in March 2018. Initial research identified 45 publications. Following full text screening, 9 studies were finally included, with a total of 1041 NUT with URS prior versus 2909 NUT alone. The primary endpoint was bladder recurrence. Secondary objectives were specific survival and overall survival. RESULTS: Bladder recurrence was reported in the 9 studies included. Diagnostic ureteroscopy was significantly associated with an increased risk of post-NUT bladder recurrence (HZ 1.42 [1.29-1.56], P<0.01). The specific survival and overall survival at 5 years, were reported in respectively 4 and 2 studies. There was no impact of the pre-NUT diagnostic URS on the specific survival (HZ 0.75 [0.54-1.03], P=0.08) or post-NUT overall survival (HZ 1.15 [0.68-1.96], P=0.59). CONCLUSION: The URS diagnostic before NUT for TVEUS is associated with a significant increase in the risk of postoperative bladder recurrence.

[Oncological results of active surveillance in prostate cancer: A retrospective multicentric cohort]. / Résultats oncologiques de la surveillance active dans le cancer de la prostate : série rétrospective multicentrique.

PURPOSE: To report oncological outcomes of patients with prostate cancer undergoing active surveillance according to SURACAP criteria. METHODS: This multicentric study included patients who were initially treated with active surveillance for localized prostate cancer according to the SURACAP criteria. The duration of active surveillance as well as the causes of discontinuing the protocol and the definitive pathological results of patients who further underwent radical prostatectomy were retrospectively evaluated. The predictors of discontinuing active surveillance were assessed using a univariable Cox Model. In addition, the predictive value of initial MRI was assessed for patients who performed such imagery. RESULTS: Between 2007 and 2013, 80 patients were included, with a median age of 64 years [47-74]. Median follow-up was 52.9 months [24-108]. At 5 years follow-up, 43.4% patients were still under surveillance. Among patients that underwent surgery, 17.8% had an extra-capsular extension. The risk of discontinuing was not significantly greater for patients with tumor size of 2 or 3mm versus 1mm (HR=0.9 [0.46-1.75], P=0.763), 2 positives cores versus 1 (HR=0.98 [0.48-2.02], P=0.967), T2a vs. T1c stage (HR=2.18 [0.77-6.18], P=0.133), increased PSA level (HR=1 [0.96-1.15], P=0.975) or the patient's age (HR=1 [0.93-1.16], P=0.966). Among the 50 patients who performed initial MRI, the results of such imagery was not significantly associated to the risk of discontinuing active surveillance MRI (HR=1.49 [0.63-3.52], P=0.36). CONCLUSION: Although this study reveals a high rate of release from active surveillance at 5 years, the rate of extra-capsular tumors reported in the group of patients that underwent surgery is among the lowest in literature. LEVEL OF EVIDENCE: 4.

The peripheral myelin protein gene PMP-22 is contained within the Charcot-Marie-Tooth disease type 1A duplication.

Charcot-Marie-Tooth disease (CMT1) is the most common form of inherited peripheral neuropathy. Although the disease is genetically heterogeneous, it has been demonstrated that the gene defect is the most frequent type (CMT1A) is the result of a partial duplication of band 17p11.2. Recent studies suggested that the peripheral hypomyelination syndrome in the trembler (Tr) mouse, a possible animal model for CMT1 disease, is associated with a point mutation in the peripheral myelin protein-22 gene (pmp-22). Expression of pmp-22 is particularly high in Schwann cells, and the protein is found in peripheral myelin. We now report that the human PMP-22 gene is contained within the CMT1A duplication. We therefore, suggest that increased dosage of the PMP-22 gene may be the cause of CMT1A neuropathy.