Lack of association between the UDP-glucuronosyltransferase 1A1 (UGT1A1) gene polymorphism and the risk of benign prostatic hyperplasia in Caucasian men.

Glucuronidation, mediated by the UDP-glucuronosyltransferase 1A1 (UGT1A1) enzyme, is an important metabolic process during which steroids are converted to more easily excreted compounds in steroid target tissues, such as the prostate. The aim of our study was to investigate the possible correlation between UGT1A1 promoter gene polymorphism and benign prostatic hyperplasia. 421 blood samples were obtained from 138 consecutive patients diagnosed with benign prostatic hypeplasia (BPH group) and 283 healthy volunteers (control group). A(TA)6TAA promoter polymorphism of UGT1A1 gene was studied using the Fragment Analysis Software of an automated DNA sequencer and three genotypes (homozygous 7/7, heterozygous 6/7 and normal homozygous 6/6) were identified. No significant differences were observed between the BPH group and controls regarding the genotyping distribution of the three UGT1A1 promoter genotypes (P = 0.39). Also, no association was found between overall disease risk and the presence of the polymorphic homozygous genotype (TA(7)/TA)7) vs. TA(6)/TA(7) + TA(6)/TA(6)) (P = 0.31). Our data suggest that the TA repeat polymorphism of UGT1A1 is not associated with increased BPH risk susceptibility in Caucasian men.

Botulinum neurotoxin A for benign prostatic hyperplasia.

PURPOSE OF REVIEW: The injection of botulinum neurotoxin A (BoNT-A) into the prostate represents an alternative, minimal invasive treatment for lower urinary tract symptoms suggestive of benign prostatic hyperplasia (BPH), which gained the interest of urologists during the last years, although it is not yet licensed. The purpose of this review is to summarize the mechanisms through which BoNT-A could inhibit the progression of BPH and eliminate the lower urinary tract symptoms according to the findings of animal studies. Furthermore, we review clinical studies to report the efficacy and safety of intraprostatic BoNT-A injection according to various injection protocols. RECENT FINDINGS: The experimental studies report induced relaxation of the prostate, atrophy, and reduction in its size through inhibition of the trophic effect of the autonomic system on the prostate gland. Also, a possible mechanism of reduction in lower urinary tract symptoms might take place through inhibition of sensory afferents from the prostate to the spinal cord. Clinical studies report symptomatic relief and improvement in the measured parameters during the follow-up period, whereas local or systematic side-effects are rare. SUMMARY: We should recognize that, at present, this therapy is still experimental. Although the results of the clinical studies are encouraging, the level of evidence is low. Clearly, we need large-scale, clinical, placebo-controlled, randomized studies, including long-term surveillance to document the evidence of this therapy and, eventually, to register BoNT-A for this indication.

Salvage perineal-retropubic AUS cuff in paraplegic patient with exstrophy-epispadias complex after previous cuff erosion at bladder neck.

Cuff erosion at the bladder neck of an implanted artificial urinary sphincter (AUS) needs complete explantation of the device. The subsequent scar tissues predispose to repeated cuff erosion, when another AUS is implanted with the cuff at a similar location. We describe a paraplegic patient with exstrophy-epispadias complex that suffered from an AUS cuff erosion at the bladder neck. We use a novel perineal-retropubic route for cuff placement, with preparation similar to a retropubic male sling. At 12 years follow-up the AUS is still functional and the patient continent.

Is botulinum neurotoxin type A (BoNT-A) a novel therapy for lower urinary tract symptoms due to benign prostatic enlargement? A review of the literature.

CONTEXT: The intraprostatic injection of botulinum neurotoxin type A (BoNT-A) is a minimally invasive but still-experimental treatment of lower urinary tract symptoms (LUTS) due to benign prostatic enlargement (BPE) based on an off-label use of the drug. OBJECTIVE: Report the mechanisms of action of BoNT-A on the prostate as well as the efficacy and safety of intraprostatic BoNT-A injection according to various injection protocols. EVIDENCE ACQUISITION: We searched the Medical Literature Analysis and Retrieval System Online (MEDLINE) database and the abstract volumes of the 2005, 2006, and 2007 European Association of Urology (EAU), American Urological Association (AUA) and International Continence Society (ICS) meetings for studies on intraprostatic BoNT-A injection. EVIDENCE SYNTHESIS: Five experimental studies and 10 clinical studies were found. The level of evidence is 1b for one study and 3 for the other studies, with grades of recommendation of A and C, respectively. The experimental studies report induced relaxation of the prostate, atrophy, and reduction of its size through inhibition of the trophic effect of the autonomic system on the prostate gland. In the clinical studies, all patients had LUTS due to BPE and prostate volume varied from <20 ml to >80 ml. The dose varied from 100U to 300U of Botox((R)). The injection was performed transperineally, transrectally, or transurethrally under general, local, or without anesthesia. The follow-up period ranged from 3 mo to 19.8 mo. All studies reported an improvement of maximum urinary flow rate, quality-of-life index and reduction of International Prostate Symptoms Score, prostate-specific antigen (PSA) level, post-void residual volume, and prostate volume. Local or systemic side effects were rare. Only patients with retention needed a urethral drainage catheter. CONCLUSIONS: BoNT-A intraprostatic injection provides improvement in patients with LUTS due to BPE refractory to medical treatment. However, there is a need for large placebo controlled-studies and long-term results. So far the therapy is still experimental.