Intraprostatic Botulinum Toxin Type A injection in patients with benign prostatic enlargement: duration of the effect of a single treatment

<p>Abstract</p> <p>Background</p> <p>Botulinum Toxin Type-A (BoNT/A) intraprostatic injection can induce prostatic involution and improve LUTS and urinary flow in patients with Benign Prostatic Enlargement (BPE). However, the duration of these effects is unknown. The objective of this work was to determine the duration of prostate volume reduction after one single intraprostatic injection of 200U of Botulinum Toxin Type-A.</p> <p>Methods</p> <p>This is an extension of a 6 month study in which 21 frail elderly patients with refractory urinary retention and unfit for surgery were submitted to intraprostatic injection of BoNT/A-200U, by ultrasound guided transrectal approach. In spite of frail conditions, eleven patients could be followed during 18 months. Prostate volume, total serum PSA, maximal flow rate (Qmax), residual volume (PVR) and IPSS-QoL scores were determined at 1, 3, 6, 12 and 18 months post-treatment.</p> <p>Results</p> <p>Mean prostate volume at baseline, 82 ± 16 ml progressively decreased from month one coming to 49 ± 9,5 ml (p = 0,003) at month six. From this moment on, prostate volume slowly recovered, becoming identical to baseline at 18 months (73 ± 16 ml, p = 0.03). Albeit non significant, serum PSA showed a 25% decrease from baseline to month 6. The 11 patients resumed spontaneous voiding at month one. Mean Qmax was 11,3 ± 1,7 ml/sec and remained unchanged during the follow-up period. PVR ranged from 55 ± 17 to 82 ± 20 ml and IPSS score from10 to 12 points.</p> <p>Conclusion</p> <p>Intraprostatic BoNT/A injection is safe and can reduce prostate volume for a period of 18 months. During this time a marked symptomatic improvement can be maintained.</p

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

Adverse effects of androgen deprivation therapy in patients with prostate cancer: Focus on metabolic complications

Prostate cancer is the most common cancer among men and androgen deprivation therapy (ADT) is the most effective treatment for this disease. The cornerstone of the treatment of prostate cancer is inhibition of testosterone production which interrupts testosterone-induced growth of the prostate tumor. The dramatic decrease in testosterone levels, however, has several undesirable effects on the metabolic profile and bone metabolism and can also lead to fatigue, loss of libido, gynecomastia, and anemia, provoke vasomotor flushing, and generally affect the quality of life. Due to the long-term survival rates of patients with prostate cancer, treatment-related adverse effects are highly relevant and thus, in each clinical setting, the benefits of ADT must be weighed against treatment-related adverse effects. The current review focuses on the more recently described metabolic complications of androgen deprivation therapy, including obesity, diabetes, lipid alterations, metabolic syndrome, and cardiovascular disease. In addition, it provides practical management recommendations drawn from the available guidelines issued by the American Diabetes Association and American Heart Association. © 2017, Hellenic Endocrine Society. All rights reserved

Adverse effects of androgen deprivation therapy in patients with prostate cancer: Focus on muscle and bone health

Androgen deprivation therapy (ADT) is the most effective systemic treatment for prostate cancer and can be succeeded either surgically or pharmaceutically. Both approaches lead to hypogonadism with a large variety of adverse events, including obesity, metabolic syndrome, osteoporosis, sarcopenia, diabetes mellitus, cardiovascular disease, gynecomastia and sexual dysfunction. In addition, undesirable effects on muscle and bone health may have a significant impact not only on the quality of life but also on life expectancy. Currently, supervised exercise seems to be the only intervention that could prevent the adverse effects of the ADT and improve quality of life. Lifestyle modification, supplementation of calcium, vitamin D and when indicated antiosteoporotic treatments improve bone health. However, patients receiving ADT must be well informed about the potential benefits as well as the risks of the treatment. © 2020 Zerbinis Publications. All rights reserved

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 enlargment (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 80 ml. The dose varied from 100 U to 300 U 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. (C) 2008 European Association of Urology. Published by Elsevier B.V. All rights reserved