[17] observed that 12 (29%) of 41 patients treated with of BoNT-A for BPH did not experience reduction of prostate volume, yet seven of these men had significant improvement of IPSS and Qmax . These data suggest that BoNT-A may act on the selleck inhibitor dynamic obstructive component of BPH. The neurotoxin was originally thought to act only by inhibiting acetylcholine release at the presynaptic neuromuscular junction [25]. Presently, other mechanisms are known to be involved such as blockage of neuroglandular junctions. It is believed that it also promotes a decrease of norepinephrine release from sympathetic endings, leading to the consequent reduction of alpha-1A adrenoceptor stimulation [26]. Furthermore, in an experimental model using rats, a dose-dependent decrease in the expression of alfa-1A adrenoceptors was demonstrated [27].

This is another possible mechanism affected by BoNT-A treatment, which may promote a decrease in density of alfa-1a adrenoceptors, which are known to be increased several-fold in BPH [28]. Different doses (range from 100 to 300U) have been studied in several series, but there is a lack of consistency in some studies [15�C21]. Some authors suggest that prostate size might influence the dosage [17, 21], but whether larger prostates require higher doses has actually not been tested. Moreover, there is no evidence whether the severity of LUTS influences the optimal dose. To the best of our knowledge, it is the first study comparing two different doses of BoNT-A. The procedure has been performed by transperineal, transrectal and transurethral approaches.

We chose the transurethral route because the vast majority of urologists are trained on cystoscopic procedures and also because it permits direct vision and injection in the transition zone of the prostate. Kuo [21] firstly described the cystoscopic approach using light general anesthesia or sedation. We have demonstrated that it is feasible to perform this technique with local anesthesia. Pain, when present, was mild and no patient required narcotics in the postoperative period. Complications were uncommon in our series and seemed to be related to the urethral manipulation rather than a direct result of BoNT-A injection. Gross hematuria, although conservatively managed, was observed in 2 (5.8%) patients. Transient urinary retention was observed in 2 (5.

8%) patients, and treated conservatively with an indwelling catheter for 5 days. Two patients (5.8%) developed acute prostatitis. As mentioned, these adverse effects seem to be associated with the route of administration of BoNT-A, since they are potential complications of any procedure requiring urethral instrumentation. Series that adopted the transperineal Batimastat or transrectal approach did not report such complications [22�C27]. Given the vascular nature of the prostate, systemic absorption of the toxin could occur.