Patients and methods This study was performed
Patients and methods
This study was performed at 3 academic centers (Chung-Ang University YongSan Hospital, Soonchunhyang University Hospital, and Chung-Ang University Hospital) in Seoul, Korea, from November 2008 to November 2010. The study protocol was approved by the institutional review boards at all participating centers. All patients gave informed consent before enrollment. The protocol was registered at http://CRiS.cdc.go.kr identifier KCT0000021.
Discussion The risk of post-ERCP pancreatitis is determined by both patient characteristics and procedure variables. Careful patient selection based on strict indication criteria is required to avoid unnecessary or marginally indicated ERCP, especially in high-risk patients. From the viewpoint of endoscopic procedures, repeated trials of selective cannulation may result in mechanical injury to the papilla and pancreatic sphincter and may cause obstruction of pancreatic outflow. Efficient cannulation is, therefore, an important determinant of post-ERCP pancreatitis. A recent study showed that the basal sphincter pressure and phasic amplitude were significantly reduced after administration of PDE-5 inhibitor (vardenafil 10 mg) in patients with suspected SOD. The hypothesized mechanism of udenafil, another PDE-5 inhibitor, in the current study was reduction of SO tone and opening of papillary access, thus allowing easier cannulation. This effect was evaluated by patency of the papillary orifice, number of cannulation attempts, and success rate of intended selective cannulation. During ERCP, the papillary orifice was observed at the first look whether papillary orifice was patulous. However, there was no significant difference in the number of patulous papillary orifices and cannulation attempts and cannulation success rate between the udenafil group and placebo group. In addition, the rates of occurrence of post-ERCP pancreatitis were also similar in the 2 groups. Udenafil (100 mg) reaches maximal Clofazimine concentration within 2 hours and produces time of onset within 1 hour, similar to other PDE-5 inhibitors at equivalent doses, including sildenafil (50 mg) and vardenafil (10 mg).32, 33 Based on this pharmacokinetics, udenafil 100 mg was given 2 hours before ERCP so that maximal plasma concentration was achieved and the anticipated effect on the SO had begun to take place. In patients with suspected SOD, vardenafil 10 mg significantly decreased SO tone. Although the equivalent udenafil dose may exhibit a similar effect on SO tone, the effect did not result in a clinically significant outcome. The pathophysiology of post-ERCP pancreatitis is multifactorial. Any prophylactic agents that intervene at only 1 step in the pathogenesis may attenuate, but not ultimately prevent, the event. After eliminating the patient-related factors by careful patient selection, both efficient cannulation with minimal mechanical trauma and early inhibition of potentially activated inflammation cascade may prevent the post-ERCP pancreatitis. For example, PDE-5 inhibitor for efficient cannulation and NSAIDs to reduce inflammation may be an effective combination. Therefore, future studies that investigate dual interventions may provide novel methods for the prevention of post-ERCP pancreatitis.
Prostate cancer is the most prevalent cancer and the second leading cause of cancer death in American men. The majority of prostate cancer, about 94%, is identified as clinically localized and treated with radical prostatectomy. Despite its surgical technique advancements, such as robot-assisted procedures with nerve sparing, more than 50% of patients experience postprostatectomy erectile dysfunction (ED) because of cavernous nerve injury. Recently, much of the research effort has been placed on the stimulation of cavernous nerve regeneration and prevention of smooth muscle atrophy in corpus cavernosum., Many preclinical evidences have shown that the intracavernous injection of stem cells with neurotrophins and growth factors contribute to the stem cell survival for nerve regeneration and differentiation., In the previous study, Piao et al have showed that the coadministration of human adipose-derived stem cell (ADSC) and brain-derived neurotrophic factor (BDNF)-immobilized poly-lactic-co-glycolic (PLGA) membrane on the injured cavernous nerve significantly increased the erectile function by promoting the nerve regeneration in a rat model of bilateral cavernous nerve injury (BCNI) model. The damage to the cavernous nerve results in vascular atrophy and apoptosis of corporal smooth muscle cell, which is significant to postprostatectomy ED. However, the previous study mainly focused on ameliorating the injured cavernous nerve after surgery, and showed limited efficacy in preventing the corpus cavernosum apoptosis. In this study, we expanded our approach to ameliorate cavernous nerve injury and corpus cavernosum apoptosis for further improving erectile function.