Deep common bile duct cannulation time at endoscopic retrograde cholangiopancreatography: a forgotten parameter for assessment of endoscopic competence?

The rate of successful deep common bile duct cannulation (DCBD) at endoscopic retrograde cholangiopancreatography (ERCP) is usually used as a surrogate marker of competence at ERCP. There are few data regarding the time spent on cannulation at ERCP. This prospective study aimed to evaluate the time spent on DCBD cannulation at ERCP and to provide a rationale for establishing the DCBD cannulation time as another parameter in assessment of ERCP competence. This is a prospective study performed in a single tertiary university-based referral center. DCBD cannulation time as well as the fluorescence time and the cost of cannulation tools during DCBD cannulation were measured. The mean DCBD cannulation was 12.5±13.6 minutes. Eighty-percent of the cannulation was achieved within 10 min, 10% achieved in 10-30 min, and the remaining in longer than 30 min. The longer cannulation time was associated with increased the cost of cannulation ($79/cannulation versus$387/ cannulation, P<0.001), as well as increasing the radiation exposure times (3.1 min/cannulation vs. 25 min/cannulation, P<0.001). In addition to the success rate of DCBD cannulation, the DCBD cannulation time should be considered as another parameter in the assessment of endoscopic competence in ERCP

GDNF rescues hyperglycemia-induced diabetic enteric neuropathy through activation of the PI3K/Akt pathway

Diabetes can result in loss of enteric neurons and subsequent gastrointestinal complications. The mechanism of enteric neuronal loss in diabetes is not known. We examined the effects of hyperglycemia on enteric neuronal survival and the effects of glial cell line–derived neurotrophic factor (GDNF) on modulating this survival. Exposure of primary enteric neurons to 20 mM glucose (hyperglycemia) for 24 hours resulted in a significant increase in apoptosis compared with 5 mM glucose (normoglycemia). Exposure to 20 mM glucose resulted in decreased Akt phosphorylation and enhanced nuclear translocation of forkhead box O3a (FOXO3a). Treatment of enteric neurons with GDNF ameliorated these changes. In streptozotocin-induced diabetic mice, there was evidence of myenteric neuronal apoptosis and reduced Akt phosphorylation. Diabetic mice had loss of NADPH diaphorase–stained myenteric neurons, delayed gastric emptying, and increased intestinal transit time. The pathophysiological effects of hyperglycemia (apoptosis, reduced Akt phosphorylation, loss of inhibitory neurons, motility changes) were reversed in diabetic glial fibrillary acidic protein–GDNF (GFAP-GDNF) Tg mice. In conclusion, we demonstrate that hyperglycemia induces neuronal loss through a reduction in Akt-mediated survival signaling and that these effects are reversed by GDNF. GDNF may be a potential therapeutic target for the gastrointestinal motility disorders related to diabetes