Risk factors for delayed hemorrhage after endoscopic sphincterotomy.

BACKGROUND: Hemorrhage is one of the most serious complications of endoscopic sphincterotomy (EST). The risk factors for delayed hemorrhage are not clear. This study aimed to explore the risk factors for post-EST delayed hemorrhage and suggest some precautionary measures. METHODS: This study analyzed 8477 patients who successfully underwent endoscopic retrograde cholangiopancreatography (ERCP) and EST between January 2007 and June 2015 in the First Affiliated Hospital of Nanchang University. Univariate and multivariate analyses were performed to find the risk factors for delayed hemorrhage after EST. RESULTS: Of the 8477 patients screened, 137 (1.62%) experienced delayed hemorrhage. Univariate analysis showed that male, the severity of jaundice, duodenal papillary adenoma and carcinoma, diabetes, intraoperative bleeding, moderate and large incisions, and directional deviation of incision were risk factors for post-EST delayed hemorrhage (P < 0.05). Multivariate analysis showed that intraoperative bleeding [odds ratio (OR) = 3.326; 95% CI: 1.785-6.196; P < 0.001] and directional deviation of incision (OR = 2.184; 95% CI: 1.266-3.767; P = 0.005) were independent risk factors for post-EST delayed hemorrhage. CONCLUSIONS: Delayed hemorrhage is the most common and dangerous complication of EST. Intraoperative bleeding and directional deviation of incision are independent risk factors for post-EST delayed hemorrhage.

Effect of vasoactive intestinal peptide (VIP) on NKG2D signal pathway and its contribution to immune escape of MKN45 cells.

OBJECTIVE: To investigate VIP effect on the cytotoxicity of NK cell to gastric cancer cells in vitro and the relation between the effect with the NKG2D signal molecules in NK cells. MATERIAL AND METHODS: NK cells were purified from peripheral blood mononuclear cells (PBMC). Before and after NK cells were incubated with VIP or its antagonist (D-p-Cl-Phe6,Leu17)-VIP, we detected the cytotoxicity of NK cells to MKN45 gastric cancer cells by MTT and detected the expressions of NKG2D, DAP10, and NF- κ B proteins and mRNAs in NK cells by immunocytochemistry and RT-PCR in those conditions. Then we analyzed the effect of VIP and its antagonist on the cytotocicity of NK cell to gastric cancer cells and on expressions of NKG2D, DAP10, and NF- κ B signal molecules in NK cells. RESULTS: VIP could inhibit the cytotoxicity of NK cells to MKN45 cells and could inhibit the expressions of NKG2D, DAP10, and NF- κ B in NK cells. However, (D-p-Cl-Phe6, Leu17)-VIP could reverse those effects. CONCLUSIONS: The VIP inhibited the cytotoxicity of NK cell to MKN45 cells which might get through inhibiting the expressions of NKG2D signal molecules in NK cells. This may be one mechanism of gastric cancer cells escaping organism immune clearance.