Outcome of Common Bile Duct Exploration without Intraoperative Cholangiography: a Case Series and Review of Literature

Background: Open or laparoscopic surgical exploration of common bile duct (CBD) is performed when endoscopic approaches fail to extract CBD stones. Intraoperative cholangiography (IOC) through T-tube is performed in order to reduce the rate of retained stones. The aim of this study was to evaluate results of CBD exploration without IOC through T-tube and reviewing existing literature.Methods: A retrospective medical chart review of 392 patients who underwent surgical CBD exploration was performed. All patients had proven CBD stones and had previously undergone failed attempts of endoscopic retrograde cholangiopancreatography (ERCP) and endoscopic sphincterotomy (ES). T-tube insertion or biliary-enteric anastomosis was performed after open CBD exploration with regard to patient’s presentation and CBD diameter. IOC was not performed after T-tube insertion and cholangiography was postponed until 7th postoperative day. Postoperative retained stone and their management were reviewed.Results: Of 392 patients with CBD explorations, T-tube was placed in 215 (54.8%) including 66 (30.7%) emergent biliary drainage and 149 (69.3%) elective operations. A number of 177 of 392 (45.2%) patients underwent biliaryenteric anastomosis. In 6 of 215 patients (2.8%) with T-tube placement, retained CBD stones were detected by T-tube cholangiography during postoperative period. All of them were treated successfully by ERCP.Conclusions: T-tube placement without IOC is accompanied by a low rate of retained stone. Omitting IOC may decrease the operation time which is especially important in emergent cases. Retained stones following CBD exploration and T-tube placement can be treated successfully using ERCP

Rectal administration of d-alpha tocopherol for active ulcerative colitis: A preliminary report

AIM: To investigate the anti-oxidant and anti-neutrophil recruitment effects of rectal d-alpha (d-α) tocopherol administration on mild and moderately active ulcerative colitis (UC)

Intestinal Dysbiosis Contributes to the Delayed Gastrointestinal Transit in High-Fat Diet Fed MiceSummary

Background & Aims: High-fat diet (HFD) feeding is associated with gastrointestinal motility disorders. We recently reported delayed colonic motility in mice fed a HFD for 11 weeks. In this study, we investigated the contributing role of gut microbiota in HFD-induced gut dysmotility. Methods: Male C57BL/6 mice were fed a HFD (60% kcal fat) or a regular/control diet (RD) (18% kcal fat) for 13 weeks. Serum and fecal endotoxin levels were measured, and relative amounts of specific gut bacteria in the feces were assessed by real-time polymerase chain reaction. Intestinal transit was measured by fluorescent-labeled marker and a bead expulsion test. Enteric neurons were assessed by immunostaining. Oligofructose (OFS) supplementation with RD or HFD for 5 weeks also was studied. In vitro studies were performed using primary enteric neurons and an enteric neuronal cell line. Results: HFD-fed mice had reduced numbers of enteric nitrergic neurons and showed delayed gastrointestinal transit compared with RD-fed mice. HFD-fed mice had higher fecal Firmicutes and Escherichia coli and lower Bacteroidetes compared with RD-fed mice. OFS supplementation protected against enteric nitrergic neuron loss in HFD-fed mice, and improved intestinal transit time. OFS supplementation resulted in a reduction in fecal Firmicutes and Escherichia coli and serum endotoxin levels. In vitro, palmitate activation of TLR4 induced enteric neuronal apoptosis in a Phosphoâc-Jun N-terminal kinaseâdependent pathway. This apoptosis was prevented by a c-Jun N-terminal kinase inhibitor and in neurons from TLR4-/- mice. Conclusions: Together our data suggest that intestinal dysbiosis in HFD-fed mice contribute to the delayed intestinal motility by inducing a TLR4-dependent neuronal loss. Manipulation of gut microbiota with OFS improved intestinal motility in HFD mice. Keywords: Myenteric Neurons, Palmitate, Gut Microbiota, LPS, TLR4, Colon Transi