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Biliary tract obstruction in chronic pancreatitis.

ABSTRACT: Bile duct strictures are a common complication in patients with advanced chronic pancreatitis and have a variable clinical presentation ranging from an incidental finding to overt jaundice and cholangitis. The diagnosis is mostly made during investigations for abdominal pain but jaundice may be the initial clinical presentation. The jaundice is typically transient but may be recurrent with a small risk of secondary biliary cirrhosis in longstanding cases. The management of a bile duct stricture is conservative in patients in whom it is an incidental finding as the risk of secondary biliary cirrhosis is negligible. Initial conservative treatment is advised in patients who present with jaundice as most will resolve once the acute on chronic attack has subsided. A surgical biliary drainage is indicated when there is persistent jaundice for more than one month or if complicated by secondary gallstones or cholangitis. The biliary drainage procedure of choice is a choledocho-jejunostomy which may be combined with a pancreaticojejunostomy in patients who have associated pain. Since many patients with chronic pancreatitis have an inflammatory mass in the head of the pancreas, a Frey procedure is indicated but a resection should be performed when there is concern about a malignancy. Temporary endoscopic stenting is reserved for cholangitis while an expandable metal stent may be indicated in patients with severe co-morbid disease.

SUBMITTER: Abdallah AA

PROVIDER: S-EPMC2215354 | biostudies-other | 2007

REPOSITORIES: biostudies-other

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Project description:Background: The farnesoid X receptor (FXR) is a key factor regulating hepatic bile acid synthesis and enterohepatic circulation. Repression of bile acid synthesis by the FXR is a potential strategy for treating cholestatic liver disease. However, the role of intestinal FXR on the intestinal barrier and intestinal microbiota needs further investigation. Materials: Intestinal tissues were collected from patients with biliary atresia or without hepatobiliary disease. Then, intestinal mRNA levels of FXR-related molecules were determined. To investigate the effect of FXR activation, bile-duct-ligation rats were treated with obeticholic acid [OCA (5 mg/kg/day)] or vehicle (0.5% methyl cellulose) per oral gavage for 14 days. The mRNA levels of intestinal FXR, SHP, TNF-α, FGF15 and bile acid transporter levels were determined. In addition, the intestinal permeability, morphologic changes, and composition of the intestinal microbiota were evaluated. Gut Microbiome was determined by 16S rDNA MiSeq sequencing, and functional profiling of microbial communities was predicted with BugBase and PICRUSt2. Finally, the role of OCA in injured intestinal epithelial cell apoptosis and proliferation was examined by pretreatment with lipopolysaccharide (LPS) in Caco-2 cells. Results: The downstream of the FXR in ileum tissues was inhibited in biliary obstruction. Activation of the FXR signaling pathway by OCA significantly reduced liver fibrosis and intestinal inflammation, improved intestinal microbiota, and protected intestinal mucosa in BDL rats. OCA also altered the functional capacities of ileum microbiota in BDL rats. Significant differences existed between the controls and BDL rats, which were attenuated by OCA in the alpha diversity analysis. Principal coordinates analysis showed that microbial communities in BDL rats clustered separately from controls, and OCA treatment attenuated the distinction. Bugbase and PICRUSt2 analysis showed that OCA changed the composition and structure of the intestinal microbiota and improved the metabolic function of the intestinal microbiota by increasing the relative abundance of beneficial bacteria and reducing the relative abundance of harmful bacteria. Moreover, OCA reduced the apoptosis induced by LPS in Caco-2 cells. Conclusion: The FXR agonist, OCA, activates the intestinal FXR signaling pathway and improves the composition and structure of the intestinal microbiota and intestinal barrier in BDL rats.

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Biliary tract obstruction in chronic pancreatitis.

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