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Pathophysiology of severe gallstone pancreatitis: A new paradigm.
World J Gastroenterol
February 2024
Clinic IB, Ibi 501-0614, Gifu, Japan.
Severe gallstone pancreatitis (GSP) refractory to maximum conservative therapy has wide clinical variations, and its pathophysiology remains controversial. This Editorial aimed to investigate the pathophysiology of severe disease based on Opie's theories of obstruction, the common channel, and duodenal reflux and describe its types. Severe GSP might be a hybrid disease with pathology polarized between acute cholangitis with mild pancreatitis (biliary type) and necrotizing pancreatitis uncomplicated with biliary tract disease (pancreatic type), in which hepatobiliary and pancreatic lesion severity is inversely related to the presence or absence of impacted ampullary stones.
View Article and Find Full Text PDFSelective deletion of ENTPD1/CD39 in macrophages exacerbates biliary fibrosis in a mouse model of sclerosing cholangitis.
Purinergic Signal
September 2019
Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Avenue, Dana 501, Boston, MA, 02115, USA.
Purinergic signaling is important in the activation and differentiation of macrophages, which play divergent roles in the pathophysiology of liver fibrosis. The ectonucleotidase CD39 is known to modulate the immunoregulatory phenotype of macrophages, but whether this specifically impacts cholestatic liver injury is unknown. Here, we investigated the role of macrophage-expressed CD39 on the development of biliary injury and fibrosis in a mouse model of sclerosing cholangitis.
View Article and Find Full Text PDFSystematic review with meta-analysis: cholecystectomy for biliary dyskinesia-what can the gallbladder ejection fraction tell us?
Aliment Pharmacol Ther
March 2019
Gastroenterology and Hepatology, Lynda K and David M Underwood Center for Digestive Disorders, Houston Methodist Hospital and Weill Cornell Medical College, Houston, Texas.
Background: Gallbladder dyskinesia (gallbladder spasm, biliary dyskinesia or chronic acalculous cholecystitis) is a poorly defined entity which presents as biliary-type pain without any identifiable organic pathology. Abnormal gallbladder ejection fraction (GBEF) is used by some to select those likely to benefit from cholecystectomy. The validity of this approach has been questioned.
View Article and Find Full Text PDFSphincter of Oddi dysfunction Type III: New studies suggest new approaches are needed.
World J Gastroenterol
May 2015
C Mel Wilcox, Division of Gastroenterology and Hepatology, University of Alabama at Birmingham, Basil I Hirschowitz Endoscopic Center of Excellence, Birmingham, AL 35294-0113, United States.
Sphincter of Oddi dysfunction (SOD) has been classified into three types based upon the presence or absence of objective findings including liver test abnormalities and bile duct dilatation. Type III is the most controversial and is classified as biliary type pain in the absence of any these objective findings. Many prior studies have shown that the clinical response to endoscopic therapy is higher based upon the presence of these objective criteria.
View Article and Find Full Text PDFVitamin D nuclear receptor deficiency promotes cholestatic liver injury by disruption of biliary epithelial cell junctions in mice.
Hepatology
October 2013
INSERM UMR_S 938, CdR Saint-Antoine, F-75012, Paris, France; UPMC Univ Paris 06, F-75012, Paris, France.
Unlabelled: Alterations in apical junctional complexes (AJCs) have been reported in genetic or acquired biliary diseases. The vitamin D nuclear receptor (VDR), predominantly expressed in biliary epithelial cells in the liver, has been shown to regulate AJCs. The aim of our study was thus to investigate the role of VDR in the maintenance of bile duct integrity in mice challenged with biliary-type liver injury.
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