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The liver, gallbladder and pancreas
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Dina G. Tiniakos, Alastair D. Burt
The gallbladder is connected to the intrahepatic and extrahepatic bile ducts by the cystic duct. It stores and concentrates bile from the liver and increases its viscosity by releasing mucus from the lining epithelium. The release of bile from the gallbladder is stimulated by food, especially fatty food, in the duodenum under the influence of cholecystokinin.
Drug-Induced Vanishing Bile Duct Syndromes
Published in Gianfranco Alpini, Domenico Alvaro, Marco Marzioni, Gene LeSage, Nicholas LaRusso, The Pathophysiology of Biliary Epithelia, 2020
Tania A. Roskams, Valeer J. Desmet
Drug-induced vanishing bile duct syndromes are part of the spectrum of drug-induced cholestatic diseases. The term cholestasis refers to a reduction or an arrest in bile secretion and/or bile flow. Cholestasis may be due to three different mechanisms: alteration of bile secretion by the hepatocyte (hepatocellular cholestasis). Hepatocellular cholestasis may be ‘pure’, i.e., without hepatocellular damage (as is the case in estrogen-induced cholestasis), or associated with some degree of hepatocellular damage, i.e., hepatitis. Hepatitis is described as cholestatic when cholestasis dominates the picture. This is frequent in drug-induced cholestasis.obstruction of intrahepatic bile ducts. In drug-induced cholestasis, the site of injury is usually the bile ductules (cholangiolitis) or the interlobular, portal bile ducts (cholangitis). Bile ductules are the finest, most peripheral branches of the biliary tree, connecting the canaliculi with the interlobular bile ducts.obstruction of extrahepatic bile ducts.
Liver and biliary system, pancreas and spleen
Published in A Stewart Whitley, Jan Dodgeon, Angela Meadows, Jane Cullingworth, Ken Holmes, Marcus Jackson, Graham Hoadley, Randeep Kumar Kulshrestha, Clark’s Procedures in Diagnostic Imaging: A System-Based Approach, 2020
A Stewart Whitley, Jan Dodgeon, Angela Meadows, Jane Cullingworth, Ken Holmes, Marcus Jackson, Graham Hoadley, Randeep Kumar Kulshrestha
ERCP/MRCP. The traditional test for imaging the extrahepatic bile ducts was endoscopic retrograde cholangio-pancreatography (ERCP). This involves passing a special endoscope into the duodenum and cannulating the distal CBD via the ampulla of Vater, in order to opacify the biliary system by retrograde injection of iodinated contrast medium. The biliary system is then imaged using fluoroscopy. This technique allows very accurate demonstration of the biliary anatomy and accurately detects stones and strictures (benign and malignant). It also permits stone extraction and/or stenting at the same procedure, but it is invasive and can have significant complications including bile duct perforation and cholangitis (infection).
ZO-2 favors Hippo signaling, and its re-expression in the steatotic liver by AMPK restores junctional sealing
Published in Tissue Barriers, 2022
Laura González-González, Helios Gallego-Gutiérrez, Dolores Martin-Tapia, José Everardo Avelino-Cruz, Christian Hernández-Guzmán, Sergio Israel Rangel-Guerrero, Luis Marat Alvarez-Salas, Erika Garay, Bibiana Chávez-Munguía, María Concepción Gutiérrez-Ruiz, Dinorah Hernández-Melchor, Esther López-Bayghen, Lorenza González-Mariscal
The formation of bile acids is one of the main functions of the liver. Bile acids are transported across the hepatocytes apical membrane into the lumen of bile canaliculi. Then, via extrahepatic bile ducts reach the intestinal tract, having a fundamental role in the solubilization of dietary lipids. Bile acids are powerful detergents, and TJs prevent their leakage to the basolateral surface and the underlying parenchyma of hepatocytes and cholangiocytes. In the liver claudins −1, −2 and −3 have been observed in hepatocyte TJs.78,79,80 Claudin-2 has been more thoroughly studied, demonstrating its importance for the paracellular water flow required for proper bile composition, as a claudin-2 deficiency in mice increased bile concentration and promoted cholesterol gallstone formation.81 In humans, the role of ZO-2 in liver TJs appears to be critical and non-redundant since homozygote20,22 and compound heterozygote23,61 mutations in TJP2 cause PFIC-4. This disease, characterized by fluctuating jaundice, persistent cholestasis, pruritus, and malabsorption, affects young children and is an end-stage liver disease that leads to cirrhosis and hepatocellular carcinoma.22,23 In PFIC-4, the mutations of TJP2 that ablate ZO-2 expression induce a severe disease only in the liver, even though ZO-2 is a protein normally expressed in all epithelial cells. These observations suggest that in the human liver, ZO-2 plays a non-redundant role at TJs that cannot be compensated by other TJ proteins like, for example, ZO-1 or ZO-3.
A significant proportion of patients with choledocholithiasis have markedly elevated alanine aminotransferase
Published in Scandinavian Journal of Gastroenterology, 2019
Helgi K. Björnsson, Einar S. Björnsson
Information on the following biochemical parameters was obtained: ALT, AST, ALP, bilirubin, amylase, and lipase. Values at baseline and maximal values during the course of the injury were documented. Furthermore, information was obtained on demographics, prior cholecystectomy, and results of radiological imaging such as the presence of gallbladder stones and CDL. Patients with confirmed CDL on imaging (abdominal ultrasound, computed tomography (CT), magnetic resonance cholangiopancreatography (MRCP), and/or ERCP) were included and those with a clinical diagnosis of CDL with a triad of new onset severe pain, elevated, and reversible liver tests and imaging features of gallbladder stones. The diameter of extrahepatic bile ducts on imaging, mostly ERCP and MRCP but also on hepatobiliary ultrasound, was analyzed.
Preclinical insights into cholangiopathies: disease modeling and emerging therapeutic targets
Published in Expert Opinion on Therapeutic Targets, 2019
Keisaku Sato, Shannon Glaser, Lindsey Kennedy, Suthat Liangpunsakul, Fanyin Meng, Heather Francis, Gianfranco Alpini
BA is a form of neonatal cholestasis caused by various factors such as viral infection or insufficient bile duct development [9–11]. The preclinical animal models available for BA research are limited. Previous studies have performed BDL utilizing 3-week-old rats, which resembled some features of BA [80]. Due to its technical difficulties, BDL is not widely performed in young mice, as should be done in the BA model to better mimic human pathology. It is well known that perinatal viral infection is associated with BA development in children [81]. Injection of rhesus rotavirus into newborn mice is the most established animal model for BA research [82,83]. Although the effects of virus injection differ depending on the strain of rotavirus, the injected virus can be delivered into cholangiocytes, thereby causing biliary damage, high serum levels of proinflammatory cytokines, and portal lymphocyte infiltration in neonatal mice [82,83]. This model has progressive jaundice, growth failure, and high mortality because of obstruction of extrahepatic bile ducts [84]. This technique can be performed in various strains of mice. Recent studies using this model have demonstrated the functional roles of the gut microbiome and bone marrow-derived mesenchymal stem cells in BA [85,86]. The viral injection model is the sole well-established BA model currently available, and studies using this model are limited.