Gallbladder

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Alan F. Hofmann - One of the best experts on this subject based on the ideXlab platform.

  • acute effects of topical methyl tert butyl ether or ethyl propionate on Gallbladder histology in animals a comparison of two solvents for contact dissolution of cholesterol gallstones
    Hepatology, 1992
    Co-Authors: Oliver Esch, Claudio D. Schteingart, John C. Spinosa, Ronald L. Hamilton, Diane L. Crombie, Joseph F. Rondinone, Jan Lillienau, Horacio B Dagostino, Alan F. Hofmann
    Abstract:

    Experiments were performed in anesthetized rabbits and piglets to assess Gallbladder mucosal injury during irrigation with methyl tert-butyl ether, a C5 ether, or ethyl propionate, a C5 ester—two organic solvents used in the contact dissolution of cholesterol gallstones. In 44 New Zealand White rabbits, the Gallbladder was exposed to individual solvents or saline solution through a transhepatic catheter for 2 hr. Gallbladders were then harvested and fixed immediately or after a recovery period of 1, 4 or 8 days. Tissue sections were examined under light microscopy, and severity of injury was graded with predefined criteria by two pathologists blinded to the animals' treatment regimens. Histological assessment showed severe mucosal injury such as necrosis of the cells at the villus tips immediately after 2 hr of exposure to either solvent. After 4 days, injury had decreased significantly; after 8 days, complete mucosal healing had taken place. A similar study was performed in 32 piglets. Solvent or saline solution was oscillated in and out of the Gallbladders of these piglets with a computer-controlled syringe pump at a pressure less than the leakage pressure of the Gallbladder. Histological assessment was performed on tissue samples obtained immediately after the procedure or 8 days later. Both solvents caused severe mucosal injury; however, after 8 days complete mucosal healing had occurred, so that Gallbladders exposed to solvent were indistinguishable from Gallbladders exposed to saline solution, which was used as control. We conclude that both methyl tert-butyl ether and ethyl propionate cause moderate to severe epithelial injury but that the Gallbladder epithelium regenerates within a few days. If these data apply to patients undergoing contact dissolution of gallstones, both methyl tert-butyl ether and ethyl propionate will cause severe but fully reversible mucosal injury. From the standpoint of toxicity to the Gallbladder mucosa, ethyl propionate appears to qualify as an alternative to methyl tert-butyl ether for contact dissolution of cholesterol gallstones. (HEPATOLOGY 1992;16:984–991.)

John K. Boitnott - One of the best experts on this subject based on the ideXlab platform.

  • diffuse lymphoplasmacytic chronic cholecystitis is highly specific for extrahepatic biliary tract disease but does not distinguish between primary and secondary sclerosing cholangiopathy
    The American Journal of Surgical Pathology, 2003
    Co-Authors: Susan C. Abraham, Pedram Argani, Emma E. Furth, Ralph H. Hruban, Marcia Cruzcorrea, John K. Boitnott
    Abstract:

    Previous studies of Gallbladder pathology in primary sclerosing cholangitis (PSC) have suggested that a distinctive histologic triad ("diffuse lymphoplasmacytic acalculous cholecystitis," composed of diffuse, mucosal-based, dense lymphoplasmacytic infiltrates) is commonly present in Gallbladders of patients with PSC and is relatively specific for that disease. However, prior control populations have included only patients with cholecystitis/cholelithiasis and hepatitis, and have not evaluated patients with non-PSC-associated extrahepatic biliary tract disease. We recently observed cases of diffuse lymphoplasmacytic chronic cholecystitis in a subset of patients with biliary tract disease associated with lymphoplasmacytic sclerosing pancreatitis and among patients undergoing Whipple resection for pancreatic head malignancy, suggesting that diffuse lymphoplasmacytic chronic cholecystitis is not specific for PSC. We studied 20 Gallbladders from patients with obstructive jaundice due to malignancies of the pancreatic head, duodenum, or ampulla and 5 Gallbladders from patients with choledocholithiasis, and compared them with 20 Gallbladders from patients with PSC and 20 Gallbladders with cholelithiasis. The following histologic features were evaluated: degree of mucosal and deep inflammation, lymphoid nodules, epithelial metaplasia, muscular hypertrophy, Rokitansky-Aschoff sinuses, fibrosis, and cholesterolosis. Gallbladders in malignancy-associated obstructive jaundice were nearly identical to Gallbladders in PSC with respect to scores for mucosal inflammation, lymphoid nodules, and frequency of diffuse lymphoplasmacytic chronic cholecystitis (60% vs. 50%, respectively). PSC Gallbladders, however, were significantly more likely to contain focal or extensive epithelial metaplasia (P = 0.01). The cholelithiasis control group was characterized by lack of significant mucosal inflammation in the majority of cases (95%) and frequent Rokitansky-Aschoff sinuses, fibrosis, and muscular hypertrophy. Gallbladders in the choledocholithiasis group showed overlapping histologic features with PSC/malignancy-associated obstructive jaundice and cholelithiasis. These results suggest that a pattern of diffuse lymphoplasmacytic chronic cholecystitis is highly specific for extrahepatic biliary tract disease but does not distinguish between primary and secondary cholangiopathies.

  • Lymphoplasmacytic Chronic Cholecystitis and Biliary Tract Disease in Patients With Lymphoplasmacytic Sclerosing Pancreatitis
    The American journal of surgical pathology, 2003
    Co-Authors: Susan C. Abraham, Marcia Cruz-correa, Pedram Argani, Emma E. Furth, Ralph H. Hruban, John K. Boitnott
    Abstract:

    Lymphoplasmacytic sclerosing pancreatitis (LPSP) represents a distinctive form of chronic pancreatitis characterized by diffuse fibroinflammatory infiltrates that can involve both the pancreatic ducts and acinar parenchyma. Several cases of inflammatory infiltrates within the Gallbladder have been reported in association with LPSP, but the spectrum of Gallbladder pathology in patients with LPSP has not been systematically reviewed. Many patients with LPSP have distal CBD fibrosis, strictures, and inflammation, features that overlap somewhat with primary sclerosing cholangitis (PSC). In PSC, a pattern of Gallbladder pathology termed "diffuse acalculous lymphoplasmacytic chronic cholecystitis" has been previously described as showing a triad of diffuse, mucosal-based, plasma cell-rich inflammatory infiltrates. We studied 20 Gallbladders from patients with LPSP and compared them with 20 Gallbladders in PSC, 20 Gallbladders with chronic cholelithiasis, and 10 Gallbladders from patients with benign (non-LPSP) pancreatic disease. The following features were evaluated: degree and composition of mucosal inflammation and deep (mural) inflammation, lymphoid nodules, metaplasia, dysplasia/neoplasia, fibrosis, muscular hypertrophy, Rokitansky-Aschoff sinuses, and cholesterolosis. The majority (60%) of Gallbladders in LPSP contained moderate or marked inflammatory infiltrates and lymphoid nodules, frequencies similar to PSC but significantly higher than in chronic cholelithiasis and benign non-LPSP pancreatic disease. LPSP Gallbladders received the highest scores for deep inflammation of all groups, and 35% of LPSP Gallbladders showed transmural chronic cholecystitis. Overall, "diffuse lymphoplasmacytic chronic cholecystitis" was present in 50% of PSC cases and 25% of LPSP cases, but in only 5% of chronic cholelithiasis and none of non-LPSP benign pancreatic disease. Mucosal inflammation in LPSP Gallbladders correlated significantly with the presence of inflammation in the extrapancreatic portion of the CBD. These findings suggest that inflammatory pathology of the Gallbladder is frequently associated with LPSP and that it is part of the spectrum of biliary tract disease in these patients, rather than a simple reflection of the pancreatitis itself.

Hiroshi Kajiya - One of the best experts on this subject based on the ideXlab platform.

  • motility of the gastrointestinal tract and Gallbladder during long term total parenteral nutrition in dogs
    Journal of Parenteral and Enteral Nutrition, 2002
    Co-Authors: Tatsuru Kaji, Hideo Takamatsu, Hiroshi Kajiya
    Abstract:

    BACKGROUND: The motility of the gastrointestinal tract during total parenteral nutrition (TPN) remains poorly understood. The objective of this study was to determine the motility pattern not only in the gastrointestinal tract but also in the Gallbladders of dogs maintained by TPN. METHODS: Central venous catheters were inserted through the external jugular vein of 5 dogs and 6 strain gauge force transducers were sewn to the stomach, small intestine, and Gallbladder. Two weeks later, oral food was discontinued and motility was recorded for 24 hours after the first migrating motor complex (MMC) was confirmed in the stomach as pre-TPN. TPN was started and continued for 4 weeks, and patterns of motor activity during TPN were recorded for 24 hours at the end of each week. RESULTS: The durations of MMC in the stomach, duodenum, and Gallbladder in pre-TPN were 118 +/- 3 minutes, 118 +/- 2 minutes, and 118 +/- 2 minutes, respectively, but in the first week of TPN they were 432 +/- 56 minutes, 431 +/- 56 minutes,...

Yongsheng Chen - One of the best experts on this subject based on the ideXlab platform.

  • phosphorylation and subcellular localization of na h exchanger isoform 3 nhe3 are associated with altered Gallbladder absorptive function after formation of cholesterol gallstones
    Journal of Physiology and Biochemistry, 2017
    Co-Authors: Yongsheng Chen, Yu Tian, Jing Kong
    Abstract:

    Na+/H+ exchanger isoform 3 (NHE3) dysfunction is thought to contribute to the altered Gallbladder absorption that occurs in cholesterol gallstone disease, but the mechanism is unknown. The current study was undertaken to examine the expression, phosphorylation, and subcellular localization of NHE3 in Gallbladder epithelium cells (GBECs) of male C57BL/6 mice on a control or lithogenic diet. Thirty-six 8-week-old male C57BL/6 mice were randomly assigned to receive a high cholesterol diet or a regular diet for 8 weeks. Gallstone formation was recorded. Gallbladder bile cholesterol, phospholipid, and total bile acids were examined. RT-PCR was used to measure NHE3 mRNA expression. NHE3 protein expression and subcellular localization were examined by Western blotting and immunofluorescence microscopy, respectively. Gallstones were formed in all mice fed the lithogenic diet. Despite higher NHE3 mRNA expression in Gallbladders of the mice on the lithogenic diet than in those on the control diet, there was no significant difference in expression of total NHE3 protein. However, a higher level of NHE3 phosphorylated at serine-552 (P-NHE3) was seen on the lithogenic diet. In immunofluorescence studies, NHE3 protein was expressed both on the apical membrane and in the cytoplasm of mouse GBEC. This pattern of subcellular distribution of NHE3 strongly corroborates an exchanger trafficking mechanism in NHE3 activity regulation in mouse GBEC. We conclude that increased phosphorylation of NHE3 following gallstone formation leads to turnover of the exchanger, resulting in decreased Gallbladder concentrating function.

  • expression and subcellular localization of nhe in the human Gallbladder epithelium
    International Journal of Clinical and Experimental Pathology, 2014
    Co-Authors: Yongsheng Chen, Jing Kong, Shuodong Wu
    Abstract:

    Background: Enhanced Gallbladder concentrating function is an important factor for the pathogenesis of cholesterol gallstone disease (CGD), but the mechanism is unknown. Potential candidates for regulation of Gallbladder ion absorption are suggested to be Na+/H+ exchanger isoform 3 (NHE3). In this study, we investigated the expression and subcellular localization of NHE3 in both acalculous and calculous human Gallbladders. Methods: Adult human Gallbladder tissue was obtained from 23 patients (7 men, 16 women) who had undergone cholecystectomy. The patients were divided into two groups: Group A (acalculous group) and Group B (calculous group). Gene expression of NHE3 was quantitatively estimated by real-time PCR. Protein expression was studied by Western blotting assays. Furthermore, expression of immunoreactive NHE3 was investigated by immunohistochemistry. Results: There was no significant difference in the NHE3 mRNA expression between calculous and acalculous human Gallbladders. NHE3 protein expression in Gallbladders from patients with cholelithiasis is increased compared to those without gallstones. Immunohistochemistry studies prove that NHE3 is located both on the apical plasma membrane and in the intracellular pool in human GBECs. Conclusions: NHE3 may play a role in the pathogenesis of human CGD. Additional studies are required to further delineate the underlying mechanisms.

Jing Kong - One of the best experts on this subject based on the ideXlab platform.

  • phosphorylation and subcellular localization of na h exchanger isoform 3 nhe3 are associated with altered Gallbladder absorptive function after formation of cholesterol gallstones
    Journal of Physiology and Biochemistry, 2017
    Co-Authors: Yongsheng Chen, Yu Tian, Jing Kong
    Abstract:

    Na+/H+ exchanger isoform 3 (NHE3) dysfunction is thought to contribute to the altered Gallbladder absorption that occurs in cholesterol gallstone disease, but the mechanism is unknown. The current study was undertaken to examine the expression, phosphorylation, and subcellular localization of NHE3 in Gallbladder epithelium cells (GBECs) of male C57BL/6 mice on a control or lithogenic diet. Thirty-six 8-week-old male C57BL/6 mice were randomly assigned to receive a high cholesterol diet or a regular diet for 8 weeks. Gallstone formation was recorded. Gallbladder bile cholesterol, phospholipid, and total bile acids were examined. RT-PCR was used to measure NHE3 mRNA expression. NHE3 protein expression and subcellular localization were examined by Western blotting and immunofluorescence microscopy, respectively. Gallstones were formed in all mice fed the lithogenic diet. Despite higher NHE3 mRNA expression in Gallbladders of the mice on the lithogenic diet than in those on the control diet, there was no significant difference in expression of total NHE3 protein. However, a higher level of NHE3 phosphorylated at serine-552 (P-NHE3) was seen on the lithogenic diet. In immunofluorescence studies, NHE3 protein was expressed both on the apical membrane and in the cytoplasm of mouse GBEC. This pattern of subcellular distribution of NHE3 strongly corroborates an exchanger trafficking mechanism in NHE3 activity regulation in mouse GBEC. We conclude that increased phosphorylation of NHE3 following gallstone formation leads to turnover of the exchanger, resulting in decreased Gallbladder concentrating function.

  • expression and subcellular localization of nhe in the human Gallbladder epithelium
    International Journal of Clinical and Experimental Pathology, 2014
    Co-Authors: Yongsheng Chen, Jing Kong, Shuodong Wu
    Abstract:

    Background: Enhanced Gallbladder concentrating function is an important factor for the pathogenesis of cholesterol gallstone disease (CGD), but the mechanism is unknown. Potential candidates for regulation of Gallbladder ion absorption are suggested to be Na+/H+ exchanger isoform 3 (NHE3). In this study, we investigated the expression and subcellular localization of NHE3 in both acalculous and calculous human Gallbladders. Methods: Adult human Gallbladder tissue was obtained from 23 patients (7 men, 16 women) who had undergone cholecystectomy. The patients were divided into two groups: Group A (acalculous group) and Group B (calculous group). Gene expression of NHE3 was quantitatively estimated by real-time PCR. Protein expression was studied by Western blotting assays. Furthermore, expression of immunoreactive NHE3 was investigated by immunohistochemistry. Results: There was no significant difference in the NHE3 mRNA expression between calculous and acalculous human Gallbladders. NHE3 protein expression in Gallbladders from patients with cholelithiasis is increased compared to those without gallstones. Immunohistochemistry studies prove that NHE3 is located both on the apical plasma membrane and in the intracellular pool in human GBECs. Conclusions: NHE3 may play a role in the pathogenesis of human CGD. Additional studies are required to further delineate the underlying mechanisms.