Gallbladder Mucosa

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Petr Mukensnabl - One of the best experts on this subject based on the ideXlab platform.

  • signet ring cell aggregates simulating carcinoma in colon and Gallbladder Mucosa
    Pathology Research and Practice, 1998
    Co-Authors: Michal Michal, A Chlumska, Petr Mukensnabl
    Abstract:

    Summary We describe three cases of benign signet-ring cell aggregates in the colon associated with pseudomembranous colitis, adenomatous polyp of the colon and ulcerated Mucosa of the Gallbladder excised for gallstones. In all cases, we found loose, benign signet-ring cell aggregates overlying the ulcerated Mucosa surface, simulating signet ring-cell carcinoma. The most important sign of the benign signet-ring cell aggregates is that they are always confined to the surface of the Mucosa of the intestine or Gallbladder Mucosa or crypts of the intestinal epithelium. In no case did we see an invasion of these cells into the lamina propria of the Mucosa. In all cases, the benign signet-ring cell aggregates were immunohistochemically positive with antibodies to cytokeratins. The occurrence of benign signet-ring cell aggregates is a rare and very misleading diagnostic pitfall which must be differentiated from signet-ring cell carcinoma of the colon and Gallbladder.

Sanjay Singh Negi - One of the best experts on this subject based on the ideXlab platform.

  • Benign signet ring cell change with multilayering in the Gallbladder Mucosa--a case report.
    Pathology research and practice, 2001
    Co-Authors: Vaishali S. Suri, Puja Sakhuja, Veena Malhotra, Ranjana Gondal, Sanjay Singh Negi
    Abstract:

    Summary We describe a case of benign signet ring cell change in the Gallbladder Mucosa. On histopathological examination of H & E-stained sections, the Gallbladder epithelium showed multilayering. The epithelial cells were large, columnar to polygonal with a small round basal or eccentric nucleus and vacuolated cytoplasm, giving them a signet ring appearance. There was no nuclear atypia, hyperchromatism or mitotic activity. The cells showed uniform positivity with mucicarmine, PAS and Alcian blue stains. The cytoplasmic vacuolations were negative for fat stains (Oil red O and Sudan IV). On immunohistochemistry, the cells showed positivity with antibodies for pancytokeratin (PCK) and epithelial membrane antigen (EMA). A diagnosis of benign signet ring cell change with multilayering in the gall bladder Mucosa was made. Thoroughly reviewing the literature, we found only one case of benign signet ring cell aggregates in the Gallbladder Mucosa documented earlier. The lesion is hereby reported because of the unique histomorphology and the diagnostic dilemma which can occur as a malignant change in situ has to be excluded.

Joar Svanvik - One of the best experts on this subject based on the ideXlab platform.

  • Acetazolamide inhibits stimulated feline liver and Gallbladder bicarbonate secretion.
    Acta physiologica Scandinavica, 2002
    Co-Authors: Bengt Nilsson, Lars Hedin, Styrbjörn Friman, J. Valantinas, Joar Svanvik
    Abstract:

    Bile acidification is a key factor in preventing calcium carbonate precipitation and gallstone formation. Carbonic anhydrase II (CA II), that is inhibited by acetazolamide, plays a role in regulation of the acid-base balance in many tissues. This study examines the effect of acetazolamide on secretin- and vasoactive intestinal peptide (VIP)-stimulated Gallbladder Mucosal bicarbonate and acid secretion. Gallbladders in anaesthetized cats were perfused with a bicarbonate buffer bubbled with CO2 in air. In 20 experiments VIP (10 ╡g kg1 h1) and in 10 experiments secretin (4 ╡g kg1 h1) were infused continuously intravenous (i.v.). Hepatic bile and samples from the buffer before and after perfusion of the Gallbladder were collected for calculation of ion and fluid transport. During basal conditions a continuous secretion of H+ by the Gallbladder Mucosa was seen. Intravenous infusion of vasoactive intestinal peptide (VIP) and secretin caused a secretion of bicarbonate from the Gallbladder Mucosa (P < 0.01). This secretion was reduced by intraluminal (i.l.) acetazolamide (P < 0.01). Bile flow was enhanced by infusion of VIP and secretin (P < 0.01) but this stimulated outflow was not affected by i.v. acetazolamide. The presence of CA II in the Gallbladder was demonstrated by immunoblotting. Biliary CA activity has an important function in the regulation of VIP- and secretin-stimulated bicarbonate secretion across the Gallbladder Mucosa.

  • Role of cyclooxygenase-2 for fluid secretion by the inflamed Gallbladder Mucosa
    Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract, 1998
    Co-Authors: Bengt Nilsson, Dick Delbro, Lars Hedin, Styrbjörn Friman, Stefan Andius, Joar Svanvik
    Abstract:

    Inflammatory fluid secretion by the Gallbladder Mucosa in experimental cholecystitis is induced by activation of cyclooxygenase, which leads to an increase in prostaglandin formation. Cyclooxygenase exists as a constitutive (cyclooxygenase-1) and an inducible (cyclooxygenase-2) isoform. The aim of this study was to demonstrate the role of cyclooxygenase-2 in inflammatory fluid secretion of the feline Gallbladder. Experiments were performed 10 weeks after a surgical procedure in which chronic cholecystitis was induced in cats by ligation of the cystic duct and implantation of a gallstone in the Gallbladder. Gallbladder fluid transport was continuously monitored via a perfusion system. In inflamed Gallbladders the continuous fluid secretion was reversed to absorption by intravenous injection of the selective cyclooxygenase-2 blocker, NS 398 (P < 0.001). Increased levels of the inducible cyclooxygenase-2 were shown by immunoblotting in inflamed Gallbladders. Selective pharmacologic blockade of cyclooxygenase-2 reduced the prostaglandin Ez release to the inflamed Gallbladder lumen (P < 0.01). These data suggest that cyclooxygenase-2 is involved in the inflammatory response during chronic cholecystitis. Selective cyclooxygenase-2 blockers may offer an alternative to traditional nonsteroidal anti-inflammatory drugs with fewer side effects in patients with cholecystitis who are awaiting operation.

  • vip antiserum and indomethacin inhibit calcium and bicarbonate secretion by the inflamed feline Gallbladder Mucosa
    Acta Physiologica Scandinavica, 1996
    Co-Authors: Bengt Nilsson, Dick Delbro, Lennart Jivegård, Anders Thune, S Friman, Joar Svanvik
    Abstract:

    Ionized calcium (Ca 2+ ) and bicarbonate (HCO 3 - ) are important ions for gallstone formation. In the present study the effect of indomethacin and vasoactive intestinal peptide-antiserum (VIP antiserum) on the Ca 2+ , HCO 3 - and fluid secretion in the inflamed Gallbladder were tested in a validated experimental model in cats. The animals were studied in acute experiments 6 weeks after cystic duct ligation and gallstone implantation During basal conditions there was a continuous secretion of Ca 2+ , HCO 3 - and fluid into the lumen of the inflamed Gallbladder Indomethacin and VIP-antiserum inhibited the Ca 2+ , HCO 3 - and fluid secretion across the inflamed Gallbladder Mucosa. Intraluminal amiloride inhibited the absorption of Ca 2+ . HCO 3 - and fluid after indomethacin infusion An impaired absorption of Ca 2+ . HCO 3 - and fluid in the inflamed Gallbladder is probably important for the solubility of calcium salts in the early stages of inflammation in the Gallbladder Mucosa

  • VIP‐antiserum and indomethacin inhibit calcium and bicarbonate secretion by the inflamed feline Gallbladder Mucosa
    Acta physiologica Scandinavica, 1996
    Co-Authors: Bengt Nilsson, Dick Delbro, Styrbjörn Friman, Lennart Jivegård, Anders Thune, Joar Svanvik
    Abstract:

    Ionized calcium (Ca 2+ ) and bicarbonate (HCO 3 - ) are important ions for gallstone formation. In the present study the effect of indomethacin and vasoactive intestinal peptide-antiserum (VIP antiserum) on the Ca 2+ , HCO 3 - and fluid secretion in the inflamed Gallbladder were tested in a validated experimental model in cats. The animals were studied in acute experiments 6 weeks after cystic duct ligation and gallstone implantation During basal conditions there was a continuous secretion of Ca 2+ , HCO 3 - and fluid into the lumen of the inflamed Gallbladder Indomethacin and VIP-antiserum inhibited the Ca 2+ , HCO 3 - and fluid secretion across the inflamed Gallbladder Mucosa. Intraluminal amiloride inhibited the absorption of Ca 2+ . HCO 3 - and fluid after indomethacin infusion An impaired absorption of Ca 2+ . HCO 3 - and fluid in the inflamed Gallbladder is probably important for the solubility of calcium salts in the early stages of inflammation in the Gallbladder Mucosa

  • inflammation reduces Mucosal secretion of hydrogen ions and impairs concentrating function and luminal acidification in feline Gallbladder
    Scandinavian Journal of Gastroenterology, 1995
    Co-Authors: Bengt Nilsson, Lennart Jivegård, S Friman, A Thune, Joar Svanvik
    Abstract:

    Background: The Gallbladder Mucosa normally absorbs fluid and secretes H+ ions. The fluid secretion in inflamed Gallbladders is induced by prostaglandins and mediated by intramural vasoactive intestinal peptide (VIP)-ergic nerves. Methods: The influence of inflammation on Gallbladder Mucosal function was studied in cats. Results: In control animals there was acidification of the Gallbladder contents due to secretion of H+ into the lumen. In animals with inflamed Gallbladders this acid secretion was reduced; there was secretion of HCO3 and no evident acidification of the Gallbladder contents. Injection of VIP antiserum or indomethacin restored H+ secretion and inhibited HCO3− and fluid secretion by the inflamed Gallbladder Mucosa. An impaired acidification of the Gallbladder contents due to Mucosal inflammation may reduce the solubility of calcium salts in Gallbladder bile and increase the risk of their precipitation in the lumen. Conclusion: Mucosal inflammation reduces H secretion and impairs acidificati...

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

  • signet ring cell aggregates simulating carcinoma in colon and Gallbladder Mucosa
    Pathology Research and Practice, 1998
    Co-Authors: Michal Michal, A Chlumska, Petr Mukensnabl
    Abstract:

    Summary We describe three cases of benign signet-ring cell aggregates in the colon associated with pseudomembranous colitis, adenomatous polyp of the colon and ulcerated Mucosa of the Gallbladder excised for gallstones. In all cases, we found loose, benign signet-ring cell aggregates overlying the ulcerated Mucosa surface, simulating signet ring-cell carcinoma. The most important sign of the benign signet-ring cell aggregates is that they are always confined to the surface of the Mucosa of the intestine or Gallbladder Mucosa or crypts of the intestinal epithelium. In no case did we see an invasion of these cells into the lamina propria of the Mucosa. In all cases, the benign signet-ring cell aggregates were immunohistochemically positive with antibodies to cytokeratins. The occurrence of benign signet-ring cell aggregates is a rare and very misleading diagnostic pitfall which must be differentiated from signet-ring cell carcinoma of the colon and Gallbladder.

Vaishali S. Suri - One of the best experts on this subject based on the ideXlab platform.

  • Benign signet ring cell change with multilayering in the Gallbladder Mucosa--a case report.
    Pathology research and practice, 2001
    Co-Authors: Vaishali S. Suri, Puja Sakhuja, Veena Malhotra, Ranjana Gondal, Sanjay Singh Negi
    Abstract:

    Summary We describe a case of benign signet ring cell change in the Gallbladder Mucosa. On histopathological examination of H & E-stained sections, the Gallbladder epithelium showed multilayering. The epithelial cells were large, columnar to polygonal with a small round basal or eccentric nucleus and vacuolated cytoplasm, giving them a signet ring appearance. There was no nuclear atypia, hyperchromatism or mitotic activity. The cells showed uniform positivity with mucicarmine, PAS and Alcian blue stains. The cytoplasmic vacuolations were negative for fat stains (Oil red O and Sudan IV). On immunohistochemistry, the cells showed positivity with antibodies for pancytokeratin (PCK) and epithelial membrane antigen (EMA). A diagnosis of benign signet ring cell change with multilayering in the gall bladder Mucosa was made. Thoroughly reviewing the literature, we found only one case of benign signet ring cell aggregates in the Gallbladder Mucosa documented earlier. The lesion is hereby reported because of the unique histomorphology and the diagnostic dilemma which can occur as a malignant change in situ has to be excluded.