Rapid communicationIntraductal acidosis in acute biliary pancreatitis
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Acknowledgements
Our research work is supported by grants from the Hungarian Scientific Research Fund to Péter Hegyi, Zoltán Rakonczay Jr and Tamás Takács (NF100677, NF105758 and K101116) and Bolyai Postdoctoral Fellowship to Zoltán Rakonczay Jr (BO00174/10/5). Conflict of interest statement. The authors have no conflict of interest to declare.
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2020, Biochemical and Biophysical Research CommunicationsCitation Excerpt :Acute pancreatitis (AP) is an inflammatory disorder in the pancreas [1]. Clinically, the increased risk of AP has been found to be correlated with marked acidosis [2,3], further supported by the observation that the luminal pH in AP patients was obviously lower than that in controls [4]. In the cerulein-induced pancreatitis, reducing extracellular pH to 6.8 sensitized pancreatic acinar cells to zymogen activation and injury, and enhanced the activation of trysinogen and pancreatic edema in vivo [5], demonstrating the promoting role of extracellular acidification in the process of AP.
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2019, Journal of Infection and ChemotherapyCitation Excerpt :It may be necessary to pay close attention to the development of ‘gallstone-related disorder’ induced by Ca-CTRX salt formation in patients receiving CTRX at a dose exceeding the normal dose, pediatric patients, old patients, and patients with a pathology reducing the bile pH such as acute biliary pancreatitis [27].
Transient High Pressure in Pancreatic Ducts Promotes Inflammation and Alters Tight Junctions via Calcineurin Signaling in Mice
2018, GastroenterologyCitation Excerpt :However, the pancreatic ductal cells exert a role in pancreatitis.44,45 Takacs et al.46 showed that elevated intraductal pressure in the setting of pancreatitis was associated with intraductal acidosis. Intraductal pH was shown in some studies to affect pancreatitis severity.
Cystic fibrosis-style changes in the early phase of pancreatitis
2015, Clinics and Research in Hepatology and GastroenterologyCitation Excerpt :Several pancreatitis associated toxic factors, such as ethanol [13], bile acids [14,15], trypsin [16] and cigarette smoke extract [17] displayed inhibitory effect on bicarbonate secretion by inhibiting the activity of CFTR chloride channel and SLC26A6/A3. Impaired HCO3− secretion disrupts the physiological interaction between acinar and duct cells, resulting in decreased intraluminal pH [26,27], premature trypsinogen activation [16,28], impaired acinar secretion [29], obstruction of the lumen with mucoprotein plugs [11,30] and finally destruction of the parenchyma [31,32], which is actually very similar to the picture we can observe in CF. Not only functional inhibition, but also genetic defects of CFTR can be causative for pancreatitis. Association between mutations and the risk for development of CP [9,10,20] indicate that insufficient electrolyte transport is clearly pathogenic for CP.
The role of pancreatic ducts in the pathogenesis of acute pancreatitis
2015, PancreatologyCitation Excerpt :The inhibition of pancreatic HCO3− secretion by high concentrations of chenodeoxycholate may be related to mitochondrial damage followed by intracellular ATP depletion which will affect apical and basolateral HCO3− transport mechanisms [15]. Notably, a small pilot study has shown that intraluminal pancreatic ductal pH is lower in patients with biliary pancreatitis vs control patients [19]. The decrease in ductal pH was greater in patients with biliary pancreatitis who had symptoms for longer time-periods before endoscopic retrograde cholangio-pancreatography.