Primary canalicular bile undergoes a process of fluidization and alkalinization along the biliary tract that is influenced by several factors including hormones, innervation/neuropeptides, and biliary constituents. Th...Primary canalicular bile undergoes a process of fluidization and alkalinization along the biliary tract that is influenced by several factors including hormones, innervation/neuropeptides, and biliary constituents. The excretion of bicarbonate at both the canaliculi and the bile ducts is an important contributor to the generation of the so-called bile-salt independent flow. Bicarbonate is secreted from hepatocytes and cholangiocytes through parallel mechanisms which involve chloride efflux through activation of Cl- channels, and further bicarbonate secretion via AE2/SLC4A2-mediated Cl-/HCO3- exchange. Glucagon and secretin are two relevant hormones which seem to act very similarly in their target cells （hepatocytes for the former and cholangiocytes for the latter）. These hormones interact with their specific G protein-coupled receptors, causing increases in intracellular levels of cAMP and activation of cAMP-dependent Cl- and HCO3- secretory mechanisms. Both hepatocytes and cholangiocytes appear to have cAMP-responsive intracellular vesicles in which AE2/SLC4A2 colocalizes with cell specific Cl- channels （CFTR in cholangiocytes and not yet determined in hepatocytes） and aquaporins （AQP8 in hepatocytes and AQP1 in cholangiocytes）, cAMP-induced coordinated trafficking of these vesicles to either canalicular or cholangiocyte lumenal membranes and further exocytosis results in increased osmotic forces and passive movement of water with net bicarbonate-rich hydrocholeresis.展开更多
Introduction Ceftriaxone(CTRX),a third-generation cephalosporin,has been extensively utilized in clinical practice due to its broad-spectrum antibacterial activity[1].However,its prolonged biliary excretion at high co...Introduction Ceftriaxone(CTRX),a third-generation cephalosporin,has been extensively utilized in clinical practice due to its broad-spectrum antibacterial activity[1].However,its prolonged biliary excretion at high concentrations can induce calcium salt deposition,resulting in reversible pseudolithiasis[2].This transient biliary complication predominantly affects the pediatric population[3].Adult cases,particularly among puerperal women,remain exceptionally rare.We present a case of CTRX-induced pseudolithiasis manifesting acute cholecystitis in a puerperal woman,with a focus on elucidating predisposing factors and optimizing therapeutic strategies.展开更多
基金the "UTE for CIMA project" as well as by a grant from the "Institute de Salud CarlosⅢ" (PI051098). J. M. B. has a grant from the Spanish Ministry of Science and Technology
文摘Primary canalicular bile undergoes a process of fluidization and alkalinization along the biliary tract that is influenced by several factors including hormones, innervation/neuropeptides, and biliary constituents. The excretion of bicarbonate at both the canaliculi and the bile ducts is an important contributor to the generation of the so-called bile-salt independent flow. Bicarbonate is secreted from hepatocytes and cholangiocytes through parallel mechanisms which involve chloride efflux through activation of Cl- channels, and further bicarbonate secretion via AE2/SLC4A2-mediated Cl-/HCO3- exchange. Glucagon and secretin are two relevant hormones which seem to act very similarly in their target cells （hepatocytes for the former and cholangiocytes for the latter）. These hormones interact with their specific G protein-coupled receptors, causing increases in intracellular levels of cAMP and activation of cAMP-dependent Cl- and HCO3- secretory mechanisms. Both hepatocytes and cholangiocytes appear to have cAMP-responsive intracellular vesicles in which AE2/SLC4A2 colocalizes with cell specific Cl- channels （CFTR in cholangiocytes and not yet determined in hepatocytes） and aquaporins （AQP8 in hepatocytes and AQP1 in cholangiocytes）, cAMP-induced coordinated trafficking of these vesicles to either canalicular or cholangiocyte lumenal membranes and further exocytosis results in increased osmotic forces and passive movement of water with net bicarbonate-rich hydrocholeresis.
基金supported by a grant from the High-quality Development Science and Technology Program Project of Xiamen(No.2024GZL-QN073).
文摘Introduction Ceftriaxone(CTRX),a third-generation cephalosporin,has been extensively utilized in clinical practice due to its broad-spectrum antibacterial activity[1].However,its prolonged biliary excretion at high concentrations can induce calcium salt deposition,resulting in reversible pseudolithiasis[2].This transient biliary complication predominantly affects the pediatric population[3].Adult cases,particularly among puerperal women,remain exceptionally rare.We present a case of CTRX-induced pseudolithiasis manifesting acute cholecystitis in a puerperal woman,with a focus on elucidating predisposing factors and optimizing therapeutic strategies.
