Secretin pentahydrochloride 29micrograms powder and solvent for solution for injection ampoules

Abstract Purpose To investigate the clinical significance of acinar filling observed during secretin-enhanced magnetic resonance cholangiopancreatography (s-MRCP) in patients undergoing pancreatic evaluation. Materials and Methods This retrospective study analyzed 1,283 consecutive s-MRCP examinations performed between 2005–2018. Acinar filling was defined as parenchymal T2 hyperintensity developing during secretin stimulation. Clinical, functional, and morphological parameters were compared between patients with and without acinar filling using univariate analysis and multivariate logistic regression. Exocrine function was assessed using duodenal filling grade (Matos score 0–3). Results Acinar filling was present in 67/1,283 patients (5.2%). In multivariate analysis, independent predictors included Cambridge grade (OR = 1.71, 95% CI 1.42–2.06, p0.001), age (OR = 1.68 per SD, 95% CI 1.27–2.22, p0.001), sphincter of Oddi dysfunction (SOD) (OR = 2.07, 95% CI 1.00-4.29, p = 0.050), and hyperenzymemia (OR = 1.75, 95% CI 1.01–3.05, p = 0.047). Importantly, acinar filling occurred predominantly in patients with preserved exocrine function (Matos score 2.8 ± 0.5, with 85% demonstrating complete duodenal filling), suggesting a functional-obstructive mechanism. The multivariate model achieved acceptable discriminative ability (AUC = 0.744). Among patients with morphologically normal pancreas (Cambridge 0), acinar filling remained associated with SOD (11.8% vs 2.7%, p = 0.006). Conclusion Acinar filling during s-MRCP is independently associated with SOD, hyperenzymemia, structural pancreatic damage, and older age. The occurrence of acinar filling predominantly in patients with preserved exocrine function supports a functional-obstructive mechanism wherein adequate pancreatic secretion accumulates in acinar spaces under conditions of relative ductal obstruction. This finding may represent a pathological marker warranting clinical attention.

Abstract licence: CC BY 4.0

AbstractSmall and large intrahepatic bile ducts consist of small and large cholangiocytes, respectively, and these cholangiocytes have different morphology and functions. The gastrointestinal peptide hormone, secretin (SCT) that binds to secretin receptor (SR), is a key mediator in cholangiocyte pathophysiology. Extracellular vesicles (EVs) are membrane-bound vesicles and cell-cell EV communication is recognized as an important factor in liver pathology, although EV communication between cholangiocytes is not identified to date. Cholangiocytes secrete proinflammatory cytokines during bacterial infection leading to biliary inflammation and hyperplasia. We demonstrate that cholangiocytes stimulated with lipopolysaccharide (LPS), which is a membrane component of gram-negative bacteria, secrete more EVs than cholangiocytes incubated with vehicle. These LPS-derived EVs induce inflammatory responses in other cholangiocytes including elevated cytokine production and cell proliferation. Large but not small cholangiocytes show inflammatory responses against large but not small cholangiocyte-derived EVs. Large cholangiocytes with knocked down either SCT or SR by short hairpin RNAs show reduced EV secretion during LPS stimulation, and EVs isolated from SCT or SR knocked down cholangiocytes fail to induce inflammatory reactions in control large cholangiocytes. This study identifies cholangiocyte EV communication during LPS stimulation, and demonstrates that the SCT/SR axis may be important for this event.

Abstract licence: CC BY 4.0