Background: The use of temporary prophylactic pancreatic duct (PD) stents in the prevention of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis in high-risk patients has been shown to be effective in multiple trials. However, there are limited data on the clinical implications of PD stents and their impact on practice outside of the trial setting.
Methods: The utility of prophylactic pancreatic stenting was evaluated in a retrospective analysis of 1,000 consecutive ERCPs performed in a single tertiary referral pancreatobiliary center over a 24-month period, based upon a predetermined protocol to identify patients at high risk of postprocedure pancreatitis.
Results: One thousand procedures performed in 688 patients were studied. Sixty-one patients were considered for stent placement and stents were successfully placed in 58 cases. The overall rate of post-ERCP pancreatitis in our study population was 3.6%. The rate of pancreatitis in the stented patients was considered high at 22.4%, but the majority (69%) were classified as mild and there were no reported severe episodes. This compares to pancreatitis in the nonstented group, in whom the majority (73.9%) experienced either moderate or severe episodes.
Conclusion: A strategy of prophylactic PD stents in this study has eliminated severe post-ERCP pancreatitis in high-risk patients. However, the high pancreatitis rate in stented patients may represent the cost to achieve this, while stent type and size employed are likely contributing factors. To maximize the benefits of PD stenting, there is a need to identify and treat all those considered at high risk.
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http://dx.doi.org/10.1007/s00464-009-0875-7 | DOI Listing |
Arq Bras Cir Dig
January 2025
Instituto D'Or de Pesquisa e Ensino, Digestive Surgery Program - Rio de Janeiro (RJ), Brazil.
Complete removal of metastatic disease and maintenance of an adequate liver remnant remains the only treatment option with curative intent concerning colorectal liver metastases. Surgery impacts on the long-term prognosis and complications adversely affect oncological results. The actual morbidity involving this scenario is debatable and estimated to be ranging from 15% to 50%.
View Article and Find Full Text PDFBJS Open
December 2024
Department of Surgery, Faculty of Medicine Vajira Hospital, Navamindradhiraj University, Bangkok, Thailand.
Background: Adverse events after endoscopic retrograde cholangiopancreatography (ERCP) are rare, and post-ERCP pancreatitis is a serious adverse event. This study aimed to determine the role of aggressive intravenous hydration with lactated Ringer's solution at a specific volume with 20% human albumin before ERCP in reducing the incidence of post-ERCP pancreatitis.
Methods: This study was a single-centre randomized clinical trial.
Gut Pathog
January 2025
Department of General, Visceral, Thoracic and Transplant Surgery, University Hospital of Giessen, Rudolf-Buchheim-Strasse 7, 35392, Giessen, Germany.
Background: The use of antibiotic therapy in acute pancreatitis remains controversial and is currently recommended only for confirmed infections of peripancreatic necrosis. However, reliable early predictors of septic complications and unfavorable outcomes are substantially lacking.
Methods: Patients with acute pancreatitis were retrospectively reviewed and divided into two groups: one with a septic course defined by pathogen detection [GERM(+)] and one without [GERM(-)].
Introduction: A pancreatic neuroendocrine tumour (NET) originates from the neuroendocrine cells responsible for producing and releasing hormones. They are uncommon findings, mainly seen arising from the head of the pancreas and their appearances may vary among different imaging modalities.
Case Report: Interesting case of an asymptomatic patient with an incidental finding of a pancreatic lesion and its variable appearances across different modalities and final histology findings.
Hepatol Commun
November 2024
Department of Medicine, University of California, San Diego, La Jolla, California, USA.
Background: Liver fibrosis is caused by chronic toxic or cholestatic liver injury. Fibrosis results from the recruitment of myeloid cells into the injured liver, the release of inflammatory and fibrogenic cytokines, and the activation of myofibroblasts, which secrete extracellular matrix, mostly collagen type I. Hepatic myofibroblasts originate from liver-resident mesenchymal cells, including HSCs and bone marrow-derived CD45+ collagen type I+ expressing fibrocytes.
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