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Background And Aims: Research on the variance of coagulation factors in acute pancreatitis (AP) with different etiologies remains limited. This study aims to explore the coagulation profiles in patients with biliary AP (BAP) and hyperlipidemic AP (HLAP), focusing on their role in predicting disease severity.
Methods: A single-center retrospective cohort study was conducted on patients diagnosed with BAP or HLAP at Beijing Chaoyang Hospital from January 2020 to December 2021.
Results: A total of 112 patients were enrolled, including 43 with BAP and 69 with HLAP. Among these, 82 had mild acute pancreatitis (MAP) and 30 had moderately severe acute pancreatitis (MSAP). HLAP patients had significantly higher levels of fibrinogen, protein C, coagulation factors II and X compared to BAP patients. Receiver Operating Characteristic (ROC) analysis identified fibrinogen, with an area under the curve (AUC) of 0.721, and coagulation factor VIII(FVIII), with an AUC of 0.700, as significant predictors of disease severity in HLAP. Correlation analysis showed significant associations between fibrinogen and FVIII with Ranson and computed tomography severity index (CTSI) scores, as well as positive correlations with cholesterol and triglyceride levels in these patients.
Conclusion: Compared with BAP, HLAP patients exhibit significant coagulation disorders from the mild stages. Fibrinogen and FVIII may be useful biomarkers for assessing HLAP severity.
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http://dx.doi.org/10.1016/j.dld.2025.03.008 | DOI Listing |
Clin Exp Immunol
September 2025
Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine, 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511, Japan.
Introduction: Conventional dendritic cells (cDCs) in the gut express the vitamin A (VA)-converting enzyme retinal dehydrogenase 2 (RALDH2) and produce significant amounts of retinoic acid (RA). RA derived from gut cDCs contributes to the generation of tolerogenic responses by promoting Treg differentiation while inhibiting Th1 and Th17 cell differentiation. In this study, we investigated whether similar RA-mediated immunoregulatory mechanisms operate in the pancreas using an experimental autoimmune pancreatitis (AIP) model.
View Article and Find Full Text PDFExp Cell Res
September 2025
Tianjin Key Laboratory of Acute Abdomen Disease Associated Organ Injury and ITCWM Repair, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin, 300100, China; Institute of Integrative Medicine for Acute Abdominal Diseases, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin 300100,
The characteristic pathological change in chronic pancreatitis (CP) is pancreatic fibrosis. In the early stages of CP development, injured acinar cells induce the infiltration of inflammatory cells, followed by pancreatic stellate cell (PSC) activation. Activated PSC induce the deposition of extracellular matrix (ECM) and promote the development of pancreatic fibrosis.
View Article and Find Full Text PDFInt J Biol Macromol
September 2025
Key Laboratory of Hepatosplenic Surgery, Ministry of Education, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Pancreatology
August 2025
Department of Dermatology, The People's Hospital of Rongchang District, Chongqing, China. Electronic address:
Gastrointest Endosc
September 2025
Department of Gastroenterology, Postgraduate Institute of Medical Education and Research, Chandigarh, India. Electronic address: