Backgrounds/aims: To analyze relationships of hepatic histopathological findings and bile microbiological profiles with perioperative outcomes and risk of late biliary stricture in individuals undergoing surgical bile duct injury (BDI) repair.
Methods: A historical cohort study was carried out at a tertiary university hospital. Fifty-six individuals who underwent surgical BDI repair from 2014-2018 with a minimal follow-up of 24 months were enrolled. Liver biopsies were performed to analyze histopathology. Bile samples were collected during repair procedures. Hepatic histopathological findings and bile microbiological profiles were then correlated with perioperative and late outcomes through uni- and multi-variate analyses.
Results: Forty-three individuals (76.8%) were females and average age was 47.2 ± 13.2 years; mean follow-up was 38.1 ± 18.6 months. The commonest histopathological finding was hepatic fibrosis (87.5%). Bile cultures were positive in 53.5%. The main surgical technique was Roux-en-Y hepaticojejunostomy (96.4%). Overall morbidity was 35.7%. In univariate analysis, liver fibrosis correlated with the duration of the operation (R = 0.3; = 0.02). In multivariate analysis, fibrosis (R = 0.36; = 0.02) and cholestasis (R = 0.34; = 0.02) independently correlated with operative time. Strasberg classification independently correlated with estimated bleeding (R = 0.31; = 0.049). The time elapsed between primary cholecystectomy and BDI repair correlated with hepatic fibrosis (R = 0.4; = 0.01).
Conclusions: Bacterial contamination of bile was observed in most cases. The degree of fibrosis and cholestasis correlated with operative time. The waiting time for definitive repair correlated with the severity of liver fibrosis.
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http://dx.doi.org/10.14701/ahbps.22-003 | DOI Listing |
BMC Pharmacol Toxicol
January 2025
Biochemistry Department, Faculty of Science, Ain-Shams University, Cairo, Egypt.
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View Article and Find Full Text PDFPhytomedicine
January 2025
Department of Gastroenterology, the First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China. Electronic address:
Background: Celastrol was recently identified as a potential treatment for obesity and hepatic steatosis. However, whether Celastrol effectively suppresses the nonalcoholic fatty liver disease (NAFLD) stage remains unknown. This study aimed to evaluate the role of Celastrol in the progression from simple steatosis to nonalcoholic steatohepatitis (NASH) and fibrosis.
View Article and Find Full Text PDFInt Endod J
January 2025
Department of Integrated Clinical Procedures, School of Dentistry, Rio de Janeiro State University (UERJ), Rio de Janeiro, Brazil.
Aim: This study aimed to explore the possible bidirectional interrelations between fructose-induced metabolic syndrome (MS) and apical periodontitis (AP).
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Lipids Health Dis
January 2025
The State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou, 510060, China.
Clinical studies have suggested that tirzepatide may also possess hepatoprotective effects; however, the molecular mechanisms underlying this association remain unclear. In our study, we performed biochemical analyses of serum and histopathological examinations of liver tissue in mice. To preliminarily explore the molecular mechanisms of tirzepatide on metabolic dysfunction-associated fatty liver disease (MAFLD), liquid chromatography-mass spectrometry (LC-MS) was employed for comprehensive metabolomic, lipidomic, and proteomic analyses in MAFLD mice fed a high-fat diet (HFD).
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
School of Life Science, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, 310053, PR China. Electronic address:
Background: Non-alcoholic steatohepatitis (NASH), an advanced manifestation of non-alcoholic fatty liver disease (NAFLD), is characterized by hepatocyte injury, inflammation, and fibrosis. Saturated fatty acids (SFAs) have emerged as key contributors to hepatocyte lipotoxicity and disease progression. Toll-like receptor 4 (TLR4) acts as a sentinel for diverse ligands, including lipopolysaccharide (LPS) and endogenous molecules like palmitic acid (PA)-induced ceramide (CER) accumulation, promoting hepatocyte demise.
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