In an effort to develop a reproducible model of liver cirrhosis and esophageal varices, we administered phenobarbital (PhB) and carbon tetrachloride (CCl4) in 32 rats that had previously undergone complete devascularization of the left renal vein (DLRV). The operation was conducted to enhance the development of cephalad collaterals mainly responsible for the induction of esophageal varices. Thirty-two rats underwent sham operation and PhB and CCl4 administration, and 24 only sham-operated rats comprised the control group. After the induction of liver cirrhosis, histopathologic examination and morphometric analysis of the lower esophagus were performed to study the submucosal veins. We separately studied number of vessels in the submucosa, mean vessel area, percentage of submucosa occupied by vessels, and area of the single most dilated vein. All variables except the number of vessels were significantly higher in cirrhotic rats that had undergone DLRV (P<0.001). We conclude that induction of liver cirrhosis in rats that previously undergo complete DLRV could present a reproducible and reliable model for the induction of liver cirrhosis and esophageal varices.
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BMC Gastroenterol
January 2025
Department of Gastroenterology, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a primary cause of chronic liver disease, with potential progression to cirrhosis and hepatocellular carcinoma (HCC). Although systemic inflammatory biomarkers are associated with liver diseases, their specific role in MASLD remains unclear. This study examines the association between systemic inflammatory biomarkers and MASLD.
View Article and Find Full Text PDFBackground And Aim: There is paucity of data about the prevalence of cirrhosis and portal hypertension in the US general population.
Methods: We used National Health and Nutrition Examination Surveys (NHANES 2017-2020) to estimate the prevalence of cirrhosis and clinically significant (CS)-portal hypertension in alcoholic liver disease (ALD), MetALD, viral hepatitis (VH) to include chronic hepatitis B (CHB) and chronic hepatitis C (CHC), and metabolic dysfunction-associated steatotic liver disease (MASLD). Cirrhosis was evaluated using liver stiffness measurement (LSM) by transient elastography or FIB-4 score; CS-portal hypertension was defined via LSM and platelet count or the use of non-selective beta-blockers in the presence of cirrhosis.
Hepatology
January 2025
Center for Individualized Medicine, Mayo Clinic, Rochester, MN, USA.
Background Aims: Metabolic dysfunction-associated steatotic liver disease (MASLD) affects about a third of adults worldwide and is projected soon to be the leading cause of cirrhosis. It occurs when fat accumulates in hepatocytes and can progress to metabolic dysfunction-associated steatohepatitis (MASH), liver cirrhosis, and hepatocellular carcinoma. MASLD pathogenesis is believed to involve a combination of genetic and environmental risk factors.
View Article and Find Full Text PDFHepatology
January 2025
AP-HP, Sorbonne Université, Liver Intensive Care Unit, Hepatogastroenterology Department, La Pitié-Salpêtrière Hospital, 47-83 Boulevard de l'Hôpital, Paris 75013, France.
Background And Aims: In cirrhosis, some patients display acute encephalopathy without hyperammonemia (NonHep E) which is not considered as overt hepatic encephalopathy (OHE). We aimed to assess the prevalence and characteristics of NonHep E and OHE in cirrhotic patients displaying acute encephalopathy, assess their respective prognosis and compare it to other causes of acute decompensation (AD) with/without hyperammonemia.
Approach And Results: We conducted a retrolective analysis from a prospective cohort of patients hospitalized for AD.
Hepatol Commun
February 2025
Department of Anesthesiology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Background: Cell therapy demonstrates promising potential as a substitute therapeutic approach for liver cirrhosis. We have developed a strategy to effectively expand murine and human hepatocyte-derived liver progenitor-like cells (HepLPCs) in vitro. The primary objective of the present study was to apply HepLPCs to the treatment of liver cirrhosis and to elucidate the underlying mechanisms responsible for their therapeutic efficacy.
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