Histidine-rich glycoprotein (HRG) reduces by complex formation with plasminogen the amount of "free" plasminogen in circulation and is therefore considered an inhibitor of fibrinolysis. We studied the levels of both HRG and plasminogen in patients with different degrees of liver cirrhosis to assess the role of HRG in enhanced fibrinolysis in these patients. In mild (Child A) cirrhosis, HRG levels unexpectedly were significantly increased. The total plasminogen level and the calculated amount of free plasminogen were decreased. In moderate (Child B) cirrhosis, both HRG levels and total plasminogen levels were reduced, resulting in a normal amount of free plasminogen in circulation. In severe (Child C) cirrhosis, HRG level, total plasminogen level, and free plasminogen level were all decreased. Because the HRG level is increased in Child A liver cirrhosis, we suggest that other mechanisms, other than simply a decreased synthetic capacity of the liver, contribute to the changes in HRG levels in patients with liver disease. Because of the reduction of free plasminogen levels in severe liver cirrhosis, we propose that the decrease in HRG levels in liver cirrhosis plays no role in enhanced fibrinolysis in these patients. The increase in the HRG level in Child A liver cirrhosis may be of importance in future studies on familial thrombosis associated with elevated levels of HRG, where mild liver dysfunction should at least be excluded.
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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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