In order to standardize the effective prevention, early screening and diagnosis of the population at risk of primary liver cancer, the Chinese Society of Hepatology and Chinese Medical Association organized the relevant domestic experts to formulate the "Consensus on Secondary Prevention of Primary Liver Cancer (2021 version)," based on the basic, clinical and preventive research progress, combined with the actual situation at home and abroad, so as to provide an important basis for the prevention, screening and early diagnosis of primary liver cancer in the population of chronic liver disease.
Carcinoma, Hepatocellular/prevention & control* ; Consensus ; Gastroenterology ; Humans ; Liver Cirrhosis ; Liver Neoplasms/prevention & control* ; Mass Screening ; Secondary Prevention

Acute Kidney Injury ; etiology ; prevention & control ; Ascites ; etiology ; prevention & control ; Humans ; Hyponatremia ; etiology ; prevention & control ; Liver Cirrhosis ; complications ; prevention & control

Acute-on-chronic liver failure (ACLF) is an increasingly recognized distinct disease entity encompassing an acute deterioration of liver function in patients with chronic liver disease. Although there are no widely accepted diagnostic criteria for ACLF, the Asia.Pacific Association for the Study of the Liver (APASL) and the American Association for the Study of Liver Disease and the European Association for the Study of the Liver (AASLD/EASL) consensus definitions are commonly used. It is obvious that the APASL and the AASLD/EASL definitions are based on fundamentally different features. Two different definitions in two different parts of the world hamper the comparability of studies. Recently, the EASL-Chronic Liver Failure Consortium proposed new diagnostic criteria for ACLF based on analyses of patients with organ failure. There are areas of uncertainty in defining ACLF, such as heterogeneity of ACLF, ambiguity in qualifying underlying liver disease, argument for infection or sepsis as a precipitating event, etc. Although the exact pathogenesis of ACLF remains to be elucidated, alteration of host response to injury, infection, and unregulated inflammation play important roles. The predisposition, infection/inflammation, response, organ failure (PIRO) concept used for sepsis might be useful in describing the pathophysiology and clinical categories for ACLF. Treatment strategies are limited to organ support but better understanding of the pathophysiology is likely to lead to discovery of novel biomarkers and therapeutic strategies in the future.
Chronic Disease ; Echocardiography ; Humans ; Liver Cirrhosis/complications ; Liver Failure/diagnosis/etiology/*pathology/prevention & control ; Liver Failure, Acute/diagnosis/etiology/*pathology/prevention & control ; Liver Transplantation ; Sepsis/complications

China ; Hepatitis B, Chronic ; complications ; Humans ; Liver Cirrhosis ; surgery ; virology ; Liver Neoplasms ; surgery ; Liver Transplantation ; trends ; Secondary Prevention ; Tissue Donors

Female ; Hepatitis B, Chronic ; prevention & control ; surgery ; therapy ; Humans ; Immunotherapy ; Liver Cirrhosis ; surgery ; Liver Transplantation ; Male ; Postoperative Complications ; prevention & control ; Preoperative Care ; methods ; Secondary Prevention

Esophageal variceal bleeding is a common complication of liver cirrhosis. Non-selective beta blockers (NSBB) have been established in numerous studies as one of the medical treatment for cirrhosis, especially in the primary and secondary prevention of variceal bleeding. The dose of NSBB is adjusted for a reduction in the resting heart rate by 25%, to 55 beat/min, or until the occurrence of adverse effect. The mean adjusted dose of propranolol in Korean study is 160 mg/day. Nevertheless, low dose propranolol is frequently used in real clinical field. A study by Kwon et al. showed that effect of propranolol in the prevention for esophageal rebleeding was superior in maximally-tolerable dose group of propranolol than low dose group. In this editorial, we have reviewed the studies of prevention for variceal rebleeding focusing on the dose of propranolol.
Esophageal and Gastric Varices ; Fibrosis ; Heart Rate ; Liver Cirrhosis ; Propranolol* ; Secondary Prevention

Globally, viral hepatitis due to hepatitis B virus (HBV) and/or hepatitis C virus (HCV) infection is the major cause of advanced liver diseases such as liver cirrhosis and hepatocellular carcinoma (HCC). Chronic inflammation resulting from persistent viral hepatitis is also associated with an increased risk of HCC recurrence. Replication of HBV and/or HCV can reactivate during anti-cancer treatments of HCC and lead to hepatic dysfunction, adversely affecting patient outcomes. The most effective way to prevent chronic viral hepatitis, cirrhosis, or HCC would be the implementation of a vaccine. Unfortunately, a vaccine for HCV is currently not available. For chronically infected patients, antiviral therapy may be the only option that can prevent or retard disease progression. Emerging evidence continues to support direct or indirect benefits from antiviral therapy for preventing liver disease progression to cirrhosis, HCC development, and recurrence after curative treatments in patients with chronic HBV or HCV infection. This paper reviews the literature on the management of viral hepatitis in patients with HCC, focusing on primary and tertiary prevention of HCC.
Carcinoma, Hepatocellular* ; Disease Progression ; Fibrosis ; Hepacivirus ; Hepatitis B virus ; Hepatitis* ; Humans ; Inflammation ; Liver Cirrhosis ; Liver Diseases ; Recurrence ; Tertiary Prevention

Chronic hepatitis C infection is an important cause of cirrhosis and hepatocellular carcinoma (HCC). Antiviral therapy (AVT) for patients with cirrhosis due to hepatitis C may retard the progression of cirrhosis and prevent both the development of HCC as well as the recurrence of hepatitis C following liver transplantation. This review highlights the issues associated with AVT for patients with compensated and decompensated cirrhosis due to hepatitis C virus.
Antiviral Agents ; therapeutic use ; Carcinoma, Hepatocellular ; prevention & control ; virology ; Disease Progression ; Hepacivirus ; Hepatitis C, Chronic ; complications ; drug therapy ; Humans ; Liver Cirrhosis ; drug therapy ; virology ; Liver Neoplasms ; prevention & control ; virology ; Liver Transplantation ; Secondary Prevention

Mesothelial cells (MCs) cover the surface of visceral organs and the parietal walls of cavities, and they synthesize lubricating fluids to create a slippery surface that facilitates movement between organs without friction. Recent studies have indicated that MCs play active roles in liver development, fibrosis, and regeneration. During liver development, the mesoderm produces MCs that form a single epithelial layer of the mesothelium. MCs exhibit an intermediate phenotype between epithelial cells and mesenchymal cells. Lineage tracing studies have indicated that during liver development, MCs act as mesenchymal progenitor cells that produce hepatic stellate cells, fibroblasts around blood vessels, and smooth muscle cells. Upon liver injury, MCs migrate inward from the liver surface and produce hepatic stellate cells or myofibroblast depending on the etiology, suggesting that MCs are the source of myofibroblasts in capsular fibrosis. Similar to the activation of hepatic stellate cells, transforming growth factor β induces the conversion of MCs into myofibroblasts. Further elucidation of the biological and molecular changes involved in MC activation and fibrogenesis will contribute to the development of novel approaches for the prevention and therapy of liver fibrosis.
Epithelial Cells/*physiology ; Epithelium/metabolism ; Hepatic Stellate Cells/*physiology ; Humans ; Liver/*cytology/injuries/*physiology ; Liver Cirrhosis/etiology/prevention & control ; Liver Regeneration/*physiology ; Mesenchymal Stromal Cells/physiology ; Myofibroblasts/physiology

Animals ; Liver Cirrhosis ; metabolism ; prevention & control ; Male ; Rats ; Rats, Inbred Strains ; Thiazolidinediones ; therapeutic use ; Tissue Inhibitor of Metalloproteinase-1 ; metabolism