Abstract

According to the fact sheet released by World Health Organization (WHO), an estimated 240 million people worldwide are chronically infected with the hepatitis B virus (HBV). HBV-related diseases, such as liver failure, liver cirrhosis, and hepatic cell carcinoma (HCC), result in approximately 600 thousand deaths per year [1]. An estimated 150 million people are infected with the hepatitis C virus (HCV), and 350 thousand mortalities per year are HCV related [2]. As one of the most widespread epidemic diseases in China, the positivity rate for the HBV surface antigen is 7.18 % [3]. In addition, epidemiological surveys revealed that in 2006, there were more than 93 million people infected with chronic HBV, of whom approximately 20 million are chronic HBV patients. Common diseases associated with HBV infection include acute and chronic HBV hepatitis, HBV-related liver cirrhosis, and HBV-related HCC. The incidence of HCC in China is approximately 350 thousand per year, accounting for 55 % of global incidences. HCC also ranks the second in cancer-related mortality, compromising the well-being of individuals and causing an enormous financial burden on the family, society, and the country. In China, 95 % of HCC originates from a background of HBV infection, and liver fibrosis plays a major role in the progression from HBV infection to liver cirrhosis and ultimately possible to HCC. Liver fibrosis is not a single disease entity but a common pathological process in almost every type of chronic liver disease. It is characterized by increased synthesis of extracellular matrix proteins, primarily via interstitial cells especially activated hepatic stellate cells, with subsequent excess deposition of fibrous connective tissue in the liver [4]. This increased synthesis and excess deposition result in structural disturbances of the hepatic lobules and the formation of pseudolobules, an effect that gradually advances to cirrhosis and liver dysfunction. The main causes of liver fibrosis are infection with hepatotropic viruses (HBV and HCV), alcohol abuse, and nonalcoholic fatty liver disease. The progression of liver fibrosis is relatively slow, usually taking a decade or even several decades for the initial fibrosis in the portal triads to form fibrous septa, which damage the hepatic lobules and to ultimately progress to cirrhosis. Excluding cirrhosis, liver fibrosis is considered to be reversible under certain circumstances; therefore, early diagnosis and dynamic surveillance of liver fibrosis is crucial. With observation, it is possible to determine the proper starting time for treatment, to evaluate drug efficacy, to stage the disease, and to evaluate its prognosis. Thereby, the accurate staging of liver fibrosis is of great importance.

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