Chronic hepatitis B patients with high liver fibrosis levels should receive antiviral treatment

Abstract

Abstract. The present study aimed to evaluate improvements in liver stiffness (LS) measured by transient elastography (TE) and associated factors in Chinese patients with chronic hepatitis B (CHB) treated with entecavir (ETV). A total of 190 consecutive CHB patients who received entecavir therapy and two LS measurements (LSMs) were enrolled in this retrospective study (average age, 47 years; 137 males [72.1%]), including 111 patients without liver cirrhosis (group 0) and 79 patients with liver cirrhosis (group 1). Each patient received LSM twice with an interval of six months. Normalized aspartate aminotransferase (AST) levels were accompanied by a significant reduction in LSM values (P<0.001) in each group. Multivariate analysis revealed that a higher initial LS value in groups 0 and 1, and a higher prothrombin time activity in group 1 was associated with a greater decline of the LS value. Higher initial quantitative hepatitis B surface antigen (qHBsAg) levels were correlated with a greater decline of the qHBsAg value in the two groups. In conclusion, LS values in CHB patients significantly improved after 24 weeks of entecavir therapy. The results suggested that higher LSM values at baseline contributed to a greater regression of LSM, and higher initial qHBsAg values could lead to greater qHBsAg reduction during ETV therapy. Extrapolating our results, we might be able to consider CHB patients who have higher initial LSM values or have higher levels of qHBsAg values when enrolled would have more benefit during ETV treatment.

RNA methylations in hepatic fibrosis, a gradually emerging new treatment strategy

“…Any factor that can lead to chronic damage of liver tissue can induce the development of HF. For example, inborn metabolic defects, alcohol abuse, viral infections, parasitic infections, and autoimmune liver disease [ 8 – 12 ]. In addition, an elevated body mass index further increases the risk of HF due to non-alcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) [ 13 – 15 ].…”

Pathophysiology and Treatment Options for Hepatic Fibrosis: Can It Be Completely Cured?

“…The pathogenesis of hepatic fibrosis is multifaceted and accompanies progressive liver injury that varies from mild to severe. It arises as a consequence of diverse biologic processes induced by alcoholic liver disease (ALD), non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), autoimmune hepatitis (AIH), drug-induced liver injury (DILI) and viral hepatitis (hepatitis B and hepatitis C) [ 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 ]. Increasing rates of obesity have further accelerated the risk of liver fibrosis due to liver injury caused by NAFLD and NASH [ 17 , 18 ].…”