Abstract
Purpose: Chronic hepatitis B virus infection affects more than 3 million people worldwide. The present study aimed to evaluate the role of pretreatment factor IV collagen as predictor of post treatment virological response with hepatic fibrosis regression. Materials and Methods: This prospective cohort study has been conducted on 74 naieve patients with chronic HBV infection with variable degree of hepatic fibrosis (F2, F3, ≥F4), viral load, and variable degree of abnormality in laboratory parameters of liver functions. All patients treated with Entecavir 0.5 mg/day or 1 mg/day according to severity of hepatic condition for 1 year. Liver fibrosis assessed using fibroscan, factor IV collagen, (APRI) and (FIB-4) scores evaluation. Results: All included patients in our study achieve post treatment Virological response with undetectable HBV DNA PCR (<16 IU/ml). With significant post treatment reduction in mean fibroscan value 10.70 ± 5.80 (p < 0.001). There were also significant end treatment improvements in mean FIB score and APRI score 1.56 ± 1.02 (p < 0.0001) and 0.50 ± 0.28 (p < 0.0001) respectively. There is significant end treatment improvement of mean factor IV collagen. In our study 49 (66.22%) of included patients showed post treatment reduction in their level of hepatic fibrosis (Responder) opposite to 25 (33.78%) had no post treatment improvement in degree of hepatic fibrosis (Non-responder). Conclusion: Low pretreatment factor IV collagen is significantly correlated with virologial response and hepatic fibrosis regression post Entecavir therapy in patients with chronic HBV infection.
Highlights
The laboratory measures among chronic Hepatitis B virus (HBV) infected patients including factor IV collagen, mean platelet count, and liver function tests together with mean FIB score and aminotransferase-to-platelet ratio index (APRI) score before and one year of regular therapy are presented in Table 2, with significant improvement of them except International normalization ratio (INR) which show non-significant post treatment improvement (p < 0.111)
Progression of hepatic fibrosis is associated with increased risk of liver decompensation, and development of hepatocellular carcinoma (HCC) [16]
We have significant post treatment improvement in the level of hepatic fibrosis in 66.22% of our patients which assessed by evaluated by the decrease parameters of hepaticfibroscan
Summary
Hepatitis B virus (HBV) infection is one of the major public health problems in Egypt; its prevalence was (1.4%) with higher prevalence in urban than rural area [1].All patients with untreated chronic hepatitis B virus infection have a high risk of development of cirrhosis and hepatocellular carcinoma [2].The aim of treatment is decreasing HBV DNA levels, decreasing hepatic inflammation and improving laboratory parameters of disease activity [3].Entecavir is a potent oral guanosine nucleoside analogue for treatment of HBeAg-positive or negative chronic HBV infection; it’s safe and effective in treatment of naive and lamivudine resistant patients [4].Chronic liver injury causes necrosis and apoptosis of parenchymal cells and replacement by extracellular matrix, with disease progression the liver parenchyma replaced by scar tissues with abnormal vascular architecture and organ dysfunction [5].Coagulation cascade is one of main factors in development of hepatic fibrosis, in which Thrombin is cause change of fibrinogen to fibrin which appear in the hepatic tissue during acute and chronic liver injury [6]. All patients with untreated chronic hepatitis B virus infection have a high risk of development of cirrhosis and hepatocellular carcinoma [2]. Entecavir is a potent oral guanosine nucleoside analogue for treatment of HBeAg-positive or negative chronic HBV infection; it’s safe and effective in treatment of naive and lamivudine resistant patients [4]. Chronic liver injury causes necrosis and apoptosis of parenchymal cells and replacement by extracellular matrix, with disease progression the liver parenchyma replaced by scar tissues with abnormal vascular architecture and organ dysfunction [5]. Coagulation cascade is one of main factors in development of hepatic fibrosis, in which Thrombin is cause change of fibrinogen to fibrin which appear in the hepatic tissue during acute and chronic liver injury [6]
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