Impact of Sustained Virological Response on Liver Function and Fibrosis Regression in Chronic Hepatitis C: A FibroScan Based Assessment

Abstract

Background: Chronic hepatitis C virus (HCV) infection is a major cause of liver fibrosis, cirrhosis, and hepatocellular carcinoma. Antiviral therapy can achieve sustained virological response (SVR) and may contribute to fibrosis regression. This study evaluated biochemical, virological, and structural liver outcomes following antiviral treatment and identified factors associated with fibrosis improvement.
Methods: A cohort study was conducted at the Department of Gastroenterology, Services Institute of Medical Sciences, Lahore, from October 2025 to April 2025 including 104 adults with chronic HCV infection. Baseline assessments included FibroScan liver stiffness measurement, liver function tests (ALT and AST), and quantitative HCV viral load. Patients received antiviral therapy according to national guidelines and were followed until 12 weeks after treatment completion (SVR12). Outcomes included changes in liver fibrosis, biochemical parameters, and viral load. Independent-samples t-tests and Chi-square tests were used for comparisons.
Results: The mean age was 44.4 ± 15.5 years; 62.5% were male and 71.2% had no comorbidities. Baseline FibroScan, ALT, and AST values were 12.6 ± 5.3 kPa, 73.1 ± 26.6 U/L, and 71.0 ± 24.0 U/L, respectively. At SVR12, significant reductions were observed in liver stiffness (10.3 ± 5.2 kPa), ALT (38.2 ± 24.4 U/L), AST (38.8 ± 23.5 U/L), and viral load. Non-responders had significantly higher viral loads (p < 0.001). Adverse events were significantly associated with poorer fibrosis improvement (p = 0.005).
Conclusion: Antiviral therapy effectively improves virological, biochemical, and fibrosis-related outcomes in chronic HCV patients. Early treatment and careful monitoring of adverse events may optimize fibrosis regression and overall clinical outcomes.