Abstract
BackgroundDirect-acting antivirals (DAAs) have revolutionized the therapy of HCV infection with higher sustained virological response (SVR) rates. Fibrosis regression after achieving SVR to DAA remains to be evaluated in chronic hepatitis C patients. One of the main inquiries here is what occurs with liver fibrosis after achieving a SVR, albeit the current DAA was not intended to be antifibrotic. Liver biopsy was replaced by various non-invasive methods, like FIB4 score and fibroscan. The aim of the study was to evaluate the impact of SVR following DAAs on liver fibrosis in chronic HCV patients.ResultsFive hundred of 1170 F4 treated patients (42.7%) improved and became 190 F3, 90 F2, and 220 F1. Also, 40 of 60 F3 patients improved and became 10 F2 and 30 F1. Also, 350 of 1230 treated patients (28.4%) transited from significant fibrosis (≥F3) to non-significant fibrosis (≤F2). There was a significant improvement of FIB-4 (p<0.001) in the improved group after DAAs were proved by liver stiffness measurement.ConclusionTreatment of chronic HCV with DAAs is associated with regression of liver fibrosis as about 28% of patients improved from significant fibrosis (≥F3) to non-significant fibrosis (≤F2) after treatment.
Highlights
Direct-acting antivirals (DAAs) have revolutionized the therapy of Hepatitis C virus (HCV) infection with higher sustained virological response (SVR) rates
In the last few years, antiviral therapy for HCV has been rapidly evolving with the introduction and proliferation of direct-acting antiviral (DAA) therapies
The aim of the current study was to assess the impact of SVR following DAAs on liver fibrosis in chronic HCV patients
Summary
Direct-acting antivirals (DAAs) have revolutionized the therapy of HCV infection with higher sustained virological response (SVR) rates. Fibrosis regression after achieving SVR to DAA remains to be evaluated in chronic hepatitis C patients. The aim of the study was to evaluate the impact of SVR following DAAs on liver fibrosis in chronic HCV patients. In the last few years, antiviral therapy for HCV has been rapidly evolving with the introduction and proliferation of direct-acting antiviral (DAA) therapies They revolutionized the therapy of HCV infection with higher efficacy and sustained virological response (SVR) rates, shortened and simplified regimens, and minimal adverse effects [3]. Previous studies on the impact of interferon-based HCV therapy on hepatic fibrosis have shown regression of fibrosis over periods of up to 48 months in some patients after therapy [4,5,6]
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