Improvement in hepatitis C virus patients with advanced, compensated liver disease after sustained virological response to direct acting antivirals

Background:The outcome of patients with chronic hepatitis C virus infection(HCV) and advanced, compensated liver disease after sustained virologicalresponse (SVR) to direct‐acting antivirals (DAAs) has not yet been completelydepicted. We aimed to assess the clinical, biochemical and instrumental outcomeof patients with advanced, compensated chronic HCV‐related liver disease withDAA‐induced SVR to DAAs and who had at least 1‐year follow‐up.Materials and methods:Fifty‐two patients with cirrhosis (n = 27) and fibrosisstage F3 (n = 25) followed up for a median of 60 weeks after successful DAAtreatment were included. Laboratory work‐up, including APRI and FIB‐4 scores,liver transient elastography and measurement of the spleen bi‐polar diameter werecarried out before treatment and at the end of follow‐up.Results:Liver stiffness decreased (P< 0.0001) from a median baseline of15.2 kPa (12.0‐20.0) to 9.3 kPa (7.5‐12.0) at follow‐up. A liver stiffness valuesuggestive of the presence (ie,≥21.0 kPa) of clinically significant portal hyperten-sion was found in 13 patients (25.0%) at baseline and in seven patients (13.5%) atfollow‐up (P= 0.037). Both APRI (P< 0.0001) and FIB‐4 score (P= 0.025)progressively decreased, while platelet count increased (143 × 109/L [117‐176] to153 × 109/L [139‐186],P= 0.003), and spleen bi‐polar diameter decreased(120 mm [112‐123] to 110 mm [102‐116],P= 0.0009) from baseline to the endof follow‐up.Conclusions:In patients advanced, compensated chronic liver disease, liver stiff-ness significantly improves in the long‐term after SVR, and this improvement isaccompanied by an amelioration of indirect indices of liver fibrosis and function,and by a decrease in parameters of portal hypertension.