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Improvement in hepatitis C virus patients with advanced, compensated liver disease after sustained virological response to direct acting antivirals
Author(s) -
Giannini Edoardo G.,
Crespi Mattia,
Demarzo Mariagiulia,
Bodini Giorgia,
Furnari Manuele,
Marabotto Elisa,
Torre Francesco,
Zentilin Patrizia,
Savarino Vincenzo
Publication year - 2019
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/eci.13056
Subject(s) - medicine , transient elastography , cirrhosis , gastroenterology , liver disease , hepatitis c virus , hepatitis c , chronic liver disease , portal hypertension , spleen , virus , liver fibrosis , immunology
Background The outcome of patients with chronic hepatitis C virus infection (HCV) and advanced, compensated liver disease after sustained virological response (SVR) to direct‐acting antivirals (DAAs) has not yet been completely depicted. We aimed to assess the clinical, biochemical and instrumental outcome of patients with advanced, compensated chronic HCV‐related liver disease with DAA‐induced SVR to DAAs and who had at least 1‐year follow‐up. Materials and methods Fifty‐two patients with cirrhosis (n = 27) and fibrosis stage F3 (n = 25) followed up for a median of 60 weeks after successful DAA treatment were included. Laboratory work‐up, including APRI and FIB‐4 scores, liver transient elastography and measurement of the spleen bi‐polar diameter were carried out before treatment and at the end of follow‐up. Results Liver stiffness decreased ( P < 0.0001) from a median baseline of 15.2 kPa (12.0‐20.0) to 9.3 kPa (7.5‐12.0) at follow‐up. A liver stiffness value suggestive of the presence (ie, ≥21.0 kPa) of clinically significant portal hypertension was found in 13 patients (25.0%) at baseline and in seven patients (13.5%) at follow‐up ( P = 0.037). Both APRI ( P < 0.0001) and FIB‐4 score ( P = 0.025) progressively decreased, while platelet count increased (143 × 10 9 /L [117‐176] to 153 × 10 9 /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 end of follow‐up. Conclusions In patients advanced, compensated chronic liver disease, liver stiffness significantly improves in the long‐term after SVR, and this improvement is accompanied by an amelioration of indirect indices of liver fibrosis and function, and by a decrease in parameters of portal hypertension.