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Regression of liver fibrosis after curing chronic hepatitis C with oral antivirals in patients with and without HIV coinfection

Lledó, Gema M.a; Carrasco, Itziarb; Benítez-Gutiérrez, Laura M.a; Arias, Anaa; Royuela, Anac; Requena, Silviab; Cuervas-Mons, Valentína; de Mendoza, Carmenb

doi: 10.1097/QAD.0000000000001966
CLINICAL SCIENCE
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Background: Treatment with direct-acting antivirals (DAA) eradicates hepatitis C virus (HCV) from most chronic carriers. Information on regression of liver fibrosis and the influence of HIV is scarce in cured patients.

Methods: All consecutive HCV-infected individuals treated with DAA at our institution were examined. Hepatic elastography was performed at baseline and at the time of SVR12. Liver fibrosis regression was defined as a shift from advanced fibrosis (Metavir F3-F4) to null–mild fibrosis (F0–F2) and/or a reduction greater than 30% kPa. AST to platelet ratio index (APRI) and fibrosis 4 (FIB-4) scores were calculated in parallel.

Results: A total of 260 patients were treated with DAA. All but 14 achieved SVR12 and represented the study population. HIV confection was present in 42%. At baseline, 57.2% had advanced liver fibrosis with a median of 11 kPa, FIB-4 of 2.4, and APRI of 0.95. At the time of SVR12, a median reduction of 2.1 kPa (P < 0.001) was recognized using elastography. A significant fibrosis regression was seen in 40%, being more frequent in patients with baseline advanced fibrosis than in those with null–mild fibrosis (52.3 vs. 22.5%; P < 0.001). Even so, 41.2% of patients with baseline F3–F4 kept within cirrhotic scores. In multivariable analysis, only baseline stiffness was significantly associated with the extent of liver fibrosis regression.

Conclusion: HCV cure with DAA is associated with regression of liver fibrosis in most patients treated with DAA, as measured using elastography, FIB-4 and APRI. This benefit is more pronounced in patients with baseline advanced fibrosis and cirrhosis. The dynamics of liver fibrosis regression are not influenced by HIV coinfection.

aInternal Medicine Department, Hospital Universitario Puerta de Hierro

bInternal Medicine Laboratory, Research Institute Puerta de Hierro-Segovia de Arana

cBiostatistic Unit. Research Institute Puerta de Hierro-Segovia de Arana. Majadahonda, Madrid, Spain.

Correspondence to Carmen de Mendoza, Department of Internal Medicine, Internal Medicine Laboratory, Research Institute Puerta de Hierro-Segovia de Arana, Calle Joaquín Rodrigo 2, 28222, Majadahonda, Spain. Tel: +34 91 1916764; e-mail: cmendoza.cdm@gmail.com.

Received 28 February, 2018

Accepted 8 June, 2018

Copyright © 2018 Wolters Kluwer Health, Inc.