Armando Tripodi (Italy)

IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Milan, Italy Angelo Bianchi Bonomi Hemophilia and Thrombosis Center and Fondazione Luigi Villa

Author of 1 Presentation

COAGULATION BALANCE AND LIVER FIBROSIS IN NON-CIRRHOTIC PATIENTS WITH CHRONIC HEPATITIS C AFTER ERADICATION BY DIRECT-ACTING ANTIVIRAL AGENTS (DAAS).

Date
Fri, 19.03.2021
Session Time
10:00 - 11:00
Room
Hall B
Lecture Time
10:28 - 10:35

Abstract

Background and Aims

Chronic HCV infection causes liver and cardiovascular damage. A procoagulant imbalance has been reported in patients with chronic hepatitis C (CHC) and has been found to be associated with the severity of liver fibrosis. Aim: to evaluate whether the eradication of HCV by Direct-acting antiviral agents (DAAs) leads to a modification of procoagulant imbalance and whether this is related to a reduction of liver damage.

Methods

From 2017 to 2019, 70 patients with CHC (mean age 58.9 + 10.5 years) without cirrhosis were enrolled. Anthropometric, clinical and biochemical parameters, cardiovascular damage by intima-media thickness, (IMT) and E/A ratio, liver fibrosis by Liver stiffness measurement (LSM) and coagulation parameters through the evaluation of endogenous thrombin potential (ETP) with/without thrombomodulin, and antithrombin and protein C (PC) – factor VIII ratio, were determined at enrollment and at 6 and 12 months after sustained viral response (SVR.

Results

At enrolment indexes of procoagulant imbalance were significantly higher in patients with CHC than in controls of general population (FVIII/PC ratio 1.7+0.7 vs 1.1+0.3; ETP ratio 0.8+0.1 vs 0.6+0.2, p<0.0001). Compared to baseline, coagulation (FVIII/PC 1.8±0.8 vs 1.3±0.5, p<0.0001) and liver fibrosis (LMS 6.4±4.8 vs 5.2±1.7 kPa,p=0.03) parameters significantly improved at 6 months after SVR, while these parameters remained stable at 12 months. No modification of IMT and E/A ratio was observed after SVR.

Conclusions

After HCV eradication by DAAs, both procoagulant imbalance and liver fibrosis improve, strengthening the direct link between coagulation alteration and HCV virus, while changes in carotid atherosclerosis may require longer follow-up to be highlighted.

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