Giuseppina Pisano (Italy)
Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico di Milano; University of Milan Unit of Internal Medicine and Metabolic Diseases, Department of Pathophysiology and TransplantationAuthor of 2 Presentations
COAGULATION BALANCE AND LIVER FIBROSIS IN NON-CIRRHOTIC PATIENTS WITH CHRONIC HEPATITIS C AFTER ERADICATION BY DIRECT-ACTING ANTIVIRAL AGENTS (DAAS).
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.
NEW ONSET STEATOSIS BUT NOT PERSISTENT STEATOSIS PREVENTS HEPATIC FIBROSIS IMPROVEMENT AFTER VIRAL ERADICATION IN PATIENTS WITH CHRONIC HEPATITIS C: EVALUATION BY FIBROSCAN
Abstract
Background and Aims
Background: In patients with chronic hepatitis C (CHC), presence of steatosis before and after sustained virological response (SVR) has been demonstrated and linked to metabolic alterations. Aim: to define the impact of post SVR steatosis on fibrosis improvement evaluated by Fibroscan in CHC patients after viral eradication.
Methods
Methods: 794 patients with CHC achieving SVR were enrolled in 2 Italian Liver Units. Data were collected the day of DAAs starting and six months after SVR. Fibroscan diagnosed steatosis (by controlled attenuation parameter (CAP) ≥ 248 dB/m) and fibrosis (by liver stiffness measurement LSM).
Results
Results: Mean age was 64±16 ys, 50% males, genotype 3 in 7%. Patients with baseline steatosis (365, 46%) presented significantly higher baseline LSM values compared to their counterpart (10.6±7.8 vs 9.4±7.4 kPa; p=0.04). After SVR, steatosis (CAP ≥ 248 dB/m) developed in 125 out of 429 (29%) without steatosis at enrollment, whereas persisted in 243 (66%) of patients with baseline steatosis. LSM significantly reduced after SVR (10±7.6 vs 8.2±7.2 kPa, p<0.001), even in presence of hepatic steatosis post SVR (10.3±7.3 vs 8.2±6.6 kPa; p<0.001). However, when the analysis was differentiated between patients with persistence and new onset steatosis, a significantly reduction of LSM in patients with persistence (10.8±7.8 vs 8.0±5.7 kPa, p<0.001) but not in those with new onset steatosis (9.4±6.4 vs 8.7±8.0 kPa, p=0.12) was confirmed.
Conclusions
Conclusion: New onset steatosis but not persistence of baseline steatosis prevents fibrosis improvement after SVR, possibly suggesting the presence of two different type of post SVR steatosis.