Hepatic benefits of HCV cure

Abstract

Direct-acting antiviral (DAA)-induced HCV clearance conceivably leads to improved outcomes at all stages of liver disease. However, available data suggest that the maximum measurable benefit is obtained by treating patients before they reach the stage of compensated advanced chronic liver disease (cACLD). Ideally, all patients with chronic hepatitis C should be treated before they develop advanced fibrosis or cirrhosis, since even if sustained virologic response (SVR) reduces the risk of hepatic events (e.g. decompensation and hepatocellular carcinoma [HCC]) and improves survival, further progression of liver disease and adverse outcomes, including hepatic deaths, cannot be entirely avoided. The hepatic venous pressure gradient (HVPG) correlates closely with the stage of liver disease. Measurements of HVPG in patients with severe fibrosis or cirrhosis treated with DAAs show that those with the highest degree of portal hypertension have the lowest probability of a meaningful reduction of portal pressure after SVR, and remain at significant risk of decompensation. Reduced liver stiffness is commonly observed in patients with cACLD but its role in predicting prognosis is yet to be demonstrated. In patients with decompensated cirrhosis, prevention of further decompensation and of HCC is only weakly associated with SVR. Overall, the main clinical predictors of a high risk of HCC in patients who obtain SVR on DAAs are all indexes strongly reflecting advanced fibrosis and impaired hepatic function. Long-term follow-up of large real-life cohorts of patients treated at all stages of liver disease, but mainly those with mild to moderate fibrosis, will be needed to confirm the impact of SVR among diverse HCV-infected populations and, more importantly, to better stratify patients at higher risk of complications in order to define their correct surveillance.

Telemedicine Chronic Viral Hepatitis C Treatment during the Lockdown Period in Romania: A Pilot Study

“…The death toll due to viral hepatitis is still high, owing to its evolution to cirrhosis and its complications. Thus, proper screening methods and direct access to the new direct antiviral agents (DAA) are being developed to cover all the shortcomings of the HCV infection [2].…”

Liver function following hepatitis C virus eradication by direct acting antivirals in patients with liver cirrhosis: data from the PITER cohort

“…Available data suggest that the maximum efficacy and benefits are obtained by treating patients before they reach the stage of advanced fibrosis or cirrhosis [2,3]. Sustained virologic response (SVR) reduces the risk of liver decompensation and of hepatocellular carcinoma (HCC) and improves survival [1,4,5]. However, a "point of non-return" in terms of deterioration of liver function, has been observed in part of patients regardless of viral eradication, potentially due to the pretreatment severe liver fibrosis and/or presence of other cofactors of liver disease progression [3,4,6].…”

“…Sustained virologic response (SVR) reduces the risk of liver decompensation and of hepatocellular carcinoma (HCC) and improves survival [1,4,5]. However, a "point of non-return" in terms of deterioration of liver function, has been observed in part of patients regardless of viral eradication, potentially due to the pretreatment severe liver fibrosis and/or presence of other cofactors of liver disease progression [3,4,6]. As a cofactor, Human Immunodeficiency Virus (HIV) coinfection negatively affect the natural course of chronic HCV infection.…”

Hepatic benefits of HCV cure: Don't forget coagulation!

“…cirrhosis (both compensated and decompensated), SVR is associated with reduced risks of decompensation, liver-related mortality, and hepatocellular carcinoma (HCC). 1 In addition to the aforementioned hepatic benefits of HCV cure, a further positive effect of SVR in patients with cirrhosis treated with DAAs is the reversal of the hypercoagulable state. 2,3 It is well known that patients with cirrhosis, particularly those who are decompensated, have complex coagulation changes that include reduced hepatic synthesis of both pro-and anticoagulant factors and increased levels of procoagulant factors synthetized outside the liver.…”