Abstract
Direct-acting antivirals (DAA) have replaced interferon (IFN)-based therapies for hepatitis C virus. In this retrospective clinical study, we examined differences in histopathologic features in paired liver biopsies collected from the same patient before and after DAA and correlated these findings with clinical outcome. Biopsies (n = 19) were evaluated by quantitative imaging analysis to measure steatosis and fibrosis. Most patients had decreased steatosis in their post-treatment, follow-up biopsies. However, one patient had a striking increase in steatosis (from 0.86 to 6.32%) and later developed decompensated cirrhosis and hepatocellular carcinoma (HCC). This patient had a marked increase in fibrosis between biopsies, with a CPA of 6.74 to 32.02. Another patient, who already had bridging fibrosis at the time of her pre-treatment biopsy, developed cholangiocarcinoma after DAA. Even though the overall inflammatory activity in the post-treatment biopsies significantly decreased after treatment, 60% of patients had persistent portal lymphocytic inflammation. In summary, DAAs decreased steatosis and hepatic inflammation in most patients, although some may have persistence of lymphocytic portal inflammation. Patients known to have advanced fibrosis at treatment initiation and who have other risk factors for ongoing liver injury, such as steatosis, should be followed closely for the development of adverse outcomes, such as portal hypertension and primary liver cancers.
Highlights
Viral hepatitis, among other etiologies, including non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), and alcohol-associated liver disease (AALD), may lead to the development of chronic liver disease[1]
Enhanced fibrosis progression in hepatitis C virus (HCV)-infected patients has been associated with heavy alcohol consumption, male gender, elevated serum ALT levels, high inflammatory activity and hepatic s iderosis[4,5]
The goal of this study was to evaluate differences in liver biopsies collected from patients pre- and post-treatment with Direct-acting antivirals (DAA) for HCV infection and to correlate the observations with clinical outcomes
Summary
Among other etiologies, including non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), and alcohol-associated liver disease (AALD), may lead to the development of chronic liver disease[1]. Direct-acting antivirals (DAA), which target the viral replicative machinery, have supplanted IFN-based therapies for treating HCV. They are the current standard therapy for the treatment of patients with HCV8. DAA therapy has increased treatment efficacy and has improved the safety profile when compared to IFNbased agents, in most HCV infected p atients[9,10]. Several factors, including HCV genotype, development of resistance associated variants, resistance to previous antiviral treatment (i.e., those that previously received Peg-IFN or Peg-IFN with ribavirin), HIV co-infection and the presence of cirrhosis, may decrease responses to DAA treatment[14,15]. Recent studies with larger participants have shown that even though they decrease the risk of HCC, achieving SVR does not completely eliminate a patient’s risk h epatocarcinogenesis[18]
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