We observed a sustained viral response (SVR) of ombitasvir/paritaprevir/ritonavir, dasabuvir and ribavirin therapy, for 12 wk, in two cases with compensated liver cirrhosis and fully destroyed early hepatocellular carcinoma (HCC). Patients were infected with hepatitis C virus (HCV) genotype 1b and were previous null responders/relapsers to interferon-alpha/ribavirin (IFN/RBV). There was a rapid suppression of HCV RNA to undetectable levels within the first two treatment weeks. SVR was achieved even after marked reduction of the RBV dose. The treatment was well tolerated. Both subjects experienced worsening of liver disease during therapy, in different patterns: severe, transient, predominantly direct hyperbilirubinemia without cytolysis (case 1) or progressive increase of aminotransferases (grade 4) without severe hyperbilirubinemia (case 2). Adverse events spontaneously resolved. The patients remained in a good clinical condition without hepatic decompensation. There was no re-occurrence of HCC. This is the first report for treatment of HCV cirrhosis after complete HCC destruction.

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The histopathology of hepatitis B is diverse and reflects the natural history of chronic HBV-infection. Liver biopsy is gold standard for assessment of disease-activity and fibrosis. Treatment-decision is based on the assessment of liver disease severity as well as on patient's age, viral load, and HBeAg status. The relationship between these parameters and liver histopathology is not studied in details. We analysed treatment-naïve patients from single canter: 231 with histologically-proven chronic hepatitis B (CHB) and 104 subjects with clinical, laboratory and ultrasound signs of liver cirrhosis (LC). Viral load and HBV-serology were measured in all cases by real-time PCR and ELISA, respectively. Histological assessment of liver biopsies was performed according to METAVIR. Our results showed that the number of HBeAg-positive patient decreases with the increase of the disease activity from A0 to A3 as well as with the increase of the fibrosis stage from F1 to F4. In HBeAg-positive CHB patients both inflammation and fibrosis were more frequently mild or moderate. Severe disease activity (A3) and advanced fibrosis were observed more frequently in HBeAg-negative subjects. HBeAg-positive patients are younger than HBeAg-negative. Such an age difference exists into all separate subgroups

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