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Letter: can persisting liver stiffness indicate increased risk of hepatocellular cell carcinoma after successful anti‐HCV therapy? – authors’ reply

SIRS, We read with interest the letter by the group of Dr Wiegand describing their experience on the potential value of liver stiffness measurement in patients receiving interferon (IFN)-free therapies of hepatitis C. Indeed, the findings are interesting and the important question to what extent liver function and liver stiffness are improving after cure of hepatitis C virus (HCV) infection should be determined in larger studies. In our study involving 80 patients with advanced liver cirrhosis, we described an overall improvement of parameters associated with liver synthesis in the far majority of patients already during therapy while platelet counts showed different (delayed) kinetics of improvement. Together with the preliminary findings by Karlas et al., and the Austrian experience recently present in this journal, we would propose that future studies need to address the following issues:(i) what is relative contribution of inflammation vs. fibrotic scarving to portal hypertension?(ii) what will be the longterm kinetics of liver function parameters and liver stiffness values after HCV clearance?(iii) which parameters are useful to identify patients at risk to develop hepatocellular carcinoma (HCC) even after HCV clearance? Our previous findings, as well as the paper by Mandorfer et al., suggest that rapid reduction of liver inflammation by blocking HCV replication has already a major influence on liver function and portal hypertension. Thus, the risk for variceal bleeding should be reduced already early during therapy which would be an argument to treat all patients with decompensated liver cirrhosis. In hepatitis B, successful antiviral therapy leads to regression of liver fibrosis 4 – which should translate also in improvements of liver stiffness values. We here describe our preliminary experience of patients followed with fibroscan for 24 weeks after the end of therapy. Indeed and in line with the data by the Wiegand group, a significant and in some patients marked decline of fibroscan values was evident in 26 of the 30 patients (Fig. 1). Overall, we suggest a two-phasic decline of portal hypertension in the context of IFN-free HCV therapies: a rapid first phase which occurs already during treatment (associated with improvement of liver inflammation) followed by a slower second phase becoming relevant only after 6–12 months of stopping HCV replication (correlate of fibrosis regression). The last question whether fibroscan values indicate a higher risk for HCC after HCV clearance remains to be answered in future studies as the case series by Karlas and colleagues included only patients who had HCC already before therapy.