HCC surveillance after SVR in patients with F3/F4 fibrosis

Abstract

HCV eradication by antiviral treatment reduces but does not eliminate HCC risk. Patients with established cirrhosis require HCC surveillance "indefinitely" after sustained virologic response (SVR) because they appear to have a high risk of HCC even many years after SVR. Patients without established or known cirrhosis may still require surveillance after SVR if they have a sufficiently high HCC risk. In all patients who achieve SVR, the key question is how we can reliably estimate HCC risk, and the change in HCC risk over time, to determine whether the patient might benefit from HCC surveillance. HCC risk is one of the most important factors that should inform decisions of whether and how to screen for HCC. Promising strategies for estimating HCC risk include simplified scoring systems (such as fibrosis-4), liver elastography and multivariable HCC risk calculators. Such tools may enable risk stratification and individualised, risk-based surveillance strategies ("precision HCC screening") in the future.

External validation of LCR1-LCR2, a multivariable HCC risk calculator, in patients with chronic HCV

“…Finally, we agree with others that stopping the surveillance of low-risk groups is questionable, and that the intensification of screening programs in intermediate- or high-risk groups is a challenge that would improve compliance with surveillance recommendations. [3] , [4] , [5] , 10 , [28] , [29] , [30] …”

Risk of hepatocellular carcinoma after HCV eradication: Determining the role of portal hypertension by measuring spleen stiffness

“…Several attempts have been made to identify high-risk patients, mainly based on biochemical, elastosonographic, multivariate, and deep learning models. 5 In particular, different models based on LSM values have been proposed for this purpose. 6,7,[21][22][23] However, none of the predictive models reported included variables reflecting the severity of portal hypertension.…”

“…6,7,[21][22][23] However, none of the predictive models reported included variables reflecting the severity of portal hypertension. 5 In their seminal paper, Faillaci et al 8 showed that large oesophageal varices and high levels of angiopoietin-2, a reflection of neoangiogenesis and extensive splanchnic collateralisation, were independent predictors of both HCC occurrence and recurrence after DAAs. This study strongly suggests that the role of DAA in liver carcinogenesis acts through the main predisposing condition: severe portal hypertension and the linked modification of hepatic and splanchnic microcirculation.…”

“…High-risk patients for HCC could benefit from a more intensive follow-up by magnetic resonance imaging or computer tomography spaced out with ultrasound. 5,24,25 In conclusion, prediction models estimating the HCC risk after HCV eradication should include parameters that mirror the presence of portal hypertension, such as spleen stiffness. The combination of LSM and SSM offers a unique possibility of capturing together liver fibrosis, portal hypertension, and their dynamic changes after specific treatment.…”

“…[2][3][4] However, some patients remain at considerable risk for HCC despite SVR achievement, so the development of adequate HCC surveillance strategies after HCV eradication is a very relevant topic. 5 Increasing evidence supports the role of liver stiffness measurement (LSM), both before and after DAA treatment, to predict HCC risk despite SVR. 6 Pons et al 7 recently described how post-SVR LSM values (<10 kPa vs. 10-20 kPa vs. > − 20 kPa), combined with albumin levels, were able to predict HCC development with good accuracy (Harrell's C index = 0.73).…”