Professor of Medicine
Director of Hepatology
Stanford University School of Medicine
Palo Alto, California
Paul Y. Kwo, MD, has disclosed that he has received consulting fees from AbbVie, Bristol-Myers Squibb, Gilead Sciences, and Merck and funds for research support from AbbVie and Gilead Sciences.
In this viral hepatitis case series, we highlight common patient case scenarios and the critical decision making that informs selection of optimal patient management strategies. This commentary features a man who achieved cure following HCV treatment. Optimal follow-up strategies for this type of patient, with a focus on the need to monitor for hepatocellular carcinoma (HCC), are discussed.
A 49-year-old white man with genotype 1b HCV infection recently completed 8 weeks of antiviral treatment, achieving a sustained virologic response at 12 weeks post treatment (SVR12). In his pretreatment assessment, he was found to have F3 liver fibrosis by transient elastography (10.6 kPa) but no esophageal varices. Is this patient at risk for developing HCC? How should he be monitored now that he has achieved SVR12?
Screening for HCC in Patients Who Have Achieved SVR
Owing to the contemporary breadth of efficacious treatment options, we can now counsel all patients with HCV—including those with cirrhosis—that successful completion of therapy typically results in SVR, or virologic cure. For patients who have achieved cure, our emphasis must shift from eradicating viral disease to managing liver disease. The complications of advanced fibrosis and cirrhosis are reduced following SVR but do not disappear completely. In particular, we must be aware of the persistent elevated risk for HCC in patients with cirrhosis or F3 fibrosis.
Data from the interferon treatment era and, more recently, from the current direct-acting antiviral era demonstrate that patients with HCV infection are at risk for developing HCC and that achievement of SVR reduces this risk—in both cirrhotic and noncirrhotic patients—by approximately 70%, although the absolute risk of development of HCC in those without cirrhosis is substantially lower than in those with cirrhosis. Both the AASLD/IDSA and EASL guidelines recommend that patients with F3-F4 fibrosis be monitored for HCC by ultrasonography every 6 months following achievement of SVR. Until further data are generated, this HCC screening should continue indefinitely. I would recommend screening the case patient in this way, as he had F3 fibrosis prior to direct-acting antiviral therapy.
In years prior to these recommendations, liver biopsies were routinely performed in the evaluation of hepatitis C and could be correlated with other clinical data (including serum markers of fibrosis and imaging information) to accurately ascertain the degree of fibrosis and decide on whether the patient truly had advanced fibrosis (F3-F4) that would necessitate continued screening for HCC. However, we are now doing fewer liver biopsies to stage fibrosis, instead relying on elastography and serum markers of fibrosis. It is hoped that with additional risk stratification models and improved biomarkers, we will be able to better identify those at highest risk for developing HCC, allowing screening to be fine-tuned to target populations most likely to develop HCC. For now, all patients who are evaluated for hepatitis C and determined to have F3 or F4 fibrosis should be screened twice annually with ultrasound following SVR, regardless of how fibrosis was assessed.
How do you approach screening for HCC in patients with HCV infection who have achieved SVR? Please add your experience to this conversation using the comments box below.
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