Abstract
Introduction: Hepatitis C has long been one of the most common causes of cirrhosis and resultant hepatocellular carcinoma (HCC). There is evidence demonstrating an increased risk of development of HCC in non-cirrhotic patients who have had sustained virologic response (SVR) after direct acting antiviral (DAA) treatment of hepatitis C. We present a case of a non-cirrhotic 72-year-old male who attained SVR with DAA treatment in 2018. After presenting to the hospital two years later with significant weight loss and fatigue, he was found to have metastatic HCC. Case Description/Methods: A 71-year-old male with a history of tobacco use, hypertension, diabetes mellitus type 2, and chronic hepatitis C who completed Harvoni in 2017 was admitted due to unintentional weight loss of fifty-five pounds associated with early satiety, epigastric pain, and weakness. He was found to have hepatitis C antibodies in 1993 and underwent a liver biopsy in 2001 that showed stage one fibrosis. In 2015, he underwent a second liver biopsy that again showed stage one portal fibrosis. In July 2017, he underwent treatment and was found to have an undetectable viral load. During his 2021 admission, CT abdomen/pelvis showed heterogeneous enhancement throughout the right lobe of the liver with scattered hyper-enhancing foci. He underwent liver biopsy showing HCC. He was offered the option of immunotherapy versus hospice care. He then opted for hospice care. Discussion: While HCC can develop in patients who achieved sustained virologic response following HCV eradication, 20% of cases can develop in non-cirrhotics. Surveillance is not performed in these cases, so HCC can present at more advanced stages. Risk factors for HCC development after HCV clearance are older age at eradication, male sex, advanced fibrosis stage, AFP levels following IFN treatment, heavy alcohol use, diabetes mellitus, hypertension, and hyperlipidemia. Clearance by DAAs had no impact on short term development of HCC but noted sofosbuvir-based treatment without Ribavirin as adding additional risk. Other guidelines proposed following the level of fibrosis and SVR but acknowledged that implementation of this strategy cannot presently be achieved in clinical practice. Although abdominal ultrasound remains the gold standard, associating the development of HCC in patients with SVR and various SNPs could identify patients at increased risk. Our case further enforces the need for increased surveillance in this patient population.
Published Version
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