2210 Resolution of Hepatocellular Carcinoma in a Patient With Chronic Hepatitis B Treated With Entecavir Therapy

Abstract

INTRODUCTION: Hepatitis B virus (HBV) is a major cause of hepatocellular carcinoma (HCC) globally. Prolonged HBV DNA suppression with nucleos(t)ide analogues is known to regress hepatic fibrosis and reduce HCC risk. This is an unusual presentation of a patient with hepatitis B-associated HCC whose liver lesion resolved on antiviral therapy alone. CASE DESCRIPTION/METHODS: Patient is a 64-year-old Chinese male with HBeAg negative chronic hepatitis B with persistent normal serum aminotransferases and was antiviral treatment naïve. He had a positive family history of HCC and was first noted to have asymptomatic elevation of alpha-fetoprotein (AFP) to 648.9 ng/ml 6 months prior to his referral to Hepatology. During his initial Liver Center visit, the AFP increased to 1,900 ng/ml with elevated AFP-L3 at 18.4%. His hepatitis B remained inactive with normal ALT and minimal detectable HBV DNA at 1.6 log IU/ml (Table 1). He was started on entecavir 0.5 mg daily in view of his age and suspicious HCC complication. Initial MRI of the abdomen revealed lesions in segment 4 (2 cm) and segment 7 (2.1 cm) of the liver with arterial enhancement, venous washout and pseudocapsule. Targeted liver biopsy of segment 7 lesion and adjacent liver was performed within 2 weeks on entecavir therapy. The targeted liver specimen revealed a necrotic focus with loss of reticulin with strong immunoreactivity for cytokeratin Hep Par1 and Glypican-3; the findings were highly suspicious for HCC. The adjacent liver had only mild inflammation (grade 0-1) and minimal fibrosis (stage 0-1). Six weeks later, AFP decreased to 19 ng/dl but AFP-L3 remained elevated at 17%. On repeat CT scan, the segment 7 lesion decreased to 1.2 cm and no longer met OPTN HCC criteria. Patient remained clinically stable with optimal HBV DNA suppression. By 7-month follow-up, both AFP and AFP-L3 normalized and the liver lesions remained stable in size (Table 1). He continued to have regular monitoring and the segment 7 liver lesion was no longer visualized on abdominal MRI after 2 years. DISCUSSION: Nucleos(t)ide analogue therapy is known to suppress HBV replication but has not been reported to have direct effect on HCC. This HCC case is unique as the liver lesion regressed and resolved on entecavir therapy alone. While the molecular mechanism leading to the HCC resolution is currently unknown, this case highlights the beneficial role of prolonged HBV DNA suppression with antiviral therapy.