Abstract
Since 1998 with the highly effective nucleos(t)ide analogues for Hepatitis B virus (HBV), we have witnessed successful viral suppression that has led to the delay or prevention of the development of hepatocellular carcinoma (HCC). Reduced incidence of HCC with anti-HBV treatment has been documented with lamivudine, entecavir and tenofovir. A number of investigators have observed that after the initial tumor was ablated, anti-HBV treatment could prevent or reduce the recurrent or subsequent new HCC. Nonetheless, as reported earlier, we are observing the persistent risk for HCC in patients in spite of successful viral suppression for over a decade with anti-HBV therapy. In this report, we present three cases who underwent initial tumor ablation and maintained negative HBV DNA with anti-HBV therapy and yet developed subsequent new or recurrent HCC at the intervals of 5,10,11 and 15 years. These persistent risks for new and recurrent HCC are attributed to the incomplete control of HBV due to the presence of cccDNA in the host’s hepatocytes. Current antiviral treatment can achieve a functional cure (suppression of HBV replication) while a complete cure of eliminating the cccDNA has not been possible. Therefore, even though HBV is not actively replicating, cccDNA remains in the nucleus of the hepatocytes and continues hepatocarcinogenic processes including HBV and host DNA integration. There is a need for HBV cure drugs.
Highlights
Chronic hepatitis B virus (HBV) places patients at an increased risk for the development of hepatocellular carcinoma (HCC) [1,2]
Since the advent of anti-HBV therapy (nucleos(t)ide analogues), a reduced incidence of HCC has been well documented with lamivudine, entecavir and tenofovir. [3,4,5,6] On the other hand, despite HBV DNA at undetectable levels, some patients, especially those with cirrhosis were found to develop HCC
We presented three cases that illustrate the persistent risk for subsequent new or recurrent HCC in spite of initial successful tumor ablation, continued anti-HBV therapy and sustained clearance of HBV DNA viremia for over ten years
Summary
Chronic hepatitis B virus (HBV) places patients at an increased risk for the development of hepatocellular carcinoma (HCC) [1,2]. In 2014, 10 years after the first tumor ablation, at age 67, on MRI a new 1.0 cm arterially enhancing lesion with washout appeared in segment 7 of the liver He underwent successful TACE one month later Since he has been on dual anti HBV therapy with lamivudine and tenofovir with sustained undetectable HBV DNA and close follow-up (Case 1). In 2005, five years after the first tumor ablation, while continued on anti-HBV therapy with undetectable HBV DNA, a 1.1 cm × 0.8 cm arterially enhancing lesion with washout appearance was noted near the treated site on abdominal MRI. Laboratory results showed AFP 24.4 ng/ml, undetectable HBV DNA, ALT 19 IU/L, platelets 125 B/L and HBeAg (-)/anti-HBe (+) Case 3 Timeline of the first and new HCC (highlighted)
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