2221 A Case of Rare Escape Mutation Type G130N and Conundrum of Heptitis B Serology

Abstract

INTRODUCTION: Hepatitis B (HB) virus is a global public health problem as it affects more than 300 million patients around the world. It's well known that once we have Anti-HBs, seroconversion takes place, and that's a marker of viral clearance and immunity. In view of their important protective role, occurrence of anti-HBs and HBsAg is perplexing. Although this has been reported in 5-20% of cases of Chronic Hep B, it remains a confusing finding to many physicians who are unaware of the existence, explanation and implications of this finding. Herein, we will present a case of such a pattern. CASE DESCRIPTION/METHODS: A 49-year-old male with diabetes and hypertension was found to have elevated liver enzymes on routine blood work. Further workup resulted in diagnosing chronic hepatitis B. The patient’s viral serology results were positive for HB core antibody, HB surface antibody, HB surface antigen, HB e antigen, and a viral load of 1,500,000 IU/ml. Liver enzymes were elevated with ALT of 250U/L and AST of 180U/L. No masses were detected on liver ultrasound. Blood sample was sent to Center for Disease Control and analysis revealed a mutation G130N within the major hydrophilic region of surface antigen. The patient was started on Entecavir. After 12 months, the VL became undetectable. Serology was still positive for both HB s Ag and Ab but he successfully achieved HB e Ab +ve status. Liver enzymes normalized. DISCUSSION: The expected pattern in chronic HB is the presence of HBsAg and lack of anti-HBs. The mechanism underlying the coexistence of HBsAg and anti-HBs remains unclear. Mutations in the viral DNA were initially suggested by researchers to explain how the subtypes of the HBsAg and anti-HBs were heterologous. It was shown that there is a relation between this special serological profile and mutations in S gene region, particularly in the 'a' determinant of the major hydrophilic region of the surface antigen, including one located at G130N. Aside from mutations in the S gene region, the presence of heterologous subtype-specific antibodies, superinfection with a new HB strain, occult HB reactivation and false positivity for anti-HBs are other possible explanations. These patients might harbor an augmented HBV replicative capacity and HBV reactivation upon receiving immunosuppression. Antiviral prophylaxis must be considered before starting immunosuppressive drugs. It was also reported that coexistent HBsAg and anti-HBs independently increased the risk of advanced fibrosis and hepatocellular carcinoma.