Chronic Hepatitis B Reactivation Subsequent to Chronic Hepatitis C Treatment: A Case Report

Abstract

Background: CHB and CHC infections are the important global health problems. Because of their shared modes of transmission, coinfection with HBV and HCV is frequent. Patients who are coin-fected have a higher risk of progression to severe liver disease (cirrhosis, decompensated liver disease), increased risk of hepato-cellular carcinoma, and unresponsiveness to treatment. In this article, a case with reactivated CHB subsequent to CHC treatment is presented. Method: A 42-year-old woman with HBV and HCV was admitted to infectious diseases clinic with a major complaint of fatigue for three months. There was no sense of the patient's history and family history. There was no smoking, alcohol, and any drug in the history. Her physical examination and vital signs were normal at the admission. The patient had no history of drug hypersensitivity, liver diseases, blood transfusion, or surgery. She refuted to use an over-the-counter and traditional Chinese medicine. Other virological and autoimmunity markers were negative. Finding were normal by USG. Result: Laboratory tests revealed an alanine transaminase (ALT) of 182 IU/L (Normal range: 0-55 IU/L), aspartate transaminase (AST) of 150 IU/L (Normal range: 0-34 IU/L), HCV-RNA of 2080195 IU/mL, HCV genotype 1b, Hepatitis B surface antigen (HBs Ag), HBV-DNA of 1184 IU/mL, whereas the results of other tests were within the normal range. Pegylated interferon (Peg-IFN) alpha-2a 180 mcg/week and ribavirin (RBV) tablet 1200 mg/day were initiated in April 2015 for CHC treatment. At the third and sixth months of CHC treatment, the liver enzymes were slightly elevated and HCV-RNA negative. HCV-RNA remained to be negative in the first year after the treatment of CHC. Patients presented with fatigue once again and elevated liver enzymes to our department after one year of CHC treatment. A liver biopsy was performed according to the health insurance guideline of Turkey in order to receive CHB treatment due to a HBV-DNA of 878215 IU/ml and elevated liver enzymes. The histopathological examination of liver tissue revealed a mildly active histologic activity (6/18) and a mildly active histological activity (1/6) according to ISHAK scoring. Tenofovir tablet 245 mg/day was administered for the CHB treatment. The patient is still followed up without any complaint at the ambulatory clinic of infectious diseases. Reactivation of HBV is thought to be a result of an immunological response to infected hepatocytes that replicate HBV after the restoration of both innate (restoration of NK cell phenotype and function) and adaptive (improvement in CD8+T cell function) immunological mechanisms with interferon treatment against CHC. Spontaneous fluctuations in the HBV-DNA levels are common in patients with HBs Ag-positive. Maylin and colleagues reported to occur the spontaneous fluctuations (>0.5 log10) in 63% of 87 patients with HBs Ag positive, normal ALT and AST. Papatheodoridis and colleagues reported that almost 50% of patients with CHB followed during a median period of time of 7.5 months (HbeAg negative) had >1log10 IU/mL fluctuations in the HBV-DNA levels. The probable risk of liver failure due to HBV reactivation, although slight, urges us to screen all patients receiving hepatitis C treatment for the presence of HBs Ag. Conclusion: As a result, patients coinfected with HBV and HCV should be followed up for the cirrhosis and hepatocellular carcinoma after CHC treatment in terms of HBV reactivation, even though they have undetectable viral load for HBV and HCV. [Figure Presented].