Prevalence of Hepatitis B Reactivation Among Chinese Individuals With Chronic Hepatitis C Treated With Pan-Oral Direct-Acting Antivirals

Shou-Wu Lee, Teng-Yu Lee, Sheng-Shun Yang, Yen-Chun Peng, Hong-Zen Yeh, Chi-Sen Chang

Abstract


Background: Clearance of hepatitis C virus (HCV) has been reported to induce the reactivation of hepatitis B virus (HBV). The aim of this study was to investigate the rate of HBV reactivation in HCV-infected Chinese patients who received treatment with pan-oral direct-acting antivirals (DAAs).

Methods: Data from HCV subjects receiving oral DAA therapy were retrospectively collected from October 2015 to May 2017. Patients who were seropositive for HBsAg or anti-HBc were enrolled. The efficacy of DAAs, including end-of-treatment virologic response (ETVR) and sustained virologic response (SVR) 12, was recorded. HBV virologic reactivation was defined as a reappearance of HBsAg, or increased HBV DNA by at least one log10 IU/mL. HBV clinical reactivation was defined as virologic reactivation and serum alanine aminotransferase (ALT) over two-fold of the upper limit of normal.

Results: There were 11 (7.2%) cases and 53 (34.6%) cases in the HBsAg group and the anti-HBc group among all 153 subjects. All individuals achieved ETVR and SVR12. There were no cases with reappearance of HBsAg during DAAs therapy. Among seven cases in the HBsAg group whose HBV DNA level was determined, HBV virological reactivation was detected in two subjects (28.6%). Among all 11 subjects in the HBsAg group, there was one (9.1%) case with HBV clinical reactivation, which was resolved following treatment with Entaclavir. The case with HBV clinical reactivation had a higher baseline HBV DNA viral load (1,380 IU/mL) compared with that of the other patients (20 - 296 IU/mL).

Conclusion: HBV virological and clinical reactivation occurred in 28.5% and 9.1% of subjects with HBsAg seropositivity. No HBV reactivation was observed in the cases with past HBV infection.




Gastroenterol Res. 2018;11(2):124-129
doi: https://doi.org/10.14740/gr971w

 


Keywords


Hepatitis B; Hepatitis C; Direct-acting antivirals

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