Background/Purpose:  Reactivation of hepatitis B virus (HBV) is one of the most serious complications in rheumatoid arthritis (RA) patients treated with biological disease-modifying anti-rheumatic drugs (bDMARDs). De novo hepatitis induced by HBV reactivation in patients with resolved HBV can easily lead to fulminant hepatitis with poor prognosis. However, few studies have addressed the incidence and risk factors of HBV reactivation in RA patients with resolved HBV by treatment of bDMARDs. The purpose of this study was to identify the prevalence and risk factors for developing HBV reactivation in RA patients with resolved HBV who received bDMARDs therapy.

Methods:  RA patients who were newly treated with bDMARDs at our department from April 2009 to March 2016 were reviewed for this study. Of these patients, registered were the patients who had been diagnosed as resolved HBV and whose HBV-DNA was repeatedly measured with the interval ranged from one to three months. The definition of resolved HBV was positive for antibody against hepatitis B core antigen (anti-HBc) and negative for hepatitis B surface antigen (HBsAg). The study endpoint was reactivation of HBV determined as an HBV-DNA level higher than 2.0 log copies/ml. The association between HBV reactivation and clinical, laboratory and treatment data were retrospectively analyzed.

Results:  A total of ninety-six RA patients with resolved HBV were included in this study. In these patients, etanercept was administered in 21 patients, abatacept (ABT) in 18, golimumab (GLM) in17, tocilizumab (TCZ) in 17, infliximab (IFX) in 11, adalimumab in 7 and certolizumab pegol in 5. The median follow-up period was 19 months (interquartile range 5-37 months). Six out of ninety-six patients (6.3%) developed HBV reactivation during the observation periods. ABT was used for 2 patients, IFX for 2, GLM for 1 and TCZ for 1. In five out of the six patients, HBV-DNA levels were below the quantitation limit (< 2.1 log copies/ml) without any antiviral therapy while they continued to receive bDMARDs. In contrast, HBV-DNA level over 2.1 log copies/ml was observed in one patient treated with ABT, however HBV-DNA became negative after the initiation of entecavil therapy. The prevalence of HBV reactivation was significantly higher in the patients negative for antibody against HBsAg (anti-HBs) (p = 0.047, Fisher’s exact test).

Conclusion:  HBV reactivation occurred in 6.3% of RA patients with resolved HBV during the bDMARDs treatment. Absence of anti-HBs can be risk for reactivation of resolved HBV in these patients.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/prevalence-and-risk-factors-of-reactivation-of-resolved-hepatitis-b-virus-in-rheumatoid-arthritis-patients-treated-with-biological-disease-modifying-anti-rheumatic-drugs/