Tumor Necrosis Factor-α Inhibitors Increase the Risk of Hepatitis B Virus Reactivation in Patients with Ankylosing Spondylitis

Abstract

Abstract Background/Purpose Biologic agents may cause hepatitis B virus (HBV) reactivation in patients with rheumatoid arthritis or hematological diseases. However, little is known about HBV reactivation (HBVr) in ankylosing spondylitis (AS) patients receiving biologics.Methods A total of 1959 AS patients were retrospectively screened from year 2005 to 2019. The medical record of 448 patients with available HBV markers were carefully reviewed. The incidence and risk factors for HBVr were examined.Results Among the 448 AS patients, 172 were enrolled in our study after excluding those with antiviral prophylaxis, negative hepatitis B core antibody (anti-HBc), and missing data. Sixty-seven (39.0%) of them were hepatitis B surface antigen (HBsAg) positive at baseline, and 14 (20.9%) developed HBVr during a follow-up of 536 patient-years. Eight were treated with tumor necrosis factor-alpha inhibitor (TNFi). The median time for the 8 patients receiving biologics to develop HBVr was 11.5 months (ranging from 5 to 71 months). Multivariate logistic regression analysis showed that receiving TNFi was an independent risk factor for HBVr in HBsAg-positive patients (hazard ratio (HR) 4.365, 95% CI: 1.4–13.9, P = .013). One (7.1%) patient with HBVr developed liver decompensation, and there was no death. Also, none of the HBsAg-negative patients experienced HBsAg reverse seroconversion.Conclusion TNFi exposure can induce HBVr in HBsAg-positive patients with AS, and the incidence was substantial. Monitoring HBV viral load is necessary for HBsAg-positive patients undergoing TNFi in the absence of antiviral prophylaxis.