Abstract
Sensitized patients received desensitization therapy with rituximab for kidney transplantation. However, the impact of rituximab dose on hepatitis B virus (HBV) reactivation is unknown. Patients who underwent living donor kidney transplantation between 2008 and 2016 were grouped according to rituximab dose (control vs. standard-dose rituximab [375 mg/m2] vs. reduced-dose rituximab [200 mg/body]) for comparison of HBV reactivation. A total of 336 hepatitis B surface antigen (HBsAg)-negative/antibody to hepatitis B core antigen (anti-HBc)-positive patients underwent kidney transplantation, of whom 91 (27.1%) received rituximab for desensitization (57 standard-dose and 34 reduced-dose rituximab). During the study period, eight patients experienced HBV reactivation (three in the control group, five in the standard-dose group). In the standard-dose group, four patients experienced hepatitis flare, and one patient died due to hepatic failure. No HBV reactivation occurred in the reduced-dose group. Standard-dose rituximab significantly decreased hepatitis B surface antigen antibody titer (anti-HBs; −99.8 IU/L) at 12 months, compared with reduced-dose rituximab (−20.1 IU/L) and control (−39.1 IU/L, P = 0.017). Standard-dose rituximab (HR, 10.60; 95% CI, 2.52–44.60; P = 0.001) and anti-HBs < 100 IU/L at transplantation (HR, 9.06; 95% CI, 1.11–74.30; P = 0.04) were independent risk factors for HBV reactivation. Standard-dose rituximab significantly increased HBV reactivation risk for HBsAg-negative/anti-HBc-positive kidney transplant patients.
Highlights
Hepatitis B virus (HBV) infection is the common chronic viral infection in the world[1]
Despite its potent cytolytic effect, rituximab is generally well tolerated with minimal toxicity; increasing evidence indicates that rituximab is associated with hepatitis B virus (HBV) reactivation[16]
The US Food and Drug Administration (FDA) issued a new boxed warning that rituximab increases the risk of HBV reactivation[17]
Summary
Hepatitis B virus (HBV) infection is the common chronic viral infection in the world[1]. Anti-HBs < 100 IU/L at the time of transplantation and standard-dose rituximab for desensitization were significant independent risk factors for HBV reactivation. At 1-year after kidney transplantation, the mean changes in anti-HBs between the standard-dose rituximab, reduced-dose rituximab, and control groups were −99.8, −20.1, and −39.1 IU/L, respectively (P = 0.017).
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