Figure 3.

The clinical course of two resolved hepatitis B patients who developed HBsAg reverse seroconversion. (A) A SLE patient had positive antibodies to HBsAg (anti-HBs) titer at baseline and lupus nephritis developed three years after SLE diagnosis. She then received immunosuppressive treatment with glucocorticoids (GC), hydroxychloroquine (HCQ), and azathioprine (AZA). Unfortunately, she progressed to end-stage renal disease (ESRD) and was treated with hemodialysis 112 months later. She received a kidney transplant 42 months later and augmented immunosuppressants with GC, mycophenolate mofetil, and cyclosporin were used to prevent graft rejection. After 37 months, anti-HBs became weakly positive and HBV reactivation (HBVr) developed 27 months later with HBsAg reverse seroconversion (HBsAg RS). The peak HBV viral load was >8 log IU/mL and peak ALT level was 427 IU/mL during HBVr. The patient received emergent entecavir treatment and survived. (B) The patient was negative for anti-HBs before the use of immunosuppressive agents. She exposed to GC treatment for 101 months with a high accumulative GC dosage (165,768 mg prednisolone) before HBsAg RS. The peak HBV viral load was missing and peak ALT level was 142 IU/mL. She did not receive antiviral treatment because of spontaneous ALT decline and survived.