Hepatitis B virus infection in heart transplant recipients in a hepatitis B endemic area

Hepatitis B virus (HBV) infection is hyperendemic in Taiwan. It is almost impossible for us to reject organ donors or recipients with positive serum hepatitis B surface antigen (HBsAg). We report our experience with HBV infection in heart transplant recipients with particular attention to outcome of recipients who were HBsAg+ or who had received donor hearts from HBsAg+ donors.

We performed a retrospective review of medical records.

In the study, we included 101 heart recipients with post-transplant survival of more than 6 months. According to pre-transplant HBV serology markers, we divided patients into 4 groups. Group 1 (n = 8) had been HBsAg+ at the time of heart transplantation. Of these, 6 patients had HBV reactivation in the post-transplant follow-up and needed lamivudine treatment. Complete response was achieved in all 6 patients; however, HBV recurrence occurred in 1 patient after 8 months of lamivudine treatment. The recurrence remained under partial control. Group 2 (n = 16) was HBV naïve at the time of heart transplantation. Of these, 2 received HBsAg+ donor hearts under perioperative hepatitis B immunoglobulin prophylaxis. HBV infection was successfully prevented in 1 patient, but the other contracted HBV hepatitis, which was successfully treated with lamivudine. In Group 2, 10 patients received donor hearts from anti-HBs+ donors, and none contracted HBV hepatitis after transplantation. Group 3 (n = 55) had protective anti-HBs antibody at the time of heart transplantation either from previous HBV vaccination (n = 10) or from natural HGB infection (n = 45). HBsAg+ donor hearts were transplanted into 2 patients with anti-HBs from previous HBV vaccination, and into 8 patients with anti-HBs form natural HBV infection. However, none of these 10 patients who received HBsAg+ donor hearts had HBV hepatitis after transplantation. Group 4 (n = 22) was HBs-, anti-HBs-, and anti-HBc+ at the time of heart transplantation. Of these, 7 patients received HBsAg+ donor hearts. Six patients experienced no HBV hepatitis after heart transplantation, and serum HBV DNA by polymerase chain reaction (PCR) at the time of heart transplantation was negative in all 6 patients. One patient had HBV hepatitis after transplantation, and serum HBV DNA by PCR at the time of heart transplantation also was positive.

HBV reactivation after the heart transplantation was common but usually well controlled with lamivudine treatment. Therefore, HBV carrier status should not contraindicate heart transplantation. HBsAg+ donor hearts were safely transplanted into anti-HBs+ recipients; therefore, HBsAg+ itself was not a contraindication to heart donation. Patients with HBsAg-, anti-HBs-, anti-HBc+, and negative HBV DNA in the serum by PCR could be protected from HBV infection from HBsAg+ donor hearts. However, patients with HBsAg-, anti-HBs-, anti-HBc+, and positive HBV DNA in the serum by PCR should be recognized as HBV carriers and closely followed for potential HBV flare-up after heart transplantation.