Reactivation of hepatitis B virus replication is a known complication of immunosuppressive therapy, which can lead to hepatocellular injury, liver failure, and death. In this report, we describe the case of a 44-year-old man with chronic hepatitis B and a dilated cardiomyopathy status after a heart transplant. Reactivation of the patient’s hepatitis B virus occurred 4 months after the heart transplant. Despite prompt administration of antiviral therapy, he developed fulminant hepatitis with hepatic encephalopathy. A successful living-related liver transplant was performed 7 months after the heart transplant. The patient was followed up for 1 year, and during that time was free of hepatitis B virus. We suggest that routine antiviral therapy should be administered to patients with chronic hepatitis B receiving immunosuppressive therapy.
Key words : Hepatitis B virus, Acute liver failure, Heart transplant, Liver transplant
Immunosuppressive therapy in hepatitis B virus (HBV) carriers can result in reactivation of viral replication, which manifests as an abrupt increase in serum HBV DNA and can lead to elevation of liver enzymes, symptoms of fulminant hepatitis, hepatocellular injury, liver failure, and death.1,2 This case report documents a heart transplant recipient who experienced HBV reactivation 4 months after he began immuno-suppressive therapy. The patient was treated with a nucleoside analogue (entecavir) after HBV reactivation, but his condition progressed to fulminant hepatitis and hepatic coma. A living-donor liver transplant was performed successfully 7 months after he had received the heart transplant. Regular administration of low doses of hepatitis B immunoglobulin (HBIG) and entecavir were used for prophylaxis of HBV recurrence.
A 44-year-old HBV carrier received a heart transplant for dilated cardiomyopathy, and was treated with tacrolimus and prednisolone as immunosuppressants. A regular follow-up examination 4 months after the transplant was significant for mildly elevated levels of liver enzymes (aspartate aminotransferase/alanine aminotransferase, 0.852/2.238 μkat/L). In addition, the patient’s HBV viral load (> 1.0 × 109 IU/mL) was detected, and he was given entecavir as antiviral treatment. However, the patient experienced general weakness and exhibited tea-colored urine after 1 month of entecavir treatment. Moreover, he continued to have elevated levels of liver enzymes (aspartate aminotransferase/alanine aminotransferase, 11.890/25.134 μkat/L) and his total bilirubin count was 87.4 μmol/L. The patient’s disease was diagnosed as an HBV flare-up of acute hepatitis, which progressed to liver failure with hepatic encephalopathy. A living-donor liver transplant, with a partial right lobe graft from his wife, was performed 7 months after the heart transplant. Prophylactic intravenous HBIG was administered intraoperatively (10 000 IU) during the anhepatic phase, 2000 IU/day postoperatively between days 2 and 7, and 2000 IU/week postoperatively from week 2 to week 4. Thereafter, the patient received long-term HBIG intramuscularly 800 IU/month.
His postoperative course was uneventful. Three weeks after the liver transplant, his liver enzymes returned to normal levels. He was given entecavir treatment (0.5 mg/d) for HBV prophylaxis and told to continue for the rest of his life. One year after the transplant, the HBV DNA viral load was undetectable, and the patient’s heart and liver functions were normal during this time.
Hepatitis B virus reactivation has been reported in 20% to 50% of HBV carriers undergoing immuno-suppressive therapy.3 In hyperendemic areas, hepatitis B virus reactivation in HBV carriers is common after a heart transplant.4 To achieve optimal clinical outcomes, administering antiviral therapy before beginning immunosuppressive therapy has been suggested.5 If the antiviral treatment does not resolve the progression of fulminant hepatitis, a liver transplant should be considered as a rescue therapy. The outcomes of an emergent living-donor liver transplant are comparable to emergent deceased-donor liver transplant and may be considered first-line treatment for patients with acute liver failure, particularly in hepatitis-endemic areas where a shortage of deceased donor organs exists.6,7 Patients other than those with undetectable HBV DNA levels during a liver transplant are advised to take lifelong prophylaxis consisting of low-dose HBIG and an antiviral agent.8 In sum, we have described our experiences managing fulminant hepatitis due to HBV reactivation after a heart transplant.
Volume : 13
Issue : 4
Pages : 369 - 370
DOI : 10.6002/ect.2014.0030
From the Department of Surgery, National Taiwan University Hospital, Taipei,
Acknowledgements: Thanks to all of our transplant team members in National Taiwan University Hospital for their incredible and unlimited love and collaboration in this difficult patient. The authors have no conflicts of interest to disclose, and there was no funding for this study.
Corresponding author: Cheng-Maw Ho, MD, National Taiwan University Hospital, No. 7, Chung-Shan South Road, Taipei 100, Taiwan
Phone: +886 2 23123456-65914
Fax: +886 2 23568810