Postliver Transplant Allograft Reinfection with a Lamivudine‐Resistant Strain of Hepatitis B Virus: Long Term Follow‐up

Canadian Journal of Gastroenterology and Hepatology - Tập 12 Số 2 - Trang 125-129 - 1998
Eric M. Yoshida1, Mang Ma2, Jennifer Davis1,3, Karl Fischer4,2, Norman M. Kneteman5, Siegfried R. Erb1,6, D. Lorne Tyrrell7,1,5, Vincent G. Bain2
1Department of Medicine, University of British Columbia
2Department of Medicine, University of Alberta, Edmonton, Alberta
3Department of, Pathology, University of British Columbia.
4Department of Medical Microbiology, University of Alberta, Edmonton, Alberta
5Department of Surgery, University of Alberta, Edmonton, Alberta
6The British Columbia Transplant Society, Vancouver, British Columbia
7Department of Immunology, University of Alberta, Edmonton, Alberta

Tóm tắt

Lamivudine is a nucleoside analogue with efficacy in the suppression of hepatitis B viral (HBV) replication. In a previously reported study, lamivudine was administered to patients with chronic, actively replicating HBV infection who subsequently underwent liver transplantation. Patients became serum HBV DNA‐negative in response to lamivudine before transplantation, which was continued in the post‐transplant period. Two of four patients surviving the immediate postoperative period developed allograft reinfection 240 and 409 days post‐transplant. The strain of the reinfecting virus was analyzed, and a mutation in the YMDD region of the viral polymerase conferring resistance to lamivudine was discovered. The long term follow‐up of these two patients is reported. The first patient developed ascites 16.5 months after allograft reinfection. A transjugular liver biopsy performed 18 months after the emergence of the lamivudine‐resistant strain revealed cirrhosis and lobular hepatitis without rejection. The gradient between hepatic vein wedged and free pressures was 13 mmHg, consistent with portal hypertension. The second patient, 16 months after allograft reinfection with the lamivudine‐resistant strain, is without clinical evidence of portal hypertension, although liver enzymes remain elevated. Both patients were given a trial of famciclovir, which did not significantly suppress HBV viremia. In conclusion, lamivudine‐resistant HBV strains with the YMDD mutation may have an aggressive clinical course with rapid progression to cirrhosis. Famciclovir did not appear to be an effective rescue agent in these two patients.

Từ khóa


Tài liệu tham khảo

Thông tin
Thông tin xuất bản

Canadian Journal of Gastroenterology and Hepatology

Tập 12 Số 2

125-129

Thông tin tác giả