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Fatal Reactivation of Precore Mutant Hepatitis B Virus Associated with Fibrosing Cholestatic Hepatitis after Bone Marrow Transplantation

Carolyn McIvor, FRACP; James Morton, MBBS; Andrew Bryant, FRACP; W. Graham Cooksley, FRACP; Simon Durrant, MRCP; and Neal Walker, FRACP
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From the Royal Brisbane Hospital, Brisbane, Queensland, Australia. Requests for Reprints: W. Graham Cooksley, MD, Clinical Research Centre, H Floor, Bancroft Center, Royal Brisbane Hospital, 300 Herston Road, Brisbane, Queensland 4029, Australia. Grant Support: In part by a Gastroenterological Society of Australia Medical Postgraduate Scholarship and by the Royal Brisbane Hospital Research Foundation.

Copyright ©2004 by the American College of Physicians

Ann Intern Med. 1994;121(4):274-275. doi:10.7326/0003-4819-121-4-199408150-00007
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Liver failure caused by reactivation of hepatitis B virus (HBV) is an uncommon complication of bone marrow transplantation [13]. Fibrosing cholestatic hepatitis is a recently described liver lesion that develops after liver transplantation for chronic HBV infection. Hepatitis B virus precore mutant infection has been associated with liver failure after cytotoxic chemotherapy [4] and with fibrosing cholestatic hepatitis after liver transplantation [56], but the relation is unclear. We describe a patient who developed fibrosing cholestatic hepatitis and HBV precore mutant infection after bone marrow transplantation.

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Figure 1.
Hepatologic course after bone marrow transplantation, including alanine aminotransferase (ALT) levels and hepatitis B virus (HBV) DNA.

Panels above the graph show the time course of drug therapies. PCR = polymerase chain reaction.

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Figure 2.
Immunohistochemical stains for hepatitis B surface antigens (top) and core antigens (bottom) on day 171.

Hepatocytes show variable cytoplasmic staining for surface antigen and intense nuclear and cytoplasmic staining for core antigen. The amount of surface antigen is greatest in severely altered hepatocytes (original magnification, × 330).

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