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发表于 2002-9-20 21:43
Gut 2002;51:597-599 2002 by Gut
CASE REPORT
Fatal hepatitis B reactivation following discontinuation of nucleoside
analogues for chronic hepatitis B
S G Lim1, C T Wai1, A Rajnakova1, T Kajiji1 and R Guan2
1 Division of Gastroenterology, Department of Medicine, National University
Hospital, 5 Lower Kent Ridge Road, Singapore (119074)
2 Mount Elizabeth Hospital, Singapore
Correspondence to:
Dr S G Lim, Division of Gastroenterology, Department of Medicine, National
University Hospital, 5 Lower Kent Ridge Road, Singapore (119074);
[email protected]
ABSTRACT
Background: Nucleoside analogues such as lamivudine for chronic hepatitis B have an excellent safety profile while patients are on therapy but
reactivation flares occur in 19-50% of patients after stopping therapy, some of whom develop liver decompensation.
Aims: To describe and report three cases who developed fatal hepatitis B
reactivation after stopping nucleoside analogue therapy.
Subjects and results: Three patients are described who developed hepatitis B reactivation and liver decompensation after stopping therapy. One of the three patients was participating in a famciclovir trial and the other two were receiving lamivudine therapy for active hepatitis B infection. All three patients had documented hepatitis B flares, and all had hepatitis B virus DNA detected at that time. All patients developed decompensated liver disease despite one patient having had a prior liver biopsy showing absence of cirrhosis. Reintroduction of lamivudine therapy failed to halt
progression of liver decompensation even after hepatitis B virus DNA had
been demonstrated to be absent. Sequencing for lamivudine resistant mutants in two cases where serum was available failed to show evidence of mutations associated with lamivudine resistance.
Conclusion: Hepatitis B virus reactivation, leading to decompensation and
death, are possible complications of treatment withdrawal and patients
should be monitored closely if therapy is ceased.
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