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Articles

Lamivudine Therapy in Acute Leukemia Patients who are Hepatitis B Surface Antigen Carriers

, , , , , , & show all
Pages 393-396 | Published online: 04 Sep 2013
 

Abstract

Background: Reactivation of hepatitis B in patients receiving chemotherapy for acute leukemia may give rise to a variety of clinical patterns including hepatitis, asymtomatic hepatic dysfunction, massive hepatic necrosis and fatal hepatic failure. Lamivudine is a nucleoside analogue which can directly suppress Hepatitis B virus (HBV) replication. We reviewed our combined experience to evaluate the role of lamivudine as prophylaxis in acute leukemia patients who were HBsAg carriers treated with chemotherapy between July 2000 and October 2002 at the Numune Education and Research Hospitals (Ankara, Turkey) retrospectively.

Methods: We investigated 75 acute leukemia patients who received chemotherapy. Thirteen (17.3%) of 75 acute leukemia patients were HbsAg positive and of 7 (53.3%) were HBV DNA positive. Two patients (patients 5 and 6) had a chemotherapy regimen that included corticosteroids and were HBsAg and HBV DNA negative but anti HBc total positive. HBsAg positive patients with or without HBV DNA positivity were treated with a dose of 100 mg/day lamivudine commencing when chemotherapy was initiated. Lamivudine started at the beginning of chemotherapy and was maintained for 6 months following the cessation of chemotherapy. During lamivudine treatment, Aspartate aminotransferase (AST), Alanine aminotransferase (ALT), Gama glutamile transpeptidase (GGT), Alkaline phosphatase (ALP) were followed.

Results: Of the 8 patients who presented with hepatic dysfunction during the first chemotherapy cycle, 4 improved during the second course. After completing chemotherapy, the levels of hepatic enzymes were in the normal range in all but one patient. With lamivudune prophylaxis, HBV DNA positivity did not develop in any of the HBV DNA negative patients. The two patients who received corticosteroids with their first chemotherapy cycle became positive for HBsAg and HBV DNA and were given Lamivudine when the seroconversion was established. Median follow up from the diagnosis of leukemia was 14.5 months. Survival rate at the end of follow up was 5 (38%) for the 13 patients.

Conclusions: As this infection is endemic in our country and the exposure to blood products is high in these patients, HBV infection is more common. Prophylaxis with daily administration of lamivudine to HBsAg carriers who are candidates for chemotherapy seems to be effective and may prevent chemotherapy induced HBV reactivation and hepatic failure.

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