Comparative effectiveness of nucleos(t)ide analogues in chronic hepatitis B patients undergoing cytotoxic chemotherapy

作者:Tseng Chao Ming; Chen Tai Been; Hsu Yao Chun*; Chang Chi Yang; Lin Jaw Town; Mo Lein Ray
来源:Asia-Pacific Journal of Clinical Oncology, 2016, 12(4): 421-429.
DOI:10.1111/ajco.12520

摘要

Background: Comparative effectiveness of different nucleos(t)ide analogues for preventing hepatitis B virus reactivation induced by cytotoxic chemotherapy has not been elucidated. The prophylactic drug of choice remains controversial. Aim: Our objective was to compare the effectiveness of tenofovir, telbivudine and entecavir with lamivudine in preventing the reactivation of hepatitis B virus caused by chemotherapy. Methods: This retrospective cohort study consecutively screened all patients who were positive for hepatitis B virus surface antigen and received chemotherapy for malignant diseases in a teaching hospital in Taiwan. Eligible patients were grouped according to whether they received nucleos(t) ide analogues before (prophylactic group) or during chemotherapy (historical control). Those who received antiviral prophylaxis were further classified by the medications that included lamivudine, telbivudine, entecavir and tenofovir. The incidence of hepatitis, liver decompensation and interruption of chemotherapy were audited. Results: A total of 212 consecutive patients were enrolled into analysis. Those who prophylactically used nucleos(t) ide analogues (n = 177) had significantly lower rates of liver decompensation (0.6% vs 20%, P < 0.01), interruption of chemotherapy (0% vs 40%, P < 0.01) and incidence of hepatitis (4.5% vs 100%, P < 0.01), as compared with their historical control (n = 35). In the prophylactic group, there was no difference among tenofovir, telbivudine, entecavir and lamivudine users in the incidence of hepatitis, liver decompensation and interruption of chemotherapy. Conclusion: Lamivudine, telbivudine, entecavir and tenofovir are all effective as the prophylactic antiviral therapy to prevent reactivation of hepatitis B induced by chemotherapy.