BACKGROUND AND AIMS: Exacerbation of liver damage during transhepatic arterial infusion chemotherapy (THAIC) is a critical complication in patients with hepatitis B virus (HBV) related hepatocellular carcinoma (HCC). We previously reported that HBe antigen positivity was the associating factor for the exacerbation of liver damage. In the present study, we investigated the effect of lamivudine administration for exacerbation of liver damage in such patients. PATIENTS AND METHODS: Seventeen patients with HBV-related hepatocellular carcinoma who received THAIC were reviewed. Eight of these patients received lamivudine administration. Nine patients did not receive lamivudine administration. All patients were HBe antigen positive. Liver function tests, liver enzymes, HBV-DNA levels, HBe antigen, HBe antibody, and mutation in the precore and core-promoter regions of HBV DNA were evaluated. RESULTS: In the lamivudine-treated group, HBV-DNA levels were significantly reduced and did not increase throughout chemotherapy. Lamivudine did not induce any changes in precore or core-promoter regions. Although levels of alanine aminotransferase (ALT), asparate aminotransferase (AST), total bilirubin, and prothrombin time (PT) in the lamivudine-treated group did not change, levels of ALT, AST and total bilirubin increased, and PT were prolonged in the untreated group by chemotherapy. No patients receiving lamivudine administration showed exacerbation of liver damage. Exacerbation of liver damage was detected in six patients without lamivudine administration. Of these, three patients died of progressive liver failure due to reactivation of HBV. CONCLUSION: These results indicate that prophylactic lamivudine administration reduces HBV-DNA levels and prevents exacerbation of liver damage throughout the period of chemotherapy in HBe antigen positive patients with hepatocellular carcinoma.
BACKGROUND AND AIMS: Exacerbation of liver damage during transhepatic arterial infusion chemotherapy (THAIC) is a critical complication in patients with hepatitis B virus (HBV) related hepatocellular carcinoma (HCC). We previously reported that HBe antigen positivity was the associating factor for the exacerbation of liver damage. In the present study, we investigated the effect of lamivudine administration for exacerbation of liver damage in such patients. PATIENTS AND METHODS: Seventeen patients with HBV-related hepatocellular carcinoma who received THAIC were reviewed. Eight of these patients received lamivudine administration. Nine patients did not receive lamivudine administration. All patients were HBe antigen positive. Liver function tests, liver enzymes, HBV-DNA levels, HBe antigen, HBe antibody, and mutation in the precore and core-promoter regions of HBV DNA were evaluated. RESULTS: In the lamivudine-treated group, HBV-DNA levels were significantly reduced and did not increase throughout chemotherapy. Lamivudine did not induce any changes in precore or core-promoter regions. Although levels of alanine aminotransferase (ALT), asparate aminotransferase (AST), total bilirubin, and prothrombin time (PT) in the lamivudine-treated group did not change, levels of ALT, AST and total bilirubin increased, and PT were prolonged in the untreated group by chemotherapy. No patients receiving lamivudine administration showed exacerbation of liver damage. Exacerbation of liver damage was detected in six patients without lamivudine administration. Of these, three patients died of progressive liver failure due to reactivation of HBV. CONCLUSION: These results indicate that prophylactic lamivudine administration reduces HBV-DNA levels and prevents exacerbation of liver damage throughout the period of chemotherapy in HBe antigen positive patients with hepatocellular carcinoma.
Authors: Rohit Loomba; Ayana Rowley; Robert Wesley; T Jake Liang; Jay H Hoofnagle; Frank Pucino; Gyorgy Csako Journal: Ann Intern Med Date: 2008-04-01 Impact factor: 25.391