A team of researchers led by Jeong Won Jang of the Department of Internal Medicine at the Catholic University of Korea in Seoul, has found that administering an antiviral drug would help prevent hepatitis B relapse in patients who are undergoing chemotherapy for the treatment of cancer.
In hepatocellular carcinoma (HCC), patients have a 55 percent chance of developing hepatitis B as a result of chemotherapy. Hepatocellular carcinoma or liver cancer is caused by hepatitis B virus. Now researchers say that giving antiviral drug lamivudine in order to prevent hepatitis B returning during chemotherapy will benefit patients in the long run. In the current study 36 patients with HCC were pretreated with lamivudine between January 2004 and February 2005.All these patients were on transarterial chemo-lipiodolization (TACL) chemotherapy. Another group of 37 patients who were undergoing chemotherapy were used as a control. The number of chemotherapy cycles was unlimited and went on till the tumors disappeared while lamivudine was continued for a year after the chemotherapy was stopped. It was found that 43 percent of the patients in the control group developed hepatitis B, while only 17 percent of the lamivudine group developed it. "Given that preemptive antiviral therapy ameliorates the hepatic morbidity seen during transarterial chemotherapy and facilitates further chemotherapy without disruptions in the treatment schedules, the expectation would be for an increased chance of survival with this approach," the authors conclude.
The study is published in the February 2006 issue of Hepatology, the official journal of the American Association for the Study of Liver Diseases (AASLD). Published by John Wiley & Sons, Inc., Hepatology is available online via Wiley InterScience at
Original Article: "A Randomized Controlled Study of Preemptive Lamivudine in Patients Receiving Transarterial Chemo-Lipiodolization," Jeong Won Jang, Jong Young Choi, Si Hyun Bae, Seung Kew Yoon, U Im Chang, Chang Wook Kim, Se Hyun Cho, Jun Yeol Han, Young Sok Lee, Hepatology; February 2006 (DOI: 10.1002.hep.21024).
Contact: David Greenberg
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