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BACKGROUND It has been reported that temozolomide treatment for malignant glioma can lead to the reactivation of Hepatitis B virus (HBV) and fulminant hepatitis. However, the frequency of HBV reactivation and the preventative effect of entecavir remains unclear. In this study, we retrospectively reviewed clinical features of the cases treated by temozolomide for malignant glioma, focusing on the reactivation of HBV and the effect of entecavir. METHODS We screened 129 cases with newly diagnosed and recurrent malignant glioma for HBs antigen, HBs antibody and HBc antibody before the administration of temozolomide. HBV-DNA were quantified by real-time PCR in the HBV carrier and the cases with occult HBV infection. HBV- DNA were monitored every 1–3 months by real-time PCR during temozolomide treatment and 12 months after completion of temozolomide. Entecavir were started before temozolomide treatment to the HB carrier, and if HBV-DNA became detectable at follow-up to the cases with occult HBV infection. Results 2 (1.5%) and 20 (15%) of 129 cases were HB carrier and had occult HBV infection, respectively. HBV- DNA in both of HB carrier turned negative after administration of entecavir, but transiently turned positive again during temozolomide treatment. In the cases with occult HBV infection, 4 (20%) patients had HBV reactivation. HBV- DNA turned negative after starting entecavir without liver dysfunction. CONCLUSION HBV carrier and the cases with occult HBV infection were not rare in Japan, and HBV reactivation developed frequently during temozolomide treatment. Because pharmacological prevention of HBV reactivation with entecavir was effective, the screening and monitoring is indispensable in the treatment of malignant glioma with temozolomide.

COT-06 HBV REACTIVATION DURING AND AFTER THE TREATMENT OF MALIGNANT GLIOMA WITH TEMOZOLOMIDE