ABSTRACT
Hepatitis B virus (HBV) reactivation has previously occurred in hepatitis B surface antigen-negative patients with malignant lymphoma who received rituximab-based combination chemotherapy. However, few reports have described cases of HBV reactivation in patients with multiple myeloma thus far. We report a case of HBV reactivation in a patient with multiple myeloma treated with chemotherapy, autologous hematopoietic stem cell transplantation, and maintenance steroid therapy. For the HBV reactivation, the patient was treated with the antiviral agent entecavir. The clinical symptoms and laboratory findings improved after 3 months. Further studies should target the identification of patients at high risk of HBV reactivation in multiple myeloma treated with autologous hematopoietic stem cell transplantation and steroid therapy for maintenance and establish viral prophylaxis strategies, especially in Korea, in which HBV infection is endemic.
Subject(s)
Humans , Drug Therapy , Drug Therapy, Combination , Hematopoietic Stem Cell Transplantation , Hepatitis B , Hepatitis B virus , Korea , Lymphoma , Multiple Myeloma , Prednisolone , TransplantationABSTRACT
BACKGROUND/AIMS: Silibinin, the main component of silymarin, is used as a hepatoprotectant and exhibits anticancer effects against various cancer cells. This study evaluated the effects of a combination of silibinin with either gefitinib or sorafenib on hepatocellular carcinoma (HCC) cells. METHODS: Several different human HCC cell lines were used to test the growth-inhibiting effects and cell toxicity of silibinin both alone and in combination with either gefitinib or sorafenib. The cell viability and growth inhibition were assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, trypan blue staining, and a colony-forming assay. Furthermore, changes in epidermal growth factor receptor (EGFR)-related signals were evaluated by Western blot analysis. RESULTS: Gefitinib, sorafenib, and silibinin individually exhibited dose-dependent antiproliferative effects on HCC cells. Combined treatment with silibinin enhanced the gefitinib-induced growth-inhibiting effects in some HCC cell lines. The combination effect of gefitinib and silibinin was synergistic in the SNU761 cell line, but was only additive in the Huh-BAT cell line. The combination effect may be attributable to inhibition of EGFR-dependent Akt signaling. Enhanced growth-inhibiting effects were also observed in HCC cells treated with a combination of sorafenib and silibinin. CONCLUSIONS: Combined treatment with silibinin enhanced the growth-inhibiting effects of both gefitinib and sorafenib. Therefore, the combination of silibinin with either sorafenib or gefitinib could be a useful treatment approach for HCC in the future.