• breast cancer
• hepatitis B
• lamivudine
• prophylaxis antiviral therapy
• reactivation

In the past few decades, chronic hepatitis B (CHB) has evolved from a disease that was untreatable and progressive, to one that can be easily controlled with antiviral therapy. However, patients with severe liver disease still remain difficult to treat despite the availability of highly potent nucleos(t)ide analogs. These include those with underlying cirrhosis, severe flares of CHB, hepatocellular carcinoma (HCC), and for those undergoing liver transplantation. For those with established cirrhosis, antiviral therapy should be considered for all, as unpredictable flares can still occur, which can be fatal for those with advanced chronic liver disease. However, even with effective viral suppression, the development of HCC can still occur. For patients with severe flares of CHB, although the use of antiviral can improve long term outcomes, a significant proportion may still die without liver transplantation. The short term prognosis of these patients is dependent on both the severity of flare and underlying pre-existing liver disease. In patients with decompensated cirrhosis, liver failure secondary to severe flares, or those with HCC, liver transplantation may be curative. After liver transplantation, long term antiviral therapy is required to prevent graft loss from recurrent hepatitis B infection. The use of hepatitis B immune globulin (HBIG) in combination with an oral antiviral agent has been the mainstay of post-transplant antiviral regimen for over a decade. With newer and more potent antiviral agents such as tenofovir and entecavir, use of these agents along with HBIG have demonstrated to be effective in preventing significant recurrence in the long term.

• Antiviral therapy
• Cirrhosis
• Liver failure
• Liver transplantation
• Hepatocellular carcinoma

• Antiviral Agents/therapeutic use
• Carcinoma, Hepatocellular/diagnosis
• Carcinoma, Hepatocellular/drug therapy
• Carcinoma, Hepatocellular/virology
• Disease Progression
• Drug Resistance, Viral
• Hepatitis B virus/drug effects
• Hepatitis B virus/pathogenicity
• Hepatitis B, Chronic/complications
• Hepatitis B, Chronic/diagnosis
• Hepatitis B, Chronic/drug therapy
• Hepatitis B, Chronic/virology
• Humans
• Liver Cirrhosis/diagnosis
• Liver Cirrhosis/drug therapy
• Liver Cirrhosis/virology
• Liver Neoplasms/diagnosis
• Liver Neoplasms/drug therapy
• Liver Neoplasms/virology
• Liver Transplantation
• Recurrence
• Severity of Illness Index
• Time Factors
• Treatment Outcome
• Virus Activation

AIM: To understand the impact of different initial hepatitis B virus (HBV) DNA copies on the efficacy and side effects of chemotherapy combined with antiviral therapy in tumor patients with hepatitis B.

METHODS: Eighty-seven tumor patients with HBV infection were randomly divided into two groups according to the initial HBV DNA copies: A and B. Group A included 44 patients with the initial HBV DNA copies ≥ 1 × 10³ GE/mL, while group B included 43 patients with the initial HBV DNA copies < 1×10³ GE/mL. All of the patients had been treated with antiviral therapy for one month before conventional chemotherapy and continued to receive antiviral therapy for three months after chemotherapy.

RESULTS: The Karnofsky performance status (KPS) score was significantly higher in group B than in group A. The short-term therapeutic effects were similar between groups A and B, while in terms of long-term efficacy, the disease progression and death risk at 6 mo after chemotherapy were significantly lower in group B than in group A. The rate of related side effects did not increase significantly during chemotherapy combined with antiviral therapy.

CONCLUSION: For tumor patients with HBV infection, chemotherapy combined with antiviral therapy is superior to chemotherapy alone in terms of improving the KPS score and side effects.

• Tumors
• Hepatitis B virus
• HBV DNA copies
• Chemotherapy combined with antiviral therapy

Reactivation of hepatitis B virus (HBV) is a frequent complication of chemotherapy in patients with HBV infection. Reactivation is characterized by increased levels of serum HBV DNA, abnormal liver function and hepatic failure. HBV reactivation inevitably leads to disruption of chemotherapy and severe clinical results in some cases. Nucleoside analogues play an important role in preventing and reducing the risk for HBV reactivation and HBV-associated morbidity and mortality. This paper gives a systematic review of the definition, mechanism and causes of HBV reactivation and summarizes the principles and problems for antiviral treatment in patients with HBV reactivation. It is strongly recommended that all patients should be screened for HBV serum markers before chemotherapy and preventive therapy with nucleoside analogues be given in patients with HBV. The use of potent antiviral drugs with low resistance potential and close viral monitoring during therapy are important for patients with HBV infection undergoing chemotherapy.

• Hepatitis B virus
• Chemotherapy
• Reactivation
• Antiviral treatment