Reactivation of HBV refers to a rise in the hepatitis B viral load caused by immunosuppression or chemotherapy in a patient with HBV infection. Reactivation of HBV is classified into reactivation from the carrier state Akt inhibitor and reactivation in a patient with resolved HBV infection (HBsAg negative, and anti-HBc antibody or anti-HBs antibody positive). Hepatitis associated with reactivation in a patient with resolved HBV infection is called “de novo hepatitis B”. Not only is severe disease common in cases of hepatitis associated with reactivation of HBV, but also treatment of concurrent conditions is made difficult by the onset of hepatitis, so it is extremely
important to prevent the onset of hepatitis itself. The basic strategy for prevention and treatment of HBV reactivation associated with powerful immunosuppressant or chemotherapy regimens should follow the guidelines summarized below, based
on the “Guidelines for the prevention of hepatitis B virus reactivation in patients receiving immunosuppressive therapy or chemotherapy (Revised version)”[310, 311] produced by an MHLW study group (Fig. 7). An MHLW study group currently conducting a multicenter nationwide prospective clinical trial of preemptive antiviral therapy to prevent BMS-354825 HBV reactivation during treatment of malignant lymphoma with rituximab has published the results of interim analyses.[312] As for HBV reactivation caused
by immunosuppressive and anti-cancer therapies rather than rituximab, the MHLW “HBV Reactivation through Immunosuppressive and/or Anti-cancer Therapies” research group has also reported its results.[313] Furthermore, the Japan College of Rheumatology has MCE公司 published “A proposal for management of rheumatic disease patients with hepatitis B virus infection receiving immunosuppressive therapy”.[314] The risk of reactivation of HBV is mainly governed by the HBV infection status and the degree of immunosuppression. The HBV infection status is classified into chronic active hepatitis, inactive carrier, and resolved infection. This corresponds to the risk of reactivation in descending order. There is no evidence available concerning asymptomatic carriers in the immune tolerance phase, the incidence of further activation of HBV, or whether NA therapy can prevent activation. The risks of HBV reactivation and the onset of hepatitis or fulminant hepatitis vary with the exact immunosuppressant or chemotherapy agents used, and the incidences of these events are unclear. When immunosuppressive therapy or chemotherapy including powerful agents such as rituximab is administered, careful attention should be paid to the possibility of reactivation in HBsAg positive patients including inactive carriers, and patients with resolved infection.