title: Prevention of hepatitis B virus reactivation in immunosuppressive therapy or chemotherapy.
abstract: In recent years, hepatitis B virus (HBV) has been found to reproliferate either during or following immunosuppressive therapy or chemotherapy, with hepatitis caused by HBV reactivation now considered a serious issue. HBV reactivation is categorized into occurrence in HBsAg- and anti-HBe-positive asymptomatic carriers, and in HBsAg-negative, anti-HBc low-titer-positive, and/or anti-HBs-positive resolved HBV infection cases. Despite the fact that "clinical cure" is claimed for such resolved HBV cases, low levels of ongoing HBV production are now recognized as being sustained within the liver or in peripheral blood mononuclear cells, with the infection thus now considered to be virologically persistent. The risk of HBV reactivation rises as the level of immunosuppression intensifies, but in recent years HBV reactivation risk has been clearly shown to increase in cases of rituximab plus steroid-containing regimen for treatment of malignant lymphoma. In particular, the incidence of fulminant hepatitis caused by HBV reactivation in cases with resolved HBV infection is reported to be higher than that brought about by acute hepatitis B. Therefore, for all cases in which immunosuppressive therapy or chemotherapy treatment regimens are used, screening for HBV infection and appropriate management in accordance with the status of HBV-related markers are crucial, aimed at preventing occurrence of HBV reactivation. The foundation of the aforementioned management, regardless of HBsAg status, is administration of nucleoside analogues, with their powerful anti-viral properties, when HBV DNA levels reach detectable levels.
authors.affiliation: Department of Clinical Studies, Radiation Effects Research Foundation, Hiroshima, Japan.
authors.forename: Waka
authors.initials: W
authors.lastname: Ohishi
authors.affiliation: Department of Medicine and Molecular Science, Division of Frontier Medical Science, Programs for Biomedical Research, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima, 734-8551, Japan. chayama@mba.ocn.ne.jp.
authors.forename: Kazuaki
authors.initials: K
authors.lastname: Chayama
mesh_terms: D058846:Antibodies, Monoclonal, Murine-Derived / Q000009:adverse effects; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000009:adverse effects*; D004279:DNA, Viral / Q000097:blood; D005938:Glucocorticoids / Q000009:adverse effects; D006509:Hepatitis B / Q000517:prevention & control*; D006510:Hepatitis B Antibodies / Q000032:analysis; D006514:Hepatitis B Surface Antigens / Q000032:analysis; D006513:Hepatitis B e Antigens / Q000276:immunology; D006515:Hepatitis B virus / Q000187:drug effects / Q000235:genetics / Q000276:immunology*; D006801:Humans; D007165:Immunosuppression Therapy / Q000009:adverse effects*; D008223:Lymphoma / Q000188:drug therapy; D000069283:Rituximab; D014775:Virus Activation / Q000276:immunology*
chemical_list: D058846:Antibodies, Monoclonal, Murine-Derived; D004279:DNA, Viral; D005938:Glucocorticoids; D006510:Hepatitis B Antibodies; D006514:Hepatitis B Surface Antigens; D006513:Hepatitis B e Antigens; D000069283:Rituximab