Department of Clinical Studies, Radiation Effects Research Foundation, Hiroshima, Japan.
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.
Clin Exp Nephrol. 2011 Oct;15(5):634-640. doi: 10.1007/s10157-011-0464-7. Epub 2011 Jun 1.
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.
近年来，人们发现乙型肝炎病毒（HBV）在免疫抑制治疗或化学治疗期间或之后会重新繁殖，由 HBV 再激活引起的肝炎现在被认为是一个严重的问题。HBV 再激活分为 HBsAg 和抗-HBe 阳性无症状携带者，以及 HBsAg 阴性、抗-HBc 低滴度阳性和/或抗-HBs 阳性已解决的 HBV 感染病例。尽管此类已解决的 HBV 病例被声称达到“临床治愈”，但现在人们认识到，肝脏或外周血单个核细胞内持续存在低水平的 HBV 产生，因此该感染现在被认为具有病毒学持续性。随着免疫抑制程度的加深，HBV 再激活的风险会增加，但近年来，利妥昔单抗联合含类固醇方案治疗恶性淋巴瘤的病例中，HBV 再激活的风险明显增加。特别是，在已解决 HBV 感染病例中，由 HBV 再激活引起的暴发性肝炎的发生率高于急性乙型肝炎。因此，对于所有使用免疫抑制治疗或化疗治疗方案的病例，筛查 HBV 感染并根据 HBV 相关标志物的状态进行适当的管理至关重要，旨在预防 HBV 再激活的发生。无论 HBsAg 状态如何，上述管理的基础都是在 HBV DNA 水平达到可检测水平时，使用具有强大抗病毒特性的核苷类似物进行治疗。
