Department of Medicine and Geriatrics, United Christian Hospital, Kwun Tong, Kowloon, Hong Kong.
Hong Kong Med J. 2011 Oct;17(5):376-80.
OBJECTIVE. To serially evaluate the viral kinetics of occult hepatitis B virus infection in lymphoma patients and perform a correlation with clinical outcomes. DESIGN. Case series with 1-year follow-up. SETTING. Regional hospital, Hong Kong. PATIENTS. Consecutive patients who were newly diagnosed to have lymphoma in the hospital between 1 April 2007 and 31 March 2008 were tested for hepatitis B (HB) surface (s) antigen (Ag), anti-HBs antibody (Ab) and anti-HB core (c) Ab. Seropositive occult hepatitis B patients as defined by being negative for HBsAg but positive anti-HBsAb and/or anti-HBcAb without a hepatitis B vaccination history were recruited. Serum HBsAg, anti-HBsAb, anti-HBcAb, hepatitis B virus deoxyribonucleic acid (DNA) level, and liver biochemistry were checked at baseline and every 4 weeks during and after chemotherapy until 12 months after the completion of chemotherapy or death. Entecavir was started if patients developed biochemical flare-up of hepatitis B associated with virological rebound. The prevalence and course of hepatitis B virus-related hepatitis, as well as any temporal relationship to viral kinetics and clinical hepatitis, were assessed. RESULTS. Of 47 patients tested, 10 (21%) with lymphoma were seropositive occult hepatitis carriers. Their median baseline hepatitis B virus DNA level was 89 IU/mL (range, <34-807 IU/mL). Virological rebound (as defined by a 10-fold increase in serum hepatitis B virus DNA level from pre-chemotherapy level persisted for 4 weeks) occurred in one of the 10 patients, followed by biochemical reactivation. Whereupon entecavir treatment was started and no liver failure ensued. Regarding the other seropositive occult patients, their serum hepatitis B virus DNA levels fluctuated, but there was no associated biochemical reactivation. CONCLUSION. Detectable baseline serum hepatitis B virus DNA is not uncommon in patients with occult hepatitis B who receive chemotherapy. Transient elevation in serum hepatitis B virus DNA levels does not predict biochemical reactivation, but antiviral treatment might be considered if virological rebound persists.
连续评估淋巴瘤患者隐匿性乙型肝炎病毒感染的病毒动力学，并与临床结果进行相关性分析。
1 年随访的病例系列。
香港地区医院。
2007 年 4 月 1 日至 2008 年 3 月 31 日期间在医院新诊断为淋巴瘤的连续患者接受了乙型肝炎（HB）表面（s）抗原（Ag）、抗-HBs 抗体（Ab）和抗-HB 核心（c）Ab 检测。定义为 HBsAg 阴性但具有抗-HBsAb 和/或抗-HBcAb 阳性且无乙型肝炎疫苗接种史的血清阳性隐匿性乙型肝炎患者被招募。在基线时和化疗期间及之后每 4 周检查血清 HBsAg、抗-HBsAb、抗-HBcAb、乙型肝炎病毒脱氧核糖核酸（DNA）水平和肝功能，直至化疗完成后 12 个月或死亡。如果患者出现乙型肝炎病毒相关肝炎的生化发作伴有病毒学反弹，则开始使用恩替卡韦。评估乙型肝炎病毒相关肝炎的发生率和病程，以及与病毒动力学和临床肝炎的任何时间关系。
在 47 例接受检测的患者中，10 例（21%）淋巴瘤患者为血清阳性隐匿性乙型肝炎携带者。他们的中位基线乙型肝炎病毒 DNA 水平为 89IU/mL（范围，<34-807IU/mL）。病毒学反弹（定义为血清乙型肝炎病毒 DNA 水平从化疗前水平增加 10 倍并持续 4 周）发生在 10 例患者中的 1 例，随后出现生化再激活。于是开始使用恩替卡韦治疗，没有导致肝功能衰竭。对于其他血清阳性隐匿性患者，他们的血清乙型肝炎病毒 DNA 水平波动，但没有相关的生化再激活。
接受化疗的隐匿性乙型肝炎患者中，可检测到的基线血清乙型肝炎病毒 DNA 并不少见。血清乙型肝炎病毒 DNA 水平的短暂升高并不能预测生化再激活，但如果病毒学反弹持续存在，可能需要考虑抗病毒治疗。
