Lee W C, Wu M J, Cheng C H, Chen C H, Shu K H, Lian J D
Department of Internal Medicine, Division of Nephrology, Taichung Veterans General Hospital, Chung-Shan Medical and Dental College, Taichung, Taiwan.
Am J Kidney Dis. 2001 Nov;38(5):1074-81. doi: 10.1053/ajkd.2001.28607.
Lamivudine is a potent inhibitor of hepatitis B virus (HBV) replication. The aim of this study is to elucidate the effectiveness of lamivudine for the treatment of HBV reactivation with or without fulminant hepatic failure in renal transplant recipients. Forty-two renal transplant recipients (30 men, 12 women) were enrolled onto this study. Eight patients presented with HBV reactivation without fulminant hepatic failure and were administered lamivudine (group I), 5 patients presented with HBV and hepatic failure and were administered lamivudine (group II), 5 patients presented with HBV and hepatic failure but were not administered lamivudine (group III), and 24 patients were asymptomatic HBV carriers who were not administered lamivudine (group IV). Lamivudine was administered at a dose of 100 or 150 mg once daily. A greater prevalence of recent use of a combination of antilymphocyte immunoglobulin (ALG) and methylprednisolone (MP) occurred in patients with hepatic failure (groups II and III) than those without hepatic failure (30% versus 6.3%; P = 0.043). However, there was no significant difference in the incidence of MP use alone (20% versus 25%; P = 0.746). Mortality rates for groups I, II, and III were significantly different (12.5%, 40%, 100%; P = 0.008). One patient in group I died of sepsis without evidence of HBV DNA, even in the terminal event. In group II, 3 of 5 patients (60%) were rescued by lamivudine therapy. In group III, without lamivudine treatment, there was a 100% mortality rate despite intensive plasmapheresis. HBV DNA was not detectable after lamivudine treatment in 7 of 8 patients in group I and 3 of 5 patients in group II. Creatinine levels did not change significantly during lamivudine treatment. Hepatitis B surface antigen and hepatitis B e antigen seroconversion rates after lamivudine treatment were 7.7% and 37.5%, respectively. We conclude that ALG is a potent trigger of HBV-related fulminant hepatic failure in renal transplant recipients, whereas lamivudine is an effective and lifesaving treatment. Prompt use of lamivudine is recommended in renal transplant recipients with evidence of HBV reactivation to prevent catastrophic fulminant hepatic failure.
拉米夫定是一种强效的乙型肝炎病毒(HBV)复制抑制剂。本研究的目的是阐明拉米夫定对肾移植受者中出现或未出现暴发性肝衰竭的HBV再激活的治疗效果。42例肾移植受者(30例男性,12例女性)纳入本研究。8例出现无暴发性肝衰竭的HBV再激活患者接受拉米夫定治疗(I组),5例出现HBV及肝衰竭的患者接受拉米夫定治疗(II组),5例出现HBV及肝衰竭但未接受拉米夫定治疗的患者(III组),24例无症状HBV携带者未接受拉米夫定治疗(IV组)。拉米夫定的给药剂量为每日100或150mg一次。肝衰竭患者(II组和III组)中近期联合使用抗淋巴细胞免疫球蛋白(ALG)和甲基泼尼松龙(MP)的比例高于无肝衰竭患者(30%对6.3%;P = 0.043)。然而,单独使用MP的发生率无显著差异(20%对25%;P = 0.746)。I组、II组和III组的死亡率有显著差异(12.5%、40%、100%;P = 0.008)。I组中有1例患者死于败血症,即使在终末期事件中也未检测到HBV DNA。在II组中,5例患者中有3例(60%)通过拉米夫定治疗获救。在III组中,未接受拉米夫定治疗,尽管进行了强化血浆置换,死亡率仍为100%。I组8例患者中有7例和II组5例患者中有3例在拉米夫定治疗后检测不到HBV DNA。拉米夫定治疗期间肌酐水平无显著变化。拉米夫定治疗后乙肝表面抗原和乙肝e抗原血清学转换率分别为7.7%和37.5%。我们得出结论,ALG是肾移植受者中HBV相关暴发性肝衰竭的强效触发因素,而拉米夫定是一种有效且挽救生命的治疗方法。建议对有HBV再激活证据的肾移植受者及时使用拉米夫定,以预防灾难性的暴发性肝衰竭。