Division of Gastroenterology & Hepatology, Department of Internal Medicine III, Medical University of Vienna, Austria.
J Viral Hepat. 2012 Nov;19(11):801-10. doi: 10.1111/j.1365-2893.2012.01601.x. Epub 2012 Mar 15.
Data on the efficacy of lamivudine (LAM)-, tenofovir (TDF)- and emtricitabine (FTC)-based antiretroviral therapy (HAART) in HBV-HIV coinfection are limited. We completed a retrospective analysis of HBV-HIV-coinfected patients treated at the Medical University of Vienna. One-hundred and ten coinfected patients were included, with 57% being initially HBV e-Antigen (HBeAg) positive. Baseline HBV load was significantly higher in HBeAg+ than in HBeAg- patients (5962 ± 3663 vs 20 ± 19 × 10(6) IU/mL; P < 0.0001). Over a median observation period of 83 month (range: 26-183), 87% received HAART and 91% showed a suppression of HBV replication. After 5 years of continuous treatment, HBeAg seroconversion was achieved in 21% of LAM-, 50% of TDF- (P = 0.042 vs LAM) and in 57% of TDF + FTC (P = 0.008 vs LAM)-treated patients, respectively. HBsAg loss after 5 years was found in 8% (LAM), 25% (TDF; P = 0.085 vs LAM) and 29% (TDF + FTC; P = 0.037 vs LAM) of HBeAg+ patients. In HBeAg- patients, HBsAg loss was achieved in 11% (LAM), 27% (TDF; P = 0.263 vs LAM) and 36% (TDF + FTC; P = 0.05 vs LAM), respectively. Pretreatment CD4+ counts did not influence rates of HBeAg seroconversion and of HBsAg loss. Patients with HBsAg loss had lower baseline HBV-DNA levels and higher AST/ALT levels than patients without HBsAg loss. Transient HAART-related hepatotoxicity was found in 32% (Grade I: 21%; II:7%; III:2%; IV:0%). Most HBV-HIV-coinfected patients achieve complete suppression of HBV replication despite high baseline viremia. TDF-based HAART leads to high rates of HBeAg seroconversion and HBsAg loss after 5 years of continuous exposure. One-third of HBV-HIV-coinfected patients may experience transient HAART-related hepatotoxicity.
在乙型肝炎病毒（HBV）-人类免疫缺陷病毒（HIV）合并感染患者中，有关拉米夫定（LAM）、替诺福韦（TDF）和恩曲他滨（FTC）为基础的抗逆转录病毒治疗（HAART）疗效的数据有限。我们对维也纳医科大学治疗的 HBV-HIV 合并感染患者进行了回顾性分析。共纳入 110 例合并感染患者，其中 57%的患者初始 HBV e 抗原（HBeAg）阳性。HBeAg+患者的基线 HBV 载量明显高于 HBeAg-患者（5962 ± 3663 与 20 ± 19×106 IU/mL；P < 0.0001）。中位观察期 83 个月（范围：26-183）内，87%的患者接受了 HAART，91%的患者显示 HBV 复制得到抑制。经过 5 年的连续治疗，LAM、TDF 和 TDF+FTC 治疗组中分别有 21%、50%（P = 0.042 与 LAM）和 57%（P = 0.008 与 LAM）的 HBeAg+患者实现了 HBeAg 血清学转换。5 年后，LAM、TDF 和 TDF+FTC 治疗组中分别有 8%（LAM）、25%（TDF；P = 0.085 与 LAM）和 29%（TDF+FTC；P = 0.037 与 LAM）的 HBsAg 转阴。在 HBeAg-患者中，LAM、TDF 和 TDF+FTC 治疗组中分别有 11%（LAM）、27%（TDF；P = 0.263 与 LAM）和 36%（TDF+FTC；P = 0.05 与 LAM）的患者 HBsAg 转阴。治疗前 CD4+计数对 HBeAg 血清学转换和 HBsAg 丢失率无影响。HBsAg 丢失患者的基线 HBV-DNA 水平较低，AST/ALT 水平较高。HAART 相关的肝毒性有 32%（I 级：21%；II 级：7%；III 级：2%；IV 级：0%）。尽管基线病毒载量较高，但大多数 HBV-HIV 合并感染患者的 HBV 复制得到完全抑制。TDF 为基础的 HAART 可导致 HBeAg 血清学转换和 HBsAg 丢失，5 年连续暴露后发生率较高。三分之一的 HBV-HIV 合并感染患者可能出现短暂的 HAART 相关肝毒性。
