Department of Liver Disease, The Second Hospital of Nanjing, Nanjing University of Chinese Medicine, Nanjing, China.
Department of Clinical Research Centre, The Second Hospital of Nanjing, Nanjing University of Chinese Medicine, Nanjing, China.
Front Cell Infect Microbiol. 2023 Jan 12;12:1053608. doi: 10.3389/fcimb.2022.1053608. eCollection 2022.
Effective antiviral therapy can significantly improve the long-term prognosis of HBV-related decompensated patients, and re-compensation may be achieved in part of the patients. To explore the re-compensation of ascites after HBV suppression and the risk factors, the clinical outcomes of 196 consecutive patients with HBV-related first decompensated cirrhosis of ascites treated with nucleos(t)ide analogue (NUC) were analyzed retrospectively. Among these patients, the median serum HBV DNA level was 5.0 (IQR, 3.0-6.0) log IU/mL before treatment. Most patients were given NUC with high barrier to resistance including ETV (152), TDF (1) and TAF (1). Initial combination of LAM plus ADV and LdT plus ADV was used in 41 patients and 1 patients, respectively. After NUC treatment, the percentage of patients with ascites regression was 77.6%, 81.4%, 70.5%, 93.8%, 80.8% at 12, 24, 36, 48, 60 months, respectively (P<0.001). The distribution of ascites severity showed that the patients' ascites improved, with the proportion of no ascites and mild ascites gradually increased. The proportion of re-compensation of ascites defined as negative HBV DNA, improved liver function and ascites regression (off diuretics) was 59.7%, 70.0%, 52.3%, 59.4%, 46.2% at 12, 24, 36, 48, 60 months (P<0.001). The rate of ascites regression was higher in viral response (VR) cohort when compared with that in non-VR cohort. Univariate and multivariable analysis showed that level of serum ALT (OR:0.988, 95%CI, p=0.029) and load of serum HBV DNA (OR:0.78895%CI, p=0.044) at baseline were risk factors of re-compensation of ascites. This study demonstrated that antiviral therapy could reverse decompensation of ascites in HBV-related first decompensated cirrhosis and the level of ALT and HBV DNA were risk factors of ascites re-compensation.
抗病毒治疗可显著改善乙型肝炎病毒（HBV）相关失代偿患者的长期预后，部分患者可实现再代偿。为了探讨 HBV 抑制后腹水再代偿及其相关因素，本研究回顾性分析了 196 例接受核苷（酸）类似物（NUC）治疗的 HBV 相关首次失代偿性肝硬化腹水患者的临床转归。这些患者的中位血清 HBV DNA 水平在治疗前为 5.0（IQR，3.0-6.0）log IU/mL。大多数患者接受了高耐药屏障的 NUC 治疗，包括恩替卡韦（ETV）（152 例）、替诺福韦酯（TDF）（1 例）和替比夫定（TAF）（1 例）。初始联合应用拉米夫定（LAM）+阿德福韦酯（ADV）和恩替卡韦（ETV）+替诺福韦酯（TDF）分别用于 41 例和 1 例患者。NUC 治疗后，12、24、36、48、60 个月时腹水消退患者比例分别为 77.6%、81.4%、70.5%、93.8%和 80.8%（P<0.001）。腹水严重程度的分布表明，患者腹水改善，无腹水和轻度腹水的比例逐渐增加。HBV DNA 阴性、肝功能改善和腹水消退（停用利尿剂）定义为腹水再代偿的比例分别为 59.7%、70.0%、52.3%、59.4%和 46.2%（P<0.001）。病毒学应答（VR）组腹水消退率高于非 VR 组。单因素和多因素分析显示，基线时血清丙氨酸氨基转移酶（ALT）水平（OR：0.988，95%CI，p=0.029）和血清 HBV DNA 载量（OR：0.78895%CI，p=0.044）是腹水再代偿的危险因素。本研究表明，抗病毒治疗可逆转 HBV 相关首次失代偿性肝硬化腹水的失代偿，ALT 水平和 HBV DNA 载量是腹水再代偿的危险因素。
