Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong SAR, China; Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China; State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong SAR, China; Department of Internal Medicine, Yonsei University College of Medicine, Seoul, South Korea; Insitute of Gastroenterology, Yonsei University College of Medicine, Seoul, South Korea; Liver Center, Severance Hospital, Seoul, South Korea.
Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong SAR, China; Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China; State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong SAR, China.
Clin Gastroenterol Hepatol. 2021 Sep;19(9):1950-1958.e7. doi: 10.1016/j.cgh.2020.08.064. Epub 2020 Sep 2.
It is unclear if anti-hepatitis B virus (HBV) treatment can eliminate incident hepatic decompensation. Here we report the incidence and predictors of hepatic decompensation among cirrhotic patients receiving antiviral therapy for chronic hepatitis B.
This is a post hoc analysis of two prospective HBV cohorts from Hong Kong and South Korea. Patients with liver stiffness measurement (LSM) ≥10 kPa and compensated liver disease at baseline were included. The primary endpoint was incident hepatic decompensation (jaundice or cirrhotic complications) with competing risk analysis.
818 patients (mean age, 54.9 years; 519 male [63.4%]) were included in the final analysis. During a mean follow-up of 58.1 months, 32 (3.9%) patients developed hepatic decompensation, among whom 34% were secondary to HCC. Three (0.4%) patients experienced variceal bleeding alone, 27 (3.3%) had non-bleeding decompensation and 13 (1.6%) had more than 2 decompensating events Baseline LSM, diabetes, alanine aminotransferase, platelet, total bilirubin, albumin, prothrombin time, and eGFR were independent predictors of hepatic decompensation. 30/506 (5.9%) patients fulfilling the Baveno VI criteria (LSM ≥20 kPa and/or platelet count <150ⅹ10/L) and 2/312 (0.6%) patients not fulfilling the criteria developed hepatic decompensation (P < .001).
Hepatic decompensation is uncommon but not eliminated in patients receiving antiviral therapy for HBV-related cirrhosis, and only a third of decompensating events are secondary to HCC. The Baveno VI criteria, which was originally designed to detect varices needing treatment, can be effectively applied in this population to identify patients at risk of decompensation.
目前尚不清楚抗乙型肝炎病毒（HBV）治疗是否可以消除新发肝失代偿。本研究报告了接受慢性乙型肝炎抗病毒治疗的肝硬化患者中肝失代偿的发生率和预测因素。
这是来自香港和韩国的两项前瞻性乙型肝炎队列研究的事后分析。纳入基线时肝脏硬度测量（LSM）≥10kPa 和代偿性肝病的患者。主要终点是采用竞争风险分析的新发肝失代偿（黄疸或肝硬化并发症）。
最终分析纳入 818 例患者（平均年龄 54.9 岁；519 例男性[63.4%]）。在平均 58.1 个月的随访期间，32 例（3.9%）患者发生肝失代偿，其中 34%继发于 HCC。3 例（0.4%）患者仅发生静脉曲张出血，27 例（3.3%）发生非出血性失代偿，13 例（1.6%）发生 2 次以上失代偿事件。基线 LSM、糖尿病、丙氨酸氨基转移酶、血小板、总胆红素、白蛋白、凝血酶原时间和 eGFR 是肝失代偿的独立预测因素。506 例符合 Baveno VI 标准（LSM≥20kPa 和/或血小板计数<150×10/L）的患者中有 30 例（5.9%）和 312 例不符合该标准的患者中有 2 例（0.6%）发生肝失代偿（P<0.001）。
在接受抗病毒治疗的乙型肝炎相关肝硬化患者中，肝失代偿并不常见，但不能消除，仅有三分之一的失代偿事件继发于 HCC。最初设计用于检测需要治疗的静脉曲张的 Baveno VI 标准可以有效地应用于该人群，以识别有失代偿风险的患者。
