Jochum C, Maischack F, Anastasiou O E, Verheyen J, Timm J, Bechmann L, Gerken G, Canbay A
Gastroenterology and Hepatology, University Hospital Essen, Germany.
Institute for Virology, University Hospital Essen, Germany.
Z Gastroenterol. 2016 Dec;54(12):1306-1311. doi: 10.1055/s-0042-120418. Epub 2016 Dec 9.
Acute hepatitis B virus (HBV) infection is still a major cause of acute liver failure (ALF), necessitating a high rate of emergency liver transplantation (LTx). Acute infection is followed by high viral replication rates leading to hepatocyte death and, ultimately, ALF. The objective of treating HBV-induced ALF thus is to eliminate, or significantly suppress, HBV replication and therefore reduce cell death and support regeneration. In this retrospective study, we want to evaluate the timing, the safety, and the long-term virological outcome of this approach. In this study, we included 32 patients (16 female and 16 males; median age 39.5 years) with ALF due to hepatitis B, who were transferred to the university hospital Essen, Germany between January 2009 and December 2013. Before treatment, transaminases were highly elevated, bilirubin was increased, and elevated international normalized ratio (INR) revealed impaired liver function. HBV-DNA and HBsAg were positive. All 32 patients received oral antiviral treatment (3 lamivudine, 21 entecavir, and 8 tenofovir) between 1 day and 4 months after diagnosis of acute hepatitis B. One patient died, 2 were transplanted, one died shortly after LTx the other patient survived after LTx. These 3 patients received treatment in a state of advanced liver failure, and 1 patient 4 months after initial diagnosis of hepatitis B. Twenty-nine patients survived without LTx. Five patients were discharged without further follow-up. All 24 remaining patients became HBV-DNA negative in median of 100 days. Twenty-two patients were followed further, and all patients lost their HBsAg in median of 108 days. Sixteen of the 22 patients experienced a seroconversion to anti-HBs in median of 137 days. Four patients who were followed for 1 more year after HBsAg did not develop anti-HBs. None of the patients developed chronic hepatitis B. Immediate treatment of HBV-induced ALF with nucleos(t)id-analogues (NUCs) appears save and prevents LTx and death, and there is no indication for increased chronicity.
急性乙型肝炎病毒（HBV）感染仍是急性肝衰竭（ALF）的主要病因，这使得紧急肝移植（LTx）的比例居高不下。急性感染后病毒复制率很高，导致肝细胞死亡，最终引发急性肝衰竭。因此，治疗HBV诱导的急性肝衰竭的目标是消除或显著抑制HBV复制，从而减少细胞死亡并支持肝脏再生。在这项回顾性研究中，我们希望评估这种治疗方法的时机、安全性和长期病毒学结果。在本研究中，我们纳入了32例因乙型肝炎导致急性肝衰竭的患者（16例女性和16例男性；中位年龄39.5岁），这些患者于2009年1月至2013年12月期间被转至德国埃森大学医院。治疗前，转氨酶高度升高，胆红素增加，国际标准化比值（INR）升高表明肝功能受损。HBV-DNA和HBsAg均为阳性。所有32例患者在诊断为急性乙型肝炎后1天至4个月内接受了口服抗病毒治疗（3例使用拉米夫定，21例使用恩替卡韦，8例使用替诺福韦）。1例患者死亡，2例接受了肝移植，1例在肝移植后不久死亡，另1例肝移植后存活。这3例患者在晚期肝衰竭状态下接受治疗，1例在初次诊断乙型肝炎4个月后接受治疗。29例患者未进行肝移植而存活。5例患者出院后未进一步随访。其余24例患者的HBV-DNA中位数在100天内转为阴性。22例患者接受了进一步随访，所有患者的HBsAg中位数在108天内消失。22例患者中有16例在中位数137天内发生抗-HBs血清学转换。4例在HBsAg消失后又随访1年的患者未出现抗-HBs。所有患者均未发展为慢性乙型肝炎。用核苷（酸）类似物（NUCs）立即治疗HBV诱导的急性肝衰竭似乎是安全的，可避免肝移植和死亡，且没有慢性化增加的迹象。
