[英语，研究]Tenofovir Improves Outcomes of HBV Acute-on-Chronic Liver Failu

StephenW

Tenofovir  Improves Outcomes of HBV Acute-on-Chronic Liver Failure
                  

SUMMARY                                                  Treatment with tenofovir (Viread) lowers HBV viral load,reduces liver injury, and decreases the risk of death  in patients with acute-on-chronic liver failure due to  hepatitis B reactivation.

                  
               
              
            
            

                   By   Liz Highleyman
                  Spontaneous reactivation of chronic hepatitis B virus (HBV) infection  can cause acute-on-chronic liver failure (ACLF), or sudden        worsening of liver disease in people who already have chronic  viral hepatitis. Liver transplantation is an accepted treatment for acute liver failure, but donor livers are in short supply and antiviral therapy would be an attractive option.
As reported in the March 2011 issue of Hepatology, Hitendra Garg and colleagues  in India evaluated the efficacy of tenofovir   -- one of most potent nucleoside/nucleotide analogs approved  for hepatitis B treatment -- and looked at predictors of mortality  in patients with ACLF. Prior research has indicated that the      older hepatitis B drug lamivudine (Epivir-HBV) is not effective for this purpose.
The study population included 27 patients with ACLF due to spontaneous  HBV reactivation who were randomly assigned to receive either   tenofovir or placebo. Most (72%) were men and the median age was 45 years. At baseline the median HBV DNA viral load was level was 900,000 IU/mL and 56% were hepatitis B "e" antigen positive.
All patients were followed for at least 3 months or until death. The primary endpoint was survival at 3 months. Liver transplants were unavailable.
  Results
                  

	At  3 months, the probability of survival was significantly  higher in the tenofovir group compared with the placebo group (57% vs 15%, respectively).
	The   typical cause of death was progressive liver failure leading    to multi-organ failure.
	HBV DNA levels declined significantly in the tenofovir group, but remained stable in the placebo group.
	After  3 months follow-up, 60% of patients in the tenofovir group   experienced HBeAg loss, compared with none in the placebo  group.
	Surviving  patients taking tenofovir experienced significant improvement   in Child-Turcotte-Pugh (CTP) and MELD liver disease scores,but these did not change in placebo group.
	Having  more than a 2 log reduction in HBV DNA at week 2 was an independent predictor of survival.

                  
               
              
            
"Tenofovir significantly reduces HBV DNA levels, improves CTP and MELD scores,   and reduces mortality in patients with severe spontaneous reactivation  of chronic hepatitis B presenting as ACLF," the researchersconcluded. "Reduction in HBV DNA levels at 2 weeks should be  a desirable goal and is a good predictor of survival."
"The pathogenesis of severe acute exacerbation is believed to be associated        with vigorous immune response, which results in severe hepatic necro-inflammation  and finally hepatic decompensation," they explained in their  discussion. "It is quite likely that [tenofovir] therapy inhibited the ongoing necro-inflammation and might even have permitted hepatic  regeneration. Our data convincingly shows that a rapid reduction  in HBV DNA was associated with improvement in indicators of injury      and even survival."
Investigator   affiliations: Department of Gastroenterology, GB Pant Hospital, New Delhi, India; Department of Hepatology, Institute of Liver &  Biliary Sciences, New Delhi, India; Special Centre for Molecular  Medicine, Jawaharlal Nehru University, New Delhi, India.
5/10/11
Reference
H Garg, SK Sarin, M Kumar, et al. Tenofovir improves the outcome  in patients with spontaneous reactivation of hepatitis B presenting as acute-on-chronic liver failure. Hepatology 53(3):774-780  (abstract). March 2011.



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StephenW

泰诺福韦提高了急性乙肝成果上，慢性肝功能衰竭
概要
与泰诺福韦治疗（VIREAD的）降低乙肝病毒载量，减少肝损伤，并降低死亡的急性上，由于慢性肝功能衰竭患者乙肝活化风险。

由Liz Highleyman

慢性乙型肝炎病毒（HBV）感染可引起急性自发性恢复上，慢性肝功能衰竭（ACLF），在人们谁已经有慢性病毒性肝炎或突然肝病恶化。肝移植是治疗急性肝功能衰竭接受治疗，但供肝短缺和抗病毒治疗是将是一个具有吸引力的选择。

正如在2011年3月发行的杂志报道，在印度Hitendra Garg和同事评估了泰诺福韦功效 - 最有力的核苷/核苷酸治疗B型肝炎批准类似物之一 - 在与ACLF患者的死亡率预测看去。此前的研究表明，旧的乙肝药物拉米夫定（拉米- HBV）是不能用于此目的的有效。

研究对象包括27例ACLF由于自发HBV再激活谁，随机指派接受替诺福韦或安慰剂。大多数（72％）是男性，平均年龄为45岁。在乙型肝炎病毒DNA中位数基线病毒载量水平为90万国际单位/毫升，56％是B型肝炎的“e”抗原阳性。

所有患者随访至少3个月或直至死亡。主要终点是生存在3个月。肝移植手术无法使用。

结果
在3个月，存活概率为显着泰诺福韦组高于安慰剂组（57％比15％，分别）。
死亡的典型原因是进步的肝功能衰竭导致多器官衰竭。
乙肝病毒DNA水平显着下降，在替诺福韦组，但仍稳定在安慰剂组。
3个月后随访，在60％的患者经历泰诺福韦组HBeAg转阴，相较于安慰剂组没有。
幸存的患者服用泰诺福韦经验在儿童特科特- Pugh分级（CTP）的肝脏疾病和MELD评分显着改善，但这些并没有改变安慰剂组。
有超过2日志的HBV DNA在第2周下降更是生存的独立预测因素。

“泰诺福韦显着降低乙肝病毒DNA水平，提高了CTP和MELD评分，并减少慢性重症乙型肝炎提出作为ACLF自发恢复患者的死亡率，”研究人员得出结论。 “在减少乙肝病毒DNA水平在2周应该是一个理想的目标，是一个很好的预测生存。”

“严重急性发作的发病机制被认为是具有积极的免疫反应，造成严重的肝脏坏死发炎的结果，最后肝功能失代偿有关，”他们解释了他们的讨论。 “这是很可能[泰诺福韦]疗法抑制不断坏死，炎症，甚至可能已批准肝再生。我们的数据令人信服地表明，在乙型肝炎病毒DNA的快速减少，在受伤甚至生存指标的改善联系在一起。”

调查背景：消化内科，国标潘特医院，新德里，印度，特殊的分子医学，贾瓦哈拉尔尼赫鲁大学，新德里，印度中心，对肝病，肝和胆管科学，新德里，印度研究所。

5/10/11

参考
ħ Garg，水库沙林，男库马尔，等。泰诺福韦改善了与乙型肝炎的急性上呈现慢性肝功能衰竭患者自发激活的结果。肝胆病53（3）:774 - 780（摘要）。 2011年3月。