我想知道大概有多少人抗病毒了病情还是不断恶化

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我想知道大概有多少人抗病毒了病情还是不断恶化，肝组织结构变差，大概有多少人肝组织结构好转了？
国际上做过抗病毒之后组织学变化的对照实验吗？这个比例大概是什么样的？
大家都来说说自己的经历

liver411

一定会有缓慢恶化或癌变的病例因为抗病毒不=100%控制/治愈了疾病。要设立比较需要比较抗病毒，不抗病毒，甚至代偿期和失代偿期的比较。 这个比较文献很多，仅举一个2003对于失代偿乙肝肝硬化患者使用拉米夫定研究的一个报告中的图像就可以说明（Semin Liver Dis 23(1):89-100, 2003. © 2003 Thieme Medical Publishers）可以在Medscape看到http://www.medscape.com/viewarticle/450891_5 ：



坐标Y是成活率，坐标X是年份。曲线从上向下，第一条为代偿肝硬化，第二条为使用拉米，第三条为失代偿没有治疗的...抗病毒绝对会提高失代偿期患者的成活率如果评估用药恰当。而那个时候因为仅仅有拉米，耐药问题造成治疗曲线绝对没有目前的好因为很多辅助耐药核心的抗病毒药物出现。

liver411

乙肝基金会，Dr. Rajander Reddy 医生在3-4年前，2005年患者年度大会上（今年在洛杉矶，St Vincent 医院，下个月举办）针对对于肝硬化患者的建议是：

Treatment of HBV patients with cirrhosis
对于患者肝硬化HBV的治疗

    * For patients with cirrhosis, treatment should be more aggressive. If they have decompensated cirrhosis, then treat with an oral antiviral and refer for liver transplant evaluation.
  * 患有肝硬化的患者，更应该积极治疗。如果属于失代偿期肝硬化，他们应该用口服抗病毒药物并给与肝脏移植评估。
    * 20% of patients with cirrhosis who had spontaneous e-antigen seroconversion risk reversion, which is why they should be treated indefinitely. If there is no cirrhosis, then the reversion rate is much lower.
* 20%带有自动转阴的HBeAg肝硬化患者(其HBeAg) 会有回跳危险，他们应该无期限治疗下去。如果没有肝硬化扯入，E抗原回跳率很低。
    * In patients with “wild type” chronic HBV, there is a histologic improvement in cirrhosis after 3 years of lamivudine therapy. This theory is now being debated.
* 感染有“野生株“病毒的慢性乙肝肝硬化患者，在3年拉米治疗后肝脏组织学提高。这个理论目前仍在讨论。（不过时过3-4年，新的药物和概念也不断出现。也就是治疗绝对优越于步治疗如果符合治疗条件和评估正确）

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感谢411老师，安心了，有没有代偿期肝硬化的对比试验结果呀

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拉米夫定组n=27?
也就是说省去的那段线因为变异存活率大幅下降？

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代偿期肝硬化没有过对照试验吗？

坚韧地活着

更踏实了一些。谢谢411。哪位来把资料翻译一下。

liver411

n=多少个患者（参加临床试药/试验的特定部分）

关于HBV抗病毒使病情减轻，恶化延缓...的文献很多（网上就有），这个就是4年前新英格兰医学期刊刊登一个关于拉米的文摘（全文也可以看到：http://content.nejm.org/cgi/cont ... eytype2=tf_ipsecsha

ABSTRACT

Background The effectiveness of antiviral therapy in preventing disease progression in patients with chronic hepatitis B and advanced fibrosis or cirrhosis is unknown.

Methods Patients with chronic hepatitis B who had histologically confirmed cirrhosis or advanced fibrosis were randomly assigned in a 2:1 ratio to receive lamivudine (100 mg per day) or placebo for a maximum of five years. Of 651 patients, 436 were assigned to receive lamivudine and 215 to receive placebo. The primary end point was time to disease progression, defined by hepatic decompensation, hepatocellular carcinoma, spontaneous bacterial peritonitis, bleeding gastroesophageal varices, or death related to liver disease. An independent data and safety monitoring board monitored the progress of the study and performed interim analyses of the data.

Results We randomly assigned 651 patients (98 percent Asian and 85 percent male) to receive lamivudine or placebo. The study was terminated after a median duration of treatment of 32.4 months (range, 0 to 42) owing to a significant difference between treatment groups in the number of end points reached. End points were reached by 7.8 percent of the patients receiving lamivudine and 17.7 percent of those receiving placebo (hazard ratio for disease progression, 0.45; P=0.001). The Child–Pugh score increased in 3.4 percent of the patients receiving lamivudine and 8.8 percent of those receiving placebo (hazard ratio, 0.45; P=0.02), whereas hepatocellular carcinoma occurred in 3.9 percent of those in the lamivudine group and 7.4 percent of those in the placebo group (hazard ratio, 0.49; P=0.047). Genotypic resistance YMDD mutations developed in 49 percent of the patients treated with lamivudine, and the Child–Pugh score was more likely to increase in patients with these mutations than in the other patients treated with lamivudine (7 percent vs. <1 percent). Overall, 12 percent of the patients in the lamivudine group and 18 percent of the patients in the placebo group reported serious adverse events.

Conclusions： Continuous treatment with lamivudine delays clinical progression in patients with chronic hepatitis B and advanced fibrosis or cirrhosis by significantly reducing the incidence of hepatic decompensation and the risk of hepatocellular carcinoma.
结论：持续拉米治疗可以推延慢性乙肝和严重纤维化或肝硬化乙肝患者临床上的恶化，比如：显著减低肝失代偿和原发性肝癌的危险。