抗病毒(hbeag+)导制表抗转阴

MiddleAgeMan

Summary:

1
97 patients(in Alaska, USA) with normal alt and lower or negative hbvdna, 16 patients lost hbsag, 14 of them came from the group with negative hbvdna. Not sure if they were treated with antiviral.

2
adefovir-resistant patients treated with tenofovir. Of all the patients (10 had adefovir-resistant), by week 156, 85% of the patients enrolled had excellent suppression of HBV DNA, down to less than 400 copies/mL.

3.
long-term efficacy of tenofovir. 4 year treatment with no drug resistence. 75% of the patients had achieved an HBV DNA less than 200 copies/mL, and 23% of the HBeAg+ patients had seroconverted, that is, had lost e antigen and had developed an e antibody. Very importantly, in the HBeAg+ patients overall, 15% of these individuals cleared the hepatitis B surface antigen.



Hello. I'm Paul Martin, Professor of Medicine, Chief of Hepatology at the University of Miami in Florida. I'm here at AASLD [American Association for the Study of Liver Diseases] 2010 in Boston [Massachusetts], and I'd like to review some of the sessions on hepatitis B for Medscape.
The first study that I wanted to discuss is what I call the inactive carrier state revisited. This is a study by Simons and colleagues from Alaska,[1] in which they studied 97 chronically infected Alaskan natives who had persistently normal alanine aminotransferase (ALT) levels with low-level hepatitis B virus (HBV) DNA levels. These individuals were followed over a period of several years.
In these 97 patients, they identified 3 patterns of activity. Some patients had a steady low-level replicative state. Other patients had fluctuating replication with a change in HBV DNA levels in a magnitude of 2-3 logs. Then, finally, a group of patients were persistently HBV DNA negative.
Very importantly, in each of these 3 groups, the ALT levels stayed normal, and these individuals would be normally characterized as in the inactive carrier state, but very importantly, the third group, who had an absence of HBV DNA during the period of follow-up, went on to lose hepatitis B surface antigen in a significant number of instances. Indeed, of the 97 patients in this study, 16 of whom have lost surface antigen, 14 of these came from the group with persistently negative HBV DNA.
The investigators have coined the term "elite control group," and this suggests that even with the apparently inactive carrier state, there are subsets of patients whose prognosis differs. It is crucial to determine for long-term follow-up whether there is a complete absence of HBV DNA, because this seems to predict a high likelihood of ultimate clearance of hepatitis B surface antigen.
The next study that I want to discuss is a study comparing tenofovir vs tenofovir and emtricitabine in adefovir-experienced patients. This was reported by Berg and colleagues.[2] The entry criteria for this particular study were adefovir use in patients who remained persistently HBV DNA negative, in this instance greater than 1000 copies/mL with ALT levels less than 10 times the upper limits of normal. Of importance, 58% of the group as a whole had previous lamivudine exposure.
In this long-term study, by week 156, 85% of the patients enrolled had excellent suppression of HBV DNA, down to less than 400 copies/mL. Very importantly, this included 10 adefovir-resistant patients, and as I mentioned earlier, more than half of the patients also had previous lamivudine exposure. Of importance, in this study, in terms of control of replication, there was no difference between tenofovir and a combination of tenofovir and emtricitabine. This suggests for patients who have had a suboptimal response to adefovir, the use of tenofovir over a protected period of time leads to excellent control of hepatitis B replication, including in this study a small group of patients who were adefovir resistant.
The final study that I want to discuss looks at long-term efficacy of tenofovir in patients who had a high baseline viral load. This was reported by Gordon and colleagues,[3] and the study included both HBeAg+ and HBeAg- patients. In this study, by the end of follow-up, 75% of the patients had achieved an HBV DNA less than 200 copies/mL, and 23% of the HBeAg+ patients had seroconverted, that is, had lost e antigen and had developed an e antibody. Very importantly, in the HBeAg+ patients overall, 15% of these individuals cleared the hepatitis B surface antigen. During this long-term study, no resistance was detected.
The important implications of this study include the fact that there is excellent control of even high-level replication in patients with chronic hepatitis B infection, and, ultimately, many of these individuals will go on to clear hepatitis B surface antigen. Finally, over a 4-year period, no resistance was observed. This confirms earlier studies that suggest there is a very low rate of intrinsic resistance with tenofovir therapy.
Thank you for joining us. This is Paul Martin for Medscape.
References





(6.合.彩).足球.篮球...各类投注开户下注

第一投注.现金网:招代理年薪10万以上:6668.cc

抗战11

都洋文看不懂,有高手翻译一下吗

小雪408

看不懂。

StephenW

[谷歌翻译是不是100％正确，仅供参考，使用。]

摘要：

1
97例患者ALT正常和低或负的HBVDNA（美国阿拉斯加），16例患者失去了乙肝表面抗原，其中14人来自本集团与负HBVDNA。不知道他们是用抗病毒药物治疗。

2
阿德福韦耐药患者的治疗与替诺福韦。所有患者（10人阿德福韦耐药），156周，85％的患者纳入了优良的抑制HBV DNA的，下降到低于400拷贝/ ml。

3。
替诺福韦的远期疗效。 4年治疗无耐药性。 75％的患者取得了乙型肝炎病毒DNA小于200拷贝/ ml，和23％+患者HBeAg的血清阳转，也就是说，已经失去了e抗原和e抗体。很重要的是，在整体的HBeAg +患者中，15％以上的个人清除乙肝表面抗原。



您好！我的医学教授保罗马丁在佛罗里达州迈阿密大学肝病行政。我在肝病学会[美国协会肝病研究] 2010年在波士顿马萨诸塞州]，我想检讨对乙肝权利。的一些会议。
第一项研究，我想讨论的是我称之为非活动携带状态，重新审视。这是一个从阿拉斯加由西门子和同事的研究，[1]在他们研究了97慢性感染者坚持正常丙氨酸转氨酶（ALT）水平与低级别的B型肝炎病毒（HBV）DNA水平的阿拉斯加当地人。这些人在随后的几年时间。
在这97例患者中，他们发现3的活动模式。有些患者有一个稳定的低层次的复制状态。其他患者在HBV DNA水平的幅度在2-3日志的变化波动的复制。然后，终于，一组病人持续HBV DNA阴转。
很重要的是，在这3组，ALT水平保持正常，这些人通常会在非活动载体状态的特点，但非常重要的，第三组，在后续期间的HBV DNA的情况下，接着失去一个显著的实例乙肝表面抗原。事实上，在这项研究中97例，其中16人已经失去了表面抗原，其中14来自持续负HBV DNA组。
研究人员已经创造的“精英对照组，”，这表明，即使有明显的不活动的载体状态，有病人的预后不同的子集。关键是要确定长期后续的HBV DNA是否有完整的情况下，因为这似乎是预测最终清除乙肝病毒表面抗原的可能性极高。
接下来的学习，我想讨论的是一个比较研究阿德福韦的患者替诺福韦与替诺福韦和恩曲他滨。这是伯格和他的同事报告。[2]这项研究的准入标准，谁仍然坚持HBV - DNA阴性的患者中阿德福韦使用，在这种情况下大于1000拷贝/毫升与ALT水平低于10倍的上限正常。 58％的组作为一个整体的重要性，以前拉米夫定曝光。
在这个长期的研究，由每周156，85％的患者纳入了优良的抑制HBV DNA的，下降到低于400拷贝/ ml。非常重要的，这包括10阿德福韦耐药患者，正如我前面提到的，超过一半的患者也有拉米夫定曝光。的重要性，在这项研究中，在复制的控制方面，有没有泰诺福韦和泰诺福韦和恩曲他滨的组合之间的差异。这表明有一个次优的响应阿德福韦的患者，经过一段时间的保护期使用替诺福韦导致乙肝复制的出色的控制，在这项研究中，包括小组阿德福韦耐药的患者。
最后我想讨论研究高基线病毒载量的患者中，替诺福韦的长期疗效。这是戈登和他的同事报告，[3]的研究包括大三阳+和HBeAg的患者。后续年底，在这项研究中，75％的患者取得了一个乙肝病毒的DNA低于200份/毫升，和23％的e抗原+的患者有血清阳转，的是，已经失去了e抗原，并制定了一项e抗体。很重要的是，在整体的HBeAg +患者中，15％以上的个人清除乙肝表面抗原。在这个长期的研究，发现无阻力。
这项研究具有重要意义的事实，有出色的控制，甚至是高层次复制的慢性乙型肝炎患者，并最终，这些人有很多人会去清除乙肝表面抗原。最后，过了4年的时间内，无阻力。这证实了早先的研究表明有一个替诺福韦治疗的内在耐药率非常低。
感谢您加入我们的行列。这是保罗马丁Medscape。
参考文献

把握当下

1. 97个alt正常、DNA低或阴患者中，16人s抗原转阴，16人中14人dna本来就是阴。这些人抗病毒情况未知
2.阿德耐药使用替诺情况。10个阿德耐药患者，156周时85%患者dna小于400 copies/mL
3. 替诺长期效果。4年无耐药。75% DNA小于200 copies/mL,  23% e抗原阳患者转小三。 15% e抗原阳患者s抗原转阴

tonychant

把握当下 发表于 2011-10-17 21:19
1. 97个alt正常、DNA低或阴患者中，16人s抗原转阴，16人中14人dna本来就是阴。这些人抗病毒情况未知
2.阿德 ...

美国人的病毒基因型（A、D）与亚洲人不同（B、C），所以我们可以看到干扰素和核苷类药物对外国人有显著效果，而在中国人身上没有作用

把握当下

tonychant 发表于 2011-10-23 19:12
美国人的病毒基因型（A、D）与亚洲人不同（B、C），所以我们可以看到干扰素和核苷类药物对外国人有显著效 ...

哪儿说了亚洲人没有效果？

我记得骆抗先还专门写了文章驳斥这个观点，至少是核苷效果还可以，记不清了

StephenW

tonychant 发表于 2011-10-23 19:12
美国人的病毒基因型（A、D）与亚洲人不同（B、C），所以我们可以看到干扰素和核苷类药物对外国人有显著效 ...

"而在中国人身上没有作用" - 这是不正确的. 对于亚洲人也有效，通常A优于B，然后C.