|
- 现金
- 62111 元
- 精华
- 26
- 帖子
- 30437
- 注册时间
- 2009-10-5
- 最后登录
- 2022-12-28
|
本帖最后由 风雨不动 于 2012-4-14 15:53 编辑
What's New in Chronic Hepatitis B: AASLD 2010Paul Martin, MD
Posted: 11/12/2010http://www.medscape.com/viewarticle/732437 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 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. 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, 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.
From Google translate, not 100% accurate 从谷歌翻译，不是100％准确
保罗马丁博士
作者及披露
发表于：11/12/2010http：/ / www.medscape.com/viewarticle/732437
你好。我是保罗马丁，医学教授，在佛罗里达州迈阿密大学肝脏病杂志主编。我在这里在美国肝病学会[美国协会肝病研究]波士顿[美国马萨诸塞州] 2010年，我想回顾为Medscape对肝炎B的一些会议。
第一项研究，我想讨论的是我所谓的非活动携带状态重新审查。这是一个由西门子，从阿拉斯加，[1]其中，他们研究了97慢性感染谁坚持正常丙氨酸转氨酶（ALT）与低级别的B型肝炎病毒（HBV）DNA水平阿拉斯加当地人同事的研究水平。这些人随访超过数年。
在这97例，他们确定了3个活动模式。有些病人有一个稳定的低水平复制状态。与其他病人有波动的HBV DNA水平在2-3级原木更改复制。然后，终于，一组患者血清HBV DNA持续阴性。
很重要的是，这3个组，每个逗留的ALT水平正常，这些人通常会被定性为载体，在非活动状态，但很重要的是，第三组，谁曾在本期的情况下遵循的HBV DNA行动，接着失去了相当数量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，这14个来自与乙型肝炎病毒DNA持续阴性组。
研究人员已经提出了“精英组”，这表明，即使与承运人的显然无效的状态，有不同的亚群患者的预后。关键是要确定长期跟进是否有完整的HBV DNA的情况下，因为这似乎预示了乙肝表面抗原最终过关的可能性极高。
接下来的研究，我想讨论的是一个比较研究阿德福韦经验的患者替诺福韦和恩曲他滨与泰诺福韦。这是由Berg和同事报告。[2]这项研究的入选标准的患者使用了阿德福韦谁仍然坚持HBV DNA阴性在这种情况下，大于1000拷贝/ ALT水平低于10倍的上限毫升正常。的重要性，58％作为整个集团先前曾拉米夫定曝光。
在这长期的研究，由156周，85％的患者参加了优秀的HBV DNA抑制，下降到不足400拷贝/毫升。非常重要的，这包括10阿德福韦耐药病人，而正如我前面提到的，超过一半的患者也曾经有过拉米夫定曝光。的重要性，在这项研究中，在控制上的复制，之间不存在泰诺福韦和恩曲他滨联合替诺福韦和差异。这种对谁产生了阿德福韦反应欠佳的病人建议，对泰诺福韦在一段时间内使用导致保护乙肝复制优秀的控制，在这项研究包括阿德福韦耐药病人谁是小团体。
最后的研究，我想讨论长期疗效患者泰诺福韦谁了高基线病毒载量的样子。这是戈登和他的同事报告，[3]和e抗原的研究包括两个+和e抗原的病人。在这项研究中，由后续行动，75％的患者取得了乙型肝炎病毒DNA小于200拷贝/ mL和23 HBeAg的％+患者血清阳转结束，也就是失去了e抗原，并已制定了一个e抗体。很重要的是，在HBeAg +患者总体而言，这些人15％清除乙肝表面抗原。在这长期的研究，没有抵抗检测。
这项研究的重要意义，包括事实，甚至是高层次患者的复制与慢性乙型肝炎感染优秀的控制，并最终，这些人很多人都会去清除乙肝表面抗原。最后，在4年期间，没有任何阻力进行了观察。这证实，这就意味着有一个内在的阻力与替诺福韦治疗率极低的早期研究。
谢谢收看。这是保罗马丁为Medscape。
(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 |
|
发表于 2010-11-13 12:43
