2017 EASL慢乙肝领域新进展—抗病毒治疗肾脏、骨骼安#8131

放牛哥哥

http://www.cmt.com.cn/article/090723/a090723a1201.htm
    2009年7月4日，第44届欧洲肝脏研究学会（EASL）年会精粹之中国行（Best of EASL 2009 China Tour）专家论坛在北京召开，来自欧洲的3位肝病领域的知名专家以及全国各地150多名感染病学专家出席了本次会议。本次专家论坛的主题是乙型肝炎的临床治疗，核心内容包括慢性乙型肝炎的治疗终点及抗病毒药物耐药机制及处理策略等。现将本次论坛的精彩内容总结如下，以飨读者。

    乙型肝炎的治疗终点

    2009年2月，EASL公布了最新的慢性乙型肝炎临床实践指南，旨在为慢性乙型肝炎患者提供最佳的诊疗方案。根据2009年EASL年会上的最新研究进展及EASL指南更新，帕夫洛夫斯基（Pawlotsky）教授从以下几个方面对乙型肝炎治疗终点的选择进行了深入解读。

    治疗目标和治疗终点

    慢性乙肝治疗目标是通过预防疾病进展至肝硬化、终末期肝病和肝细胞癌（HCC）来改善患者的生活质量并提高其生存率。最新 EASL指南的3个治疗终点为：①理想终点（ideal end-point） 对于所有HBeAg阳性和阴性患者，出现持续的乙肝表面抗原（HBsAg）转阴，伴或不伴HBsAg血清学转换；②满意终点（satisfactory end-point） 对于HBeAg阳性患者，出现持久的HBeAg血清学转换；③下一最期望终点（next most desirable end-point） 对于HBeAg阳性但未获得HBeAg血清学转换的患者及HBeAg阴性患者，通过核苷（酸）类似物（NUC）治疗，使HBV DNA维持在检测不到的水平，或接受有限疗程的干扰素（IFN）治疗后，HBV DNA持续检测不到。

    在以上3个终点中，理想终点和满意终点是比较难达到的，而HBV DNA的持续抑制则是可以达到的现实目标，也是基本目标。

    对HBV DNA的持续抑制

    HBV DNA水平是HBV相关肝病进展的重要决定因素。HBV DNA病毒载量>105 copies/ml（20000 IU/ml）时，肝硬化和HCC的发生率明显增高，其生存率也明显低于HBV DNA<105 copies/ml的患者。此外，HBV DNA的下降也是肝组织学改善的重要指征。HBeAg阳性患者使用恩替卡韦治疗2年或2年以上，约90%的病例能够维持HBV DNA检测不到（表1），而接受 聚乙二醇干扰素（Peg-IFN）治疗后，经过3~4年随访，仅不足20%的病例能够持续HBV DNA检测不到。

    HBeAg血清学转换

    发生HBeAg血清学转换的患者，其HCC的发生风险也明显下降。40岁以上才发生HBeAg血清学转换的患者，其HCC风险明显高于那些转换时年龄<40岁者。治疗1年时，PEG-IFN、拉米夫定、阿德福韦、恩替卡韦、替比夫定和替诺福韦的HBeAg血清学转换率分别为30%、22%、12%、21%、23%和21%，且随着治疗时间的延长，HBeAg血清学转换率逐渐增高。恩替卡韦的作用随着时间的延长更加突出（图1）。

    HBsAg转阴

    HBsAg转阴表明HBV复制得到了长期稳定的控制，HCC、肝功能失代偿、与肝脏相关的死亡率明显下降，是乙型肝炎理想的治疗终点。一项研究显示，HBsAg转阴后，患者1年时HBV DNA降至检测不到水平的比例为86.6%，10年以上可达96.3%，丙氨酸氨基转移酶（ALT）持续正常的比例达82.1%。现有乙肝治疗药物的HBsAg转阴率都比较低，但经长期治疗，该比例有增加趋势（图2）。


HBV对核苷（酸）类似物耐药的机制与处理

    在NUC治疗慢性乙肝过程中，最常见的问题是HBV对NUC的耐药。耐药的发生是由于宿主体内对抗病毒药物耐药的病毒株大量复制或发生突变，成为主导病毒株而导致的。在治疗初始阶段，对药物敏感的病毒株处于主导地位，仅有少部分耐药病毒株。随着治疗时间的延长，对药物敏感的优势株因受到抑制而不断减少，而原本数量较少的“弱势”耐药株在此期间不断复制逐渐成为优势株。此外，少部分耐药的病毒株在治疗过程中会发生突变，成为适应力强的新变异株。

    耐药的发生除了与病毒和药物本身相关外，也与宿主的免疫压力相关，病毒、宿主和药物这3方面的因素相互作用导致了耐药的发生。然而，HBV的结构和生物学特性既有利于耐药的发生，也有利于预防耐药，这与人类免疫缺陷病毒（HIV）和丙肝病毒（HCV）不同。

    HBV主要有以下3个可防止耐药的病毒学特性：① 部分重叠开放读码框的保守性限制了病毒的突变，② 大多数被感染者的免疫系统可以在一定程度上抑制病毒复制，③ 某些药物对HBV有较高的耐药屏障。

    因此，2009年EASL指南推荐，对于初治的慢性乙肝患者，宜选择最强效且耐药发生率最低的药物用于一线单药治疗（如恩替卡韦或替诺福韦），以尽可能强效且持久地抑制HBV复制。高HBV DNA水平不仅与HBV耐药有关，还与肝脏疾病的进展相关，因此，在治疗伊始尽快且持续抑制HBV复制尤为重要。

    对于不同的NUC类药物，HBV的耐药位点不尽相同，其耐药性也有显著差别（表2）。拉米夫定5年累计耐药发生率高达70%左右，因此不建议作为初治乙型肝炎患者的一线单药治疗。替比夫定的耐药发生率虽然低于拉米夫定，但研究显示，其2年的耐药率在HBeAg阳性患者和HBeAg阴性患者中仍分别达到21.6%和8.6%，且随着治疗时间的延长，其耐药发生率可能会相应升高。同样，研究结果表明，阿德福韦耐药发生率也较高，其5年耐药率达29%。

    与上述药物不同的是，恩替卡韦是一种高耐药基因屏障药物，至少需要3个位点发生突变才会产生耐药。研究显示，其6年累计耐药发生率小于1.2%。因此，2009年 EASL指南推荐恩替卡韦作为一线单药治疗慢性乙肝的药物。关于替诺福韦的耐药率，虽然初步报告也很低，但目前尚无足够数据证明其长期使用后的耐药情况。

    一旦发生对初治单一NUC类药物耐药，就应选用最为有效、与该药无交叉耐药位点且多重耐药危险性最低的药物进行挽救治疗。由于加用药物比换用药物出现耐药的概率要低，因此最有效的策略是加用另一种无交叉耐药的药物。但某些联合治疗方案的长期安全性尚须进一步研究。

放牛哥哥

Lamivudine = LAM (Epivir HBV, Zeffix, 3TC) : FDA approved 1998 for children & adults.
Adefovir Dipivoxil = ADV (Hepsera) ; FDA approved 2002 for adults.
Entecavir = ETV (Baraclude) : FDA approved 2005 for adults.
Telbivudine = LdT (Tyzeka, Sebivo) : FDA approved 2006 for adults.
Tenofovir = TDF (Viread) : FDA approved 2008 for adults.
Emtricitabine (FTC) : Phase 3 trials , expected to be FDA approved soon

与乙肝共舞

学生作文
学生作文，谈《我的理想》。一生写道：拿沙特工资，住英国房子，用瑞典手机，戴瑞士手表，娶韩国女人，包日本二奶，做泰国按摩，开德国轿车，坐美国飞机，喝法国红酒，吃澳洲海鲜，抽古巴雪茄，穿意大利皮鞋，玩西班牙女郎，看奥地利歌剧，买俄罗斯别墅，雇菲律宾女佣，配以色列保镖，洗土耳其桑拿，当中国干部......
　　老师批语：啰嗦！只需说当中国干部就行。。。。

放牛哥哥

原帖由 juanbaby 于 2009-7-30 09:32 发表
初来什么都不懂,请教一个很简单的问题,乙肝转阴就是拿金牌吗?那拿银牌又是指什么呀?
==================
1，铜牌：dna阴。
2，银牌：dna阴+e抗原阴（如果是核苷治的，必须还加上e抗体阳）
3，金牌：银牌基础上+hbsag阴

放牛哥哥

关于复发率，补充一下：
同时给药1年，针对e抗原阳性的患者，最后都达到三终点的。复发率是这样的：
派罗欣：5-10％；
国产干扰素15-30％，
佩乐能大概介于两者之间（这句话是上周群内某战友看南方医院的骆抗先教授时候，他说的一句话）

放牛哥哥

恩替和派罗欣连续治疗比较派罗欣单独治疗e抗原阳性慢乙肝患者
http://clinicaltrials.gov/ct2/sh ... rm=hbv&rank=249
目的：从大规模的临床随机实验看来，同时使用口服核苷类抗病毒药物和干扰素a 没有显示出比单独使用干扰素a更优越的治疗效果。最近，先使用拉米四周，再使用干扰素a已经显示出比单独用干扰素a更好的e抗原血清转换率。

Purpose
Currently, peginterferon alfa-2a or oral nucleos(t)ides are approved for the treatment with HBeAg positive CHB, with the overall HBeAg seroconversion far from satisfactory. Therefore, efforts on the various combinations with the currently available drugs are needed to improve the overall response rates. The simultaneous combination therapy with oral nucleoside and peginterferon alfa-2a from large-scaled randomized trials did not show a superior response rate over peginterferon alfa-2a monotherapy. Recently, sequential monotherapy with lamivudine for the first 4 weeks, followed by weekly peginterferon alfa-2a has shown favorable HBeAg seroconversion rate over peginterferon alfa-2a monotherapy, based on the assumption that early viral suppression by lamivudine can restore the immune function to facilitate the later immunomodulatory response by peginterferon alfa-2a. With the recent introduction of entecavir, the more potent oral nucleoside with few drug resistance, sequential monotherapy with entecavir can potently suppress HBV DNA with 4 weeks of treatment, which may facilitate the response of peginterferon alfa-2a to achieve HBeAg seroconversion. Therefore, we aimed to conduct a placebo controlled randomized control trial to evaluate of adding entecavir early in the course of therapy can improve the treatment response.

Arms  Assigned Interventions  
Entecavir and peginterferon: Experimental
Entecavir 0.5 mg/day at week 1-4, followed by peginterferon alfa-2a 180 ug/week at week 5-52  Drug: Entecavir and peginterferon alfa-2a
Entecavir (Baraclude) 0.5 mg/day po at week 1-4 Peginterferon alfa-2a (Pegasys) 180 ug/week sc at week 5-52  
Placebo and peginterferon: Active Comparator
Placebo 0.5 mg/day at week 1-4, followed by peginterferon alfa-2a 180 ug/week at week 5-52  Drug: Placebo and peginterferon
Placebo 0.5 mg/day po at week 1-4 Peginterferon alfa-2a (Pegasys) 180 ug/week sc at week 5-52  

Detailed Description:
Chronic hepatitis B (CHB) is prevalent in the world, with estimated chronic carriers of 350 millions worldwide.

Currently, peginterferon alfa-2a or oral nucleos(t)ides are approved for the treatment with HBeAg positive CHB, with the overall HBeAg seroconversion far from satisfactory. Therefore, efforts on the various combinations with the currently available drugs are needed to improve the overall response rates. The simultaneous combination therapy with oral nucleoside and peginterferon alfa-2a from large-scaled randomized trials did not show a superior response rate over peginterferon alfa-2a monotherapy. Recently, sequential monotherapy with lamivudine for the first 4 weeks, followed by weekly peginterferon alfa-2a has shown favorable HBeAg seroconversion rate over peginterferon alfa-2a monotherapy, based on the assumption that early viral suppression by lamivudine can restore the immune function to facilitate the later immunomodulatory response by peginterferon alfa-2a. With the recent introduction of entecavir, the more potent oral nucleoside with few drug resistance, sequential monotherapy with entecavir can potently suppress HBV DNA with 4 weeks of treatment, which may facilitate the response of peginterferon alfa-2a to achieve HBeAg seroconversion. Therefore, we aimed to conduct a placebo controlled randomized control trial to evaluate of adding entecavir early in the course of therapy can improve the treatment response.

放牛哥哥

Currently, peginterferon alfa-2a or oral nucleos(t)ides are approved for the treatment with HBeAg positive CHB, with the overall HBeAg seroconversion far from satisfactory. Therefore, efforts on the various combinations with the currently available drugs are needed to improve the overall response rates. The simultaneous combination therapy with oral nucleoside and peginterferon alfa-2a from large-scaled randomized trials did not show a superior response rate over peginterferon alfa-2a monotherapy. Recently, sequential monotherapy with lamivudine for the first 4 weeks, followed by weekly peginterferon alfa-2a has shown favorable HBeAg seroconversion rate over peginterferon alfa-2a monotherapy, based on the assumption that early viral suppression by lamivudine can restore the immune function to facilitate the later immunomodulatory response by peginterferon alfa-2a. With the recent introduction of entecavir, the more potent oral nucleoside with few drug resistance, sequential monotherapy with entecavir can potently suppress HBV DNA with 4 weeks of treatment, which may facilitate the response of peginterferon alfa-2a to achieve HBeAg seroconversion. Therefore, we aimed to conduct a placebo controlled randomized control trial to evaluate of adding entecavir early in the course of therapy can improve the treatment response

放牛哥哥

牛哥：你介绍的这个循环疗法，停干扰素，吃一个月拉米，英文我看不懂，道理是什么？是让拉米降一下DNA？还是需要停拉米后让ALT升起来，启动一下免疫？还是我猜测的这两点都不对？麻烦牛哥给解答一下。
另外,我还有一个问题问你，如果停干扰素，拉米1个月，再继续干扰素，是不是相当于干扰又从零开始了？1个月后停了拉米继续干扰后，会不会转氨酶强烈反弹，拉米能停得下来吗
＝＝＝＝＝＝＝＝
1，其原理是基于前期已有小规模国际临床试验结论的一个假设“干扰初期，使用lam 4周，降低dna载量后，有利于重建肌体免疫系统，更有助于派罗欣激发和构建体内免疫清除病毒的效率，使得在结束48周派罗欣给药后，e抗原血清转换率升高”。本临床试验项目在上述假设的基础上，进一步的提出一个目的或曰结论的求证：利用etv替换lam，看能否产生更高的应答。
2，该试验的用药方案是etv给药4周后，立马上派罗欣。不是傻等alt的升高。
3，如果停干扰素，拉米1个月，再继续干扰素，是不是相当于干扰又从零开始了？
＝＝
不是。派罗欣为例：正常成年人在180ug剂量给药8周后，血清药物浓度达到整个疗程的峰值水平，当然，这个浓度也大于正常的治疗所需要的药物浓度。而派在体内的清除，肾功能正常的人，平均清除率是56天，血清药物浓度不会在你停针后立马降低到0。
4，1个月后停了拉米继续干扰后，会不会转氨酶强烈反弹，拉米能停得下来吗。
＝＝
停lam后，因为你还在用药，使用的是抗病毒路线中的另一条线路治疗，同样会抑制病毒，控制炎症，所以，一般不用担心停掉lam的反弹（之前为重肝的患者除外。此类患者用次方法，估计要严密监控alt）

放牛哥哥

http://www.hbvhbv.com/forum/view ... page%3D1&page=3

尽管DNA高的人肝功能一直正常，肝穿出来几乎个个就是肝炎
DNA高的就比DNA低的癌变率高，高10倍
DNA高久的就比DNA短时期高的癌变率高
抗病毒的，癌变率会降低一半
DNA越高，治疗成功率就越低
DNA高的，ALT越接近正常，治疗成功率就越低，但不是没疗效
拉米耐药的，间隔一段时间还可以再次拉米，但这次拉米耐药比上一次更快些
没用拉米时变异病毒像平地的雨点，用拉米之后变异病毒像山坡的雨点，能汇成河
变异病毒没有比没变异的更残忍，只是更狡猾了
因为乙肝死掉的，肝癌只占1/10
大多数死掉的，是因为肝硬化
肝硬化的，大多是没抗病毒的
没抗病毒的，有这么几类人
1.担心病毒变异的（多可笑呀！担心当八路小命保不住，结果叫日本鬼子枪毙了）
2.没钱治病的
3.粗心大意不查体的
4.虔诚信中医的

http://www.hbvhbv.com/forum/thread-390409-52-1.html
1026#
人得了病，有这么几种结果
1.不治而愈
2.不治不愈不加重
3.不治加重，治则减轻，但难愈
4.治则愈，不治不愈，
5.除痛求死

急肝者多为1
携带者多为2
变异者多为3
肝炎者多为4
硬化及肝癌晚期者多为5

对于重肝来说，治愈意味着出院后3年没发生肝硬化肝癌，至于有没有纤维化和传染性没人要求。
对于慢肝来说，治愈意味着出院后3年没发生肝功能反复损害，至于有没有传染性没人要求。
对于大三阳携带者来说，治愈意味着治疗结束后3年没发生DNA阳性，至于有没有澳抗转阴没人要求。
对于小三阳携带者来说，治愈意味着治疗结束后3年没发生澳抗阳性，至于有没有产生抗体没人要求。
以上四种类型，治一个好一个是不可能的，治几个好一个是很现实的

[ 本帖最后由 放牛哥哥 于 2010-3-28 21:58 编辑 ]

放牛哥哥

Gilead Announces Long-Term Data from Two Pivotal Phase III Studies Evaluating Viread(R) For Chronic Hepatitis B
No Evidence of Viral Resistance Through Three Years of Treatment

BOSTON--(BUSINESS WIRE)--Oct. 31, 2009-- Gilead Sciences, Inc. (Nasdaq:GILD) today announced the presentation of three-year (144-week) open label data from two pivotal Phase III clinical trials, Studies 102 and 103, evaluating the safety and efficacy of once-daily Viread® (tenofovir disoproxil fumarate) among adult patients with chronic hepatitis B virus (HBV) infection. These data will be presented at the annual meeting of the American Association for the Study of Liver Diseases (The Liver Meeting 2009) being held this week in Boston, October 30-November 3.

These new data show that the majority of patients who received Viread for up to 144 weeks experienced sustained suppression of HBV DNA levels in the blood to below 400 copies/mL (87 percent in Study 102 and 71 percent in Study 103). Additionally, cumulatively over 144 weeks, 8 percent of all patients in Study 103 (HBeAg-positive) experienced “s” antigen (HBsAg) loss, which can contribute to resolution of chronic hepatitis B infection. Notably, no mutations associated with resistance to Viread developed in any patients up to 144 weeks of treatment.

“The development of resistance is a significant challenge for practitioners treating patients with chronic hepatitis B,” said Patrick Marcellin, MD, of Hôpital Beaujon in Clichy, France, and the principal investigator of Study 102. “The robust and comprehensive resistance surveillance in these studies provides important information for the medical community and shows that Viread offers a high barrier to resistance.”

Clinical practice guidelines recommending Viread as a first-line therapy for the treatment of chronic hepatitis B were issued earlier this year by both the American Association for the Study of Liver Diseases and the European Association for the Study of the Liver. The U.S. Food and Drug Administration (FDA) approved Viread for chronic hepatitis B in adults in 2008 based on earlier (48-week) results from Studies 102 and 103, and recently approved the inclusion of 96-week data in the product’s label.

“These data underscore the rationale for Viread’s position as a recommended first-line therapy for chronic hepatitis B infection,” said Jenny Heathcote, MD, of the University of Toronto, Canada, and the principal investigator for Study 103. “In particular, the loss of the hepatitis B ‘s’ antigen in 8 percent of patients, which is associated with resolution of HBV infection, is significant from a clinical perspective.”

Nine additional presentations examining the efficacy of Viread across a variety of patient populations, including treatment-experienced patients, patients new to therapy, patients of Asian descent, pregnant women and patients with decompensated liver disease, also will be presented during The Liver Meeting.

About Studies 102 and 103

Studies 102 and 103 were multi-center, randomized, double-blind Phase III clinical trials comparing Viread to Hepsera® (adefovir dipivoxil) among HBeAg-negative presumed pre-core mutant (n=375) and HBeAg-positive (n=266) chronic hepatitis B patients with compensated liver disease, respectively. The majority of patients were treatment-naïve upon study initiation, although some patients were lamivudine-experienced.

Patients originally randomized to Hepsera in both studies rolled over to open-label Viread (n=196) at week 48, while patients originally randomized to Viread continued open-label Viread treatment (n=389). After 72 weeks, patients with confirmed viremia (HBV DNA levels at or above 400 copies/mL on two consecutive visits) had the option of adding emtricitabine treatment by substituting Truvada® (emtricitabine and tenofovir disoproxil fumarate) for Viread. By 144 weeks, 87 percent of patients remained in Study 102 (n=328) and 80 percent of patients remained in Study 103 (n=214).

Study 102 Results (Poster Presentation #481)

HBeAg-negative patients

A long-term evaluation algorithm through 144 weeks showed that 87 percent of patients achieved virologic suppression (HBV DNA levels below 400 copies/mL), and similar efficacy was observed between patients who received Viread monotherapy throughout (206/238, 87 percent) compared to those who initially received Hepsera and then rolled over to Viread (107/121, 88 percent).

Three patients receiving Viread had HBV DNA of 400 copies/mL or more at week 144, and one additional viremic patient discontinued Viread during year three. Three patients in Study 102 added emtricitabine treatment at or after week 72 due to confirmed viremia, and all three achieved HBV DNA levels below 400 copies/mL at week 144.

Levels of alanine aminotransferase (ALT, an enzyme that serves as a measure of liver damage), which had been high at baseline, remained at normal levels through 144 weeks of treatment (overall mean ALT value of 33 U/L).

Viread was well tolerated by study subjects during open-label treatment through 144 weeks. The incidence of serious adverse events considered drug-related was low, with one event (mild renal impairment) reported in the Viread group and none reported in the Hepsera-to-Viread group. The incidence of grade 3-4 laboratory abnormalities was similar between groups; 14 percent for Viread and 15 percent in the Hepsera-to-Viread group. During the study, three patients on Viread discontinued treatment due to adverse events (hepatocellular carcinoma, dizziness/fatigue/lack of concentration and septic shock). No patients experienced a confirmed 0.5 mg/dL increase in serum creatinine or a decrease in creatinine clearance to less than 50 mL/min. There were three deaths during open-label treatment, but the causes (nasopharyngeal cancer, metastatic liver cancer and cervical cancer) were not considered related to study drug.

No resistance to Viread developed among patients who received Viread for up to three years.

Study 103 Results (Poster Presentation #483)

HBeAg-positive patients

Using a long-term evaluation algorithm through 144 weeks, 71 percent of patients achieved HBV DNA levels below 400 copies/mL, with similar response between patients who received Viread monotherapy throughout (118/165, 72 percent) and those who initially received Hepsera and rolled over to Viread (63/89, 71 percent) after week 48.

Five patients on Viread had HBV DNA of 400 copies/mL or more at week 144, and one additional viremic patient discontinued Viread during year three. Thirty-one patients in Study 103 added emtricitabine treatment between 72 and 144 weeks due to confirmed viremia; 17 achieved HBV DNA levels below 400 copies/mL at week 144.

As with Study 102, ALT levels, which had been elevated at baseline in both patient groups, remained stable at near-normal levels by week 144 (mean of 38.6 U/L).

Among all patients who continued Viread treatment to week 144, 34 percent achieved loss of HBeAg and 26 percent experienced HBeAg seroconversion. Seroconversion is defined as both the disappearance of the hepatitis B “e” antigen, a marker of HBV replication (rendering the patient “HBe-antigen negative”), and the detection of antibodies specific for this antigen (making the patient “HBe-antibody positive”). Cumulatively, 8 percent of patients experienced “s” antigen (HBsAg) loss, which contributes to resolution of chronic hepatitis B infection.

As in Study 102, Viread was well tolerated by study subjects during open-label treatment through 144 weeks. The incidence of serious adverse events considered drug-related was low, with two events (increase of ALT and facial spasm) reported in the Viread group and two events (increase of ALT) reported in the Hepsera-to-Viread group. The incidence of grade 3-4 laboratory abnormalities was 12.3 percent in the Viread group and 15.5 percent in the Hepsera-to-Viread group. During the study, one patient on Viread discontinued treatment due to an unconfirmed 0.5 mg/dL increase in creatinine. Two patients (initially randomized to Hepsera) experienced a confirmed 0.5 mg/dL increase in creatinine. No patients experienced a decrease in confirmed creatinine clearance to less than 50 ml/min.

As with Study 102, no resistance to Viread developed among patients who received Viread for up to three years.

Continued treatment with Viread for 144 weeks in Studies 102 and 103 did not reveal any new adverse reactions and no change in the tolerability profile observed during the first 48 weeks of treatment. The most common adverse reaction (all grades) was nausea, observed in 9 percent of patients taking Viread at week 48. Other treatment-related adverse events observed in greater than 5 percent of patients during the first 48 weeks of Studies 102 and 103 included abdominal pain, diarrhea, headache, dizziness, fatigue, nasopharyngitis, back pain and skin rash.

Important Information About Viread for Chronic Hepatitis B and HIV