老年慢性乙型肝炎患者基因多态性与其耐药变异的相关性

目的研究老年慢性乙型肝炎患者基因多态性与其耐药变异的相关性。方法选取接受抗病毒治疗的老年慢性乙型肝炎患者188例。检测患者在使用不同核苷类抗病毒药物后血清样本,进行基因测序和分型。结果 C基因型占比显著高于B基因型、D基因型;且B基因型占比高于D基因型(均P<0.05)。C基因型YIDD突变占比显著高于B基因型(χ2=7.918,P=0.005),而B基因型的YVDD突变高于C基因型(χ2=8.965,P=0.000)。B基因型与YVDD突变存在显著正相关(r=0.783,P=0.000),同样C基因型与YIDD突变存在显著正相关(r=0.819,P=0.000)。单一耐药中阿德夫韦耐药率显著高于拉米夫定与恩替卡韦,在共同耐药中拉米夫定+阿德夫韦+替米夫定共同耐药率显著高于拉米夫定+阿德夫韦+替米夫定+恩替卡韦、拉米夫定+阿德夫韦、拉米夫定+替米夫定以及拉米夫定+恩替卡韦。阿德夫韦、拉米夫定+阿德夫韦+替米夫定耐药均与B基因型YIDD突变、C基因型YVDD突变显著正相关(r=0.748,P=0.000;r=0.583,P=0.000;r=0.673,P=0.000;r=0.617,P=0.000)。结论乙型肝炎病毒(HBV)基因型中B基因型与YVDD突变、C基因型与YIDD突变均正相关,阿德夫韦、拉米夫定+阿德夫韦+替米夫定耐药与B基因型YIDD突变、C基因型YVDD突变正相关。通过对HBV基因分型以及耐药位点的检测,对临床及时调整用药方案有一定帮助。     

恩替卡韦治疗104例乙型肝炎肝硬化患者96周的疗效观察

目的 观察恩替卡韦治疗乙型肝炎肝硬化的临床疗效.方法 随机选择就诊于长春市中日联谊医院消化内科未经过抗病毒治疗的乙型肝炎肝硬化患者104例,给予恩替卡韦0.5 mg,每日1次口服,连续口服96周时总结临床疗效.观察患者治疗前、后血清HBV DNA水平、肝功能及HBV标志物,其中37例患者治疗前及治疗96周后行肝组织学检查.率的比较采用χ~2检验,相关性分析采用Pearson相关系数.结果 恩替卡韦治疗4周时,HBV DNA水平平均下降3.1 log_(10),至96周时平均下降幅度达到5.1 log_(10),HBV DNA不可测率达到98.1%,ALT复常率达到80.7%;72例HBeAg阳性患者96周时HBeAg/抗-Hbe血清转换率为13.9%.104例乙型肝炎肝硬化患者中,C基因型HBV感染者64例,占61.5%,B基因型28例,占26.9%.不同基因型HBV感染者患者接受恩替卡韦治疗后的HBV DNA不可测率、ALT复常率以及HBeAg血清转换率差异无统计学意义.Child-Pugh C级2例(2/21,9.5%),Child-Pugh B级1例(1/52,1.9%)出现疾病进展,Child-Pugh A级患者31例,未出现疾病进展.37例行肝组织学检查的乙型肝炎肝硬化患者治疗96周时,肝组织学改善者Child-Pugh A级17例(17/21,81.0%),B级6例(6/9,66.7%),C级3例(3/7,42.9%).治疗前HBV DNA水平越高,Knodell HAI评分越高,r=0.80.抗病毒治疗96周后血清HBV DNA下降水平与Knodell HAI评分下降水平仍呈正相关,r=0.93.结论 恩替卡韦抗病毒治疗乙型肝炎肝硬化患者疗效显著,可延缓及阻止肝硬化患者的疾病进展.     

秦皇岛市136例慢性乙型肝炎患者拉米夫定的疗效及其与HBV基因型的关系

目的:探讨秦皇岛市慢性乙型肝炎(CHB)患者拉米夫定治疗疗效与基因型的关系。方法:136例CHB患者口服拉米夫定,100mg/次,1次/d,疗程48周,用药前采用PCR方法测定乙型肝炎病毒(HBV)A～D基因型。结果:秦皇岛市CHB患者基因型以C型为主,占75.74%,其次为B基因型占16.91%,B/C混合型占7.35%,B基因型在拉米夫定抗病毒治疗48周时显示HBV DNA阴转率、HBeAg血清转换率、ALT复常率、治疗有效率4方面均高于C型及B/C基因型(P0.05),B基因型HBV感染者有较低的YMDD变异发生率。结论:拉米夫定抗病毒疗效与基因型有关,HBV基因型测定可作为预测拉米夫定抗病毒疗效的指标。     

HBV基因型与恩替卡韦抗病毒疗效间的关系

目的:探讨慢性乙型肝炎(CHB)患者基因型与恩替卡韦(博路定)抗病毒治疗疗效、病毒变异间的关系。方法:对2010-01-01-2011-12-31接受治疗的的CHB患者首先进行基因型检测,选择B和C型患者共168例,研究其恩替卡韦抗病毒治疗24周及96周后丙氨酸氨基转移酶(ALT)、乙型肝炎病毒基因(HBV-DNA)低于检测下限率(20U/ml)、乙肝e抗原(HBeAg)血清学转换率以及治疗结束(96W)后HBV P基因的变异情况。结果:168例患者中B基因型有98例(58.33%),C基因型70例(占41.67%)。恩替卡韦抗病毒治疗24周时和96周时,B型与C型患者ALT复常率、HBV-DNA低于检测下限率和HBeAg血清学转换率间差异无统计学意义(P0.05);但治疗96周时B型和C型感染者间均较治疗24周时有显著提高;治疗结束时,B型感染者发生基因变异1例,C型感染者发生变异7例,两者比较差异有统计学意义(连续校正χ2=5.415,P0.05)。结论:HBV-DNA与恩替卡韦抗病毒疗效间无明显关系,延长疗程可明显提高其疗效,但随着疗程的增加,C型CHB患者P基因变异率明显高于B型。     

武汉地区157例乙型肝炎病毒基因分型和耐药性分析

目的了解武汉市乙型肝炎病毒基因型分布特点和乙型肝炎病毒耐药情况。方法采用基因测序法检测武汉市区157例患者HBV基因型,目标检测基因型为A~H等8个基因型,检测HBV 11个耐药位点:rt L80、rt L169、rt V173、rt L180、rt A181、rt T184、rt A194、rt S202、rt M204、rt N236和rt M250,判断对HBV耐药的核苷类似物。结果武汉市区157例HBV感染者中,检出3种HBV基因型,其中B型占72.61%,C型占26.75%,D型占0.64%。共有68例(43.31%)耐药,其中B型70.59%,C型29.41%,基因B型和C型的HBV相比,耐药发生差异无统计学意义(χ2=0.379,P0.05)。对拉米夫定耐药41例,占全部耐药病例的60.29%,其中B型占73.17%,C型占26.83%;204I位点耐药17例,180M+204I位点耐药6例,180M+204V位点耐药12例,180M+204V/I位点耐药6例。对阿德福韦酯耐药20例,占全部耐药病例的29.41%,基因B型占75.0%,基因C型占25.0%,耐药位点为236T为9例,耐药位点为181T/V为7例,236T和181T/V联合耐药4例。对恩替卡韦耐药5例,占全部耐药病例的7.35%,基因B型3例,基因C型2例。拉米夫定和阿德福韦酯联合耐药2例,占全部耐药病例的2.94%,均为基因C型。替比夫定耐药与其他核苷类似物耐药分析结果重复,共32例,占47.06%,基因B型75.0%,基因C型25.0%。结论武汉市区157例乙型肝炎病毒感染者中男性较多,感染HBV主要基因型为B型,其次为C型,患者主要表现为拉米夫定、替比夫定和阿德福韦酯耐药。临床应根据患者HBV基因型和耐药情况个体化制定治疗方案。     

不同核苷(酸)类药物治疗乙型肝炎相关性肝癌患者成本效益分析

目的探讨不同核苷(酸)类药物治疗乙型肝炎相关性肝癌患者的疗效与成本-效益。方法采用随机数字表法将144例乙型肝炎相关性肝癌患者分为A、B、C、D四组,每组36例,在TACE术后分别口服恩替卡韦、拉米夫定、阿德福韦酯和替比夫定抗病毒治疗,观察48 w。采用Cochran Armitage趋势检验进行成本-效益分析。结果 A组和B组血清ALT复常率分别为94.4%和88.9%,均显著高于C组的77.8%和D组的75.0%(P0.05),HBV DNA转阴率分别为100.0%和100.0%,均显著高于C组的91.6%和D组的91.6%(P0.05);A、B、C、D四组ALT复常率成本-效益分别为33.81%、36.29%、38.87%和75.71%,HBV DNA转阴成本-效益分别为114.82%、129.04%、155.88%和255.77,呈递增趋势。结论乙型肝炎相关性肝癌患者优选的核苷(酸)类药物是恩替卡韦和拉米夫定。     

340例慢性乙型肝炎患者乙型肝炎病毒多位点耐药相关突变分析

目的 分析慢性乙型肝炎患者HBV逆转录酶基因与核苷(酸)类似物耐药相关的12个位点上的突变情况及其临床意义.方法 提取血清HBV DNA,扩增HBV逆转录酶基因,对PCR产物进行DNA双向测序,对测序成功的样本进行基因型分析.检测逆转录酶基因12个位点上的碱基突变情况,分析不同核苷(酸).类似物使用情况、患者的耐药相关突变情况及不同核苛(酸)类似物耐药的突变形式. 结果 检出拉米夫定耐药突变63例,阿德福韦耐药突变10例,恩替卡韦耐药突变8例,替比夫定耐药突变1例.拉米夫定耐药突变中以M204V和M204I最常见,前者通常伴随L180M突变,后者常单独出现,阿德福韦耐药中以N236T±A181位碱基替换为主;恩替卡韦耐药突变发生在拉米夫定耐药基础上,以T184位碱基替换为主;替比夫定的耐药突变为M204I.少数未接受过核苷(酸)类似物治疗的患者也可检出耐药相关突变.结论 检测HBV逆转录酶基因多位点耐药相关突变,有助于临床及时发现和确认乙型肝炎患者是否存在HBV耐药,合理进行抗病毒治疗.     

替比夫定与恩替卡韦用于慢性乙型肝炎初治者的疗效观察

替比夫定是国内最新上市的核苷(酸)类似物,其抗病毒疗效优于拉米夫定,亦优于阿德福韦酯[1],在体外实验和人体临床试验均显示了很强的抗HBV活性,而恩替卡韦的临床试验同样显示了其强大的病毒抑制作用.目前尚无完整的两者对比研究.本文通过对177例慢性乙型肝炎(CHB)初治患者使用替比夫定或恩替卡韦观察分析其1年时的疗效.     

慢性乙型肝炎患者HBV基因型分布及其耐药基因突变分析

目的探讨慢性乙型肝炎(CHB)患者HBV基因型及其耐药突变发生情况。方法纳入240例接受核苷(酸)类似物单药或联合或序贯治疗的CHB患者,采用PCR扩增HBV逆转录(RT)区和序列测定鉴定耐药基因突变,采用HBV S基因测序法鉴定基因型。结果在35例单用拉米夫定治疗的CHB患者中,发生耐药突变14例(40.0%),突变位点为rt L80I/V、rt Vl73L、rt Ll80M、rt M204V/I和rt V207I,23例单用阿德福韦治疗者发生耐药突变11例(47.8%),突变位点为rt Al81T/V、rt S213T/N、rt V214A、rt Q215S/H/P、rtl233V、rt N236T、rt P237H和rt N/H238A/K/D/S,70例单用恩替卡韦治疗者发生耐药突变10例(14.3%),突变位点为rt M204I,12例单用替比夫定治疗者发生耐药突变5例(41.7%),突变位点为rt I169T、rt L180M、rt T184G/S/A/I/L/F、rt S202I/G、rt M204V和rt M250V/I/L,100例接受联合或序贯治疗者发生耐药突变51例(51.0%),突变位点为rt A194T,恩替卡韦治疗患者耐药突变发生率最低(P0.05);240例CHB患者中,HBV基因B型21例(8.8%)、C型216例(90.0)和D型3例(1.2%);在发生耐药突变的91例患者中,B型6例(6.6%)、C型83例(91.2%)和D型2例(2.2%,x2=1.22,P0.05);在发生耐药突变的6例B型感染者中有2例(33.3%)和83例C型感染者中有15例(18.1%)发生了多重耐药突变。结论检测CHB患者感染HBV基因型并及时获得耐药突变基因分布,将有助于指导临床治疗。     

恩替卡韦、拉米夫定治疗乙型重型肝炎的疗效和安全性

目的评估恩替卡韦、拉米夫定治疗HBV相关重型肝炎的疗效和安全性。方法选择2010年1月1日至2015年12月31日在本科住院治疗HBV相关慢加亚急性肝衰竭患者157例,分3组,恩替卡韦组52例,拉米夫定组55例,对照组50例。3组患者均接受内科综合治疗,恩替卡韦、拉米夫定组分别口服恩替卡韦、拉米夫定抗病毒治疗。观察指标包括:24周生存率,12周HBV DNA转阴率、肝功能、凝血酶原活动度(PTA)变化,住院时间,腹水、肝性脑病、消化道出血、肝肾综合征、自发性腹膜炎等并发症的发生率。结果恩替卡韦、拉米夫定组患者的24周生存率分别为69.2%(36/52)、72.7%(40/55),高于对照组56%(28/50)(P均0.05)。治疗12周,恩替卡韦、拉米夫定组较对照组患者的TBil、ALT、AST均显著下降(P均0.05)、PTA显著升高(P0.05);HBV DNA的转阴率分别为88.5%(46/52)、85.5%(47/55),高于对照组10%(5/50)(P均0.05)。恩替卡韦、拉米夫定组肝性脑病、肝肾综合征、腹水发生率均低于对照组(P均0.05),平均住院时间分别为(85±48.6)d、(79±44.3)d,低于对照组(124.3±58.5)d(P均0.05)。结论恩替卡韦、拉米夫定可提高乙型重型肝炎患者的生存率、减少并发症、缩短住院时间,安全性良好。     

拉米夫定和阿德福韦酯抗乙型肝炎病毒耐药位点检测及临床意义

目的对应用拉米夫定或阿德福韦酯治疗后耐药的慢性乙型肝炎患者给予联合治疗,观察治疗前后乙型肝炎病毒（HBV）变异模式的变化及对疗效的影响。方法在142例对拉米夫定耐药患者中,给予72例拉米夫定联合阿德福韦酯、70例给予恩替卡韦联合阿德福韦酯冶疗,在72例对阿德福韦酯耐药患者中,给予36例联合拉米夫定、另36例联合恩替卡韦治疗,各组均治疗48 w,测定和比较治疗前后所有患者HBV DNA聚合酶逆转录区相关变异位点变化。结果在拉米夫定初治发生耐药的患者中,发生M204V和IL180M变异率分别为98.6%（140/142）和56.3%（80/142）,接受拉米夫定联合阿德福韦酯治疗患者HBV DNA阴转率为86.1%,与恩替卡韦联合阿德福韦酯治疗患者（97.1%）比,无显著性差异;在阿德福韦酯初治发生耐药的患者中,A181V和N236T变异频率分别为63.9%（46/72）和52.8%（38/72）,接受阿德福韦酯联合拉米夫定治疗患者HBV DNA阴转率为52.8%,显著低于阿德福韦酯联合恩替卡韦组（77.8%,P〈0.05）;在阿德福韦酯联合拉米夫定治疗的36例患者中,19例（52.8%）HBV DNA阴转,在阿德福韦酯联合恩替卡韦治疗的36例患者中,28例（77.8%）患者HBV DNA阴转,差异具有显著性（x2=4.963,P〈0.05）。结论以rtM204变异为主的拉米夫定耐药在联合阿德福韦酯进行挽救治疗后疗效确定;以rtA181变异为主的阿德福韦酯耐药患者在接受阿德福韦酯联合恩替卡韦治疗后的疗效优于联合拉米夫定。     

Therapeutic strategies in the management of patients with chronic hepatitis B virus infection

Currently available options for the treatment of chronic hepatitis B virus (HBV) infection include standard and pegylated interferon alfa and four oral antiviral agents (lamivudine, adefovir, entecavir, and telbivudine). These treatment strategies are either therapies of finite duration that aim to achieve sustained off-therapy responses, or long-term treatments that aim to maintain on-therapy remission. Pegylated interferon alfa may offer higher sustained off-therapy responses after 1 year, but most patients do not respond. Oral antivirals are the only candidates for long-term treatment of patients with chronic HBV infection. Viral suppression has favourable effects on patients' outcome and modifies the natural history of the disease. Viral resistance is the main drawback of long-term antiviral therapy. Lamivudine monotherapy is associated with higher resistance (year 1, 10-27%; year 2, 37-48%; year 4, 60-65%) than adefovir (year 1, 0%; year 2, 3%; year 5, 29%) or telbivudine (year 1, 3-4%; year 2, 9-22%). Entecavir resistance is rare in naive individuals (year 4, <1%), but increases over time in lamivudine-resistant patients (year 4, 43%). The best strategy for long-term therapy in chronic HBV infection has yet to be established.     

核苷（酸）类似物治疗慢性乙型肝炎致血清肌酸激酶升高的临床观察与处理

目的观察核苷（酸）类似物拉米夫定（LAM）、阿德福韦酯（ADV）、替比夫定（LdT）和恩替卡韦（EDV）治疗慢性乙型肝炎（GHB）患者血清肌酸激酶（CK）升高的发生率、意义和处理方法。方法370例CHB患者分别接受LAM（n=108）、ADV（n=146）、LdT（n=78）和ETV（n=38）治疗52周。将血清CK升高分为轻度、中度和重度，同时观察肌肉、关节疼痛情况，并作相应的处理。结果在LAM治疗组，出现血清CK轻度升高10例（9．25％）；在ADV治疗组，CK轻度升高12例（8．22％）；在LdT治疗组，出现CK升高13例（16．7％），其中10例（12．9％）为轻度升高，2例（2．6％）为中度升高，1例（1．3％）为重度升高；在EDV治疗组，2例（0．53％）轻度升高。结论核苷（酸）类似物在治疗CHB过程中均可有血清CK一过性升高，轻度升高者无需停药，能自行缓解，对重度升高者，应换药治疗。CK升高的发生率并未随治疗时间的延长而增加。     

Hepatitis B virus infection and pregnancy

Pregnancy only mildly affects that natural progression of acute and chronic infection by the hepatitis B virus (HBV) but it does bring to light three important questions. Mother to child (vertical) transmission risk is best prevented by mandatory HBs antigen testing in all pregnant women in their second trimester and by systemic serovaccination of newborns of infected mothers. In mothers with high viral load, vertical infection in utero could be prevented by lamivudine, telbivudine or tenofovir treatment. Invasive obstetric or gynecological procedures (such as amniocentesis, forceps, etc.) do not seem to increase the risk of vertical infection. Breastfeeding is not contraindicated in maternal HBV infection after serovaccination of the newborn. This holds true for mothers on active treatment with tenofovir which is not absorbed into breast milk. When it comes to managing active antiviral treatment, in absence of virosuppression with lamivudine, tenofovir remains a logical step-up treatment; in absence of virosuppression with adefovir, tenofovir also remains a logical step-up choice as do tenofovir/emtricitabine combinations or lamivudine in absence of preexisting resistance which may have been induced during combination treatment of adefovir and lamivudine. In cases of effective virosuppression with treatment by analogues, lamivudine should be continued and entecavir should eventually be replaced by lamivudine, telbivudine or tenofovir; adefovir should be replaced by tenofovir or lamivudine in absence of resistance (which would require tenofovir therapy) or adefovir which would restrict lamivudine therapy.     

Current treatment of chronic HBV infection: A North American perspective

Chronic hepatitis B virus (HBV) infection remains a major cause of liver disease and hepatocellular carcinoma worldwide. Although less prevalent in the United States than in other areas of the world, HBV infection results in a significant disease burden in many American immigrant communities. Seven treatments are approved by the US Food and Drug Administration for the treatment of chronic HBV infection: interferon-α (standard interferon-α2b or pegylated interferon-α2a), and the nucleos(t)ide analogues lamivudine, adefovir dipivoxil, entecavir, telbivudine, and tenofovir disoproxil fumarate. There is preliminary evidence that the disease burden from HBV infection may be diminishing in the United States, reflecting not only HBV vaccine progress but also more than a decade of antiviral therapy.     

Long-term efficacy of entecavir therapy in chronic hepatitis B patients with antiviral resistance to lamivudine and adefovir

No studies have reported the long-term effects of entecavir switching in patients with multidrug resistance who developed resistance after lamivudine/adefovir sequential therapy. We evaluated the efficacy of 96 weeks of entecavir therapy in patients with resistance to lamivudine/adefovir sequential therapy. In total, 33 patients with chronic hepatitis B virus (HBV) infection with evidence of active viral replication (HBV DNA levels ≥ 10(5) copies/mL) or a history of treatment failure to lamivudine/adefovir sequential therapy between April 2007 and July 2009 were treated with entecavir (1.0 mg daily) for at least 48 weeks. The rates of alanine transaminase (ALT) normalization and HBV DNA negativity were 66.7% (14/21) and 24.2% (8/33) at 48 weeks, respectively. The initial HBV DNA level was the only factor that was inversely associated with serum HBV DNA negativity after 48 weeks of entecavir therapy (P < 0.023). At 96 weeks, the rates of ALT normalization and HBV DNA negativity were 77.8% (7/9) and 16.7% (3/18), respectively. Viral breakthrough occurred in 21.2% (7/33) and 78.9% (15/19) of patients at 48 and 96 weeks, respectively. Patients who achieved a HBV DNA level of <4 log(10) copies/mL at 48 weeks maintained a similar HBV DNA level and a normal ALT level until 96 weeks. Entecavir monotherapy for 96 weeks was not efficacious for patients with lamivudine/adefovir-resistant HBV. The initial HBV DNA level was the only predictive factor for antiviral efficacy. However, patients who achieved a HBV DNA level of <4 log(10) copies/mL with a normal ALT level at 48 weeks should maintain, rather than stop, entecavir therapy.     

Management of antiviral-resistant chronic hepatitis B virus infection

Substantial progress has been made in the treatment of chronic hepatitis B during the past decade. Nucleos(t)ide analogues are now widely used due to their convenience, less side effects, and considerable response rates. However, development of antiviral resistance is a major problem being considered as the most important factor for the treatment failure. Viral breakthrough associated with selection of antiviral-resistant hepatitis B virus (HBV) is usually followed by biochemical breakthrough, clinical deterioration, and even progressive liver failure. Therefore, appropriate management of antiviral resistance is critical for improving treatment outcomes. Strategies for the management of antiviral-resistant chronic HBV infection are described herein considering recently published guidelines. Lamivudine/telbivudine resistance can be managed by adding adefovir. Switching to adefovir or entecavir is also a viable option. However, careful follow-up of viral load is mandatory to detect any primary or secondary treatment failure in case of sequential monotherapy. Interferon or peg-interferon therapy can also be considered in case of young patients with compensated liver disease. For adefovir resistance, lamivudine can be added, but adding or switching to entecavir is a more reasonable option. Likewise, adding or switching to adefovir can be considered for entecavir resistance. Adding or switching to tenofovir needs to be considered upon availability. Experiences for clevudine resistance are still lacking, and need to be studied further upon the isolation of clinically resistant strains. To avoid emergence of resistant mutations, antiviral therapy should be initiated after careful balance of risk and benefit, and the most potent antiviral agent with the lowest resistance rate should be selected.     

Hepatitis B virus treatment in HIV-infected patients

Hepatitis B virus (HBV) infection is common in HIV-infected persons and is associated with increased risk of liver-related morbidity and mortality. Agents available to treat HBV infection in coinfected patients include lamivudine, entecavir, emtricitabine, adefovir, peginterferon alfa, and the recently approved telbivudine. Treatment decisions should take into account a number of factors, including antiretroviral therapy status, HBV genotype, prior experience of lamivudine, and the need to avoid drug resistance in both HIV- and HBV-infected persons. This article summarizes a presentation on treatment and management of HBV infection in HIV-infected patients made by Chloe L. Thio, MD, at the 9th Annual Ryan White CARE Act Update in Washington, DC. The original presentation is available as a Webcast at www.iasusa.org.     

原发性肝癌局部化疗后肝炎及乙型肝炎抗病毒治疗的临床研究

目的分析肝癌化疗后肝炎发生的病因,探讨核苷类似物抗病毒治疗对化疗后乙肝病毒再激活肝炎疗效。方法收集明确诊断乙型肝炎后肝细胞癌患者120例,男108例,女12例,年龄28~85岁,平均（53.88±12.16）岁。肝癌患者均接受1次经导管肝动脉化疗栓塞（TACE）治疗;并分为抗病毒治疗组35例;未行抗病毒治疗组85例。抗病毒组中TACE前2周23例服拉米夫定;12例服阿德福韦酯,维持抗病毒治疗TACE后4周为观察终点。随访4周后,监测2组患者TACE前后肝功能及HBV载量水平变化和肝炎发生情况,观察核苷类似物抗病毒治疗HBV再激活肝炎的疗效。结果肝细胞癌患者化疗后HBV再激活33例,化疗后未再激活87例,HBV再激活发生率为27.50%。HBV再激活肝炎23例,发生率为69.70%;化疗药物性肝炎11例,发生率为12.64%,2种肝炎的发生之间差异有统计学意义（P=0.00）。抗病毒治疗组与未抗病毒组之间HBV再激活肝炎的发生差异有统计学意义（2χ=5.78,P〈0.05）,2组间药物性肝炎的发生差异无统计学意义。结论肝细胞癌化疗后发生HBV再激活肝炎和化疗药物性肝炎;HBV再激活肝炎的发生较化疗药物性肝炎多。核苷类似物（拉米夫定/阿德福韦酯）抗病毒治疗可明显降低肝细胞癌患者化疗后HBV再激活肝炎的发生。