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1.
抗病毒治疗乙型肝炎相关慢加急性肝衰竭患者的临床研究   总被引:1,自引:0,他引:1  
目的:探讨抗病毒治疗乙型肝炎相关慢加急性肝衰竭(acute on chronic liver failure,ACLF)的临床意义。方法:回顾性分析2007年8月~2013年8月我院收治的乙型肝炎相关慢加急性肝衰竭的住院患者80例,按照患者有无接受抗病毒治疗分为抗病毒治疗组(A组)50例和未抗病毒治疗组(B组)30例,分析患者接受治疗后的近期与远期疗效、并发症及生存率。结果:1出院时A组好转率70%;B组好转率33.3%。两组比较差异有统计学意义(x2=10.243,P=0.0010.05)。2治疗14周后A组乙肝病毒DNA阴转率72%;B组阴转率30%,两组比较差异有统计学意义(x2=13.440,P=0.0000.05)。3A组出现细菌感染45例,电解质紊乱41例,消化道出血5例,肝性脑病10例,肝肾综合征10例,B组出现细菌感染30例,电解质紊乱27例,消化道出血6例,肝性脑病10例,肝肾综合征12例,两组比较差异无统计学意义(x2=2.755,P=0.0970.05)。4随访5年,A组存活36例,死亡14例,12、36和60个月累积生存率分别为78.5%、71.2%、71.2%,B组存活5例,死亡25例,12、36和60个月累积生存率分别为35.4%、27.5%、27.5%,两组比较差异有统计学意义(P0.05)。结论:对乙型肝炎相关慢加急性肝衰竭患者给予抗病毒治疗可明显改善预后,提高生存率。  相似文献   

2.
目的观察丽珠肠乐及莫沙必利治疗慢加急性(亚急性)肝衰竭临床疗效。方法将2003年1月至2007年12月间住院的慢加急性(亚急性)肝衰竭患者随机分为治疗组和对照组,对照组仅给予内科综合治疗,治疗组在此基础上加用丽珠肠乐及莫沙必利口服治疗,疗程1月。结果治疗组有效率(79%)优于对照组(43%),治疗组治疗后出血、感染、肝性脑病、肝肾综合征、腹水并发症少于对照组。结论丽珠肠乐及莫沙必利治疗慢加急性(亚急性)肝衰竭临床疗效显著,预后改善明显。  相似文献   

3.
目的:探讨药物性肝衰竭的病因、临床特征及预后相关因素,提高对药物性肝衰竭的认识,减少不良事件发生的几率。方法:对2007年1月至2011年12月我院56例药物性肝衰竭患者进行回顾性分析,对患者用药情况、临床表现、肝衰竭的分型、并发症的发生、生化指标的特点及治疗与预后进行相关性分析。结果:导致肝衰竭前三位的药物分别是中药占30.3%、抗结核药占26.8%和非甾体类抗炎药占23.2%。发病时常见的临床表现为乏力64.2%、纳差60.7%、尿黄60.7%。并发症发生率最高的是感染73.2%、其次为肝性脑病66.1%、腹水64.3%。感染部位以腹腔最常见,占46.4%,其次为肺部41%。治愈好转者为18例(26.2%),治疗无效者14例(25.0%);死亡者为24例(42.9%)。从患者发病到死亡的中位时间为35天。治愈好转组的肝性脑病和消化道出血的发生率明显低于无效死亡组,激素治疗与好的预后密切相关(P〈0.05)。结论:药物性肝衰竭的主要致病药物有中药、抗结核药和解热镇痛药。患者的临床表现无明显特异性,肝性脑病和消化道出血一旦出现提示预后差。在疾病早期采用适当的激素治疗,可以明显改善肝衰竭患者的预后。  相似文献   

4.
目的:探讨前列腺素E1(PGE1)对早期乙型肝炎慢加急性肝衰竭患者的临床疗效及安全性。方法:采用随机对照方法进行前瞻性试验。将100例早期乙型肝炎慢加急性肝衰竭患者随机分为前列腺素E1治疗组和综合治疗组(对照组),前列腺素E1治疗组在常规内科综合治疗的基础上加用PGE1 10μg治疗,每天1次,疗程4周,综合治疗组为常规内科综合治疗。观察和比较治疗前后两组的肝功能指标水平、消化道和全身症状以及不良反应的发生情况,评价两组的临床疗效。结果:治疗过程中,前列腺素E1治疗组的总有效率为80%,显著优于综合治疗组的62%(P0.05)。治疗过程中,两组患者血清胆红素水平均明显下降,但前列腺素E1治疗组下降幅度较对照组更加明显。治疗第2周时,治疗组和对照组患者血清胆红素水平分别为252±103μmol/L和269±113.2μmol/L(P0.05),4周时,则分别为89.8±53.2μmol/L和114.8±62.5μmol/L(P0.01),显著低于第2周时水平。临床症状好转率和其他化验指标(如ALT、GGT)均较治疗前显著降低,但无统计学差异(P0.05)。前列腺素E1治疗组不良反应的发生率为14%,而综合治疗组未见不良反应发生。结论:PGE1治疗早期乙型肝炎慢加急性肝衰竭患者的疗效明显优于综合内科治疗组,能显著改善肝功能,促进黄疸消退,不良反应少。  相似文献   

5.
目的探讨牙周组织再生术(PTR)联合无托槽隐形矫治对牙周炎患者龈沟液炎症因子的影响,为该类患者的治疗提供参考。方法选取2017年3月至2019年3月我院收治的120例牙周炎患者为研究对象,依据随机数字表分为再隐组和再直组,每组60例。再隐组患者给予PTR联合无托槽隐形矫治,再直组患者给予PTR联合直丝弓矫治。比较两组患者龈沟液炎症因子[白介素6(IL-6)、C反应蛋白(CRP)、肿瘤坏死因子α(TNF-α)]水平、牙周健康状况[牙周探诊深度(PD)、牙龈指数(GI)、龈沟出血指数(SBI)、牙菌斑指数(PLI)、临床附着丧失(CAL)]、治疗疗效和并发症情况。结果再隐组和再直组患者治疗后龈沟液IL-6、CRP、TNF-α水平及PD、GI、SBI、PLI、CAL明显低于治疗前,再隐组患者治疗后龈沟液IL-6、CRP、TNF-α水平及PD、GI、SBI、PLI、CAL明显低于再直组,差异均有统计学意义(均P0.05)。再隐组患者治疗有效率为95.00%,明显高于再直组的80.00%,差异有统计学意义(χ~2=6.171,P=0.013)。再隐组患者并发症发生率为5.00%,明显低于再直组的16.67%,差异有统计学意义(χ~2=4.227,P=0.040)。结论 PTR联合无托槽隐形矫治可有效改善牙周炎患者龈沟液炎症因子水平及牙周健康状况,有利于提高疗效和减少并发症,值得临床推广。  相似文献   

6.
目的分析儿童隐球菌性脑膜炎临床特点。方法回顾性分析76例隐球菌性脑膜炎患儿临床资料。结果男47例,女29例,平均年龄(6.34±3.67)岁;主要临床表现为发热(100%)、头痛(78.95%)、呕吐(81.58%);首次脑脊液墨汁染色阳性46例(60.53%),首次脑脊液真菌培养阳性21例(27.63%),两性霉素B联合5-氟胞嘧啶抗真菌治疗好转率(74.19%),两性霉素B联合氟康唑治疗好转率(62.96%),差异无统计学意义(P=0.75)。结论儿童隐球菌性脑膜炎极易误诊、漏诊,反复、多次腰穿有助于早期诊断;两性霉素B联合5-氟胞嘧啶是抗真菌治疗首选方案,早期诊断、积极降颅压是改善预后的关键。  相似文献   

7.
微生态调节剂在慢性重型肝炎患者的治疗作用   总被引:2,自引:0,他引:2  
目的探讨微生态调节剂整肠生和乳果糖在慢性重型肝炎的治疗作用。方法 162例慢性重型肝炎患者被随机分为治疗组(84例)和对照组(78例)。对照组给予常规的综合治疗,治疗组在对照组的基础上给予整肠生胶囊4粒、乳果糖口服液10 ml每日3次口服,疗程为4周。比较2组病例治疗后主要症状和体征、肝功能、凝血功能、内毒素、血氨、并发症发生率及病死率。结果与对照组比较,治疗组更有效地改善患者临床症状、肝功能及凝血功能,降低血浆内毒素、血氨浓度,减少自发性腹膜炎(SBP)、肝性脑病(HE)和肝肾综合征(HRS)等并发症发生率和患者病死率。结论微生态制通过调整肠道失调菌群,能改善患者肝功能和凝血功能,降低血氨和内毒素血症,减少并发症和病死率,对慢性重型肝炎有明显治疗作用。  相似文献   

8.
目的:阐明乙型肝炎相关急性肝衰竭的预后因素和恩替卡韦的疗效。方法:本研究回顾性选取了47名因感染乙型肝炎病毒而明确诊断急性肝衰竭的患者,其中5名短期内行肝移植手术被排除,其余42名患者的数据被总结分析。结果:42名患者中12名患者服用了恩替卡韦,在诊断之初,服用恩替卡韦组和未服用恩替卡韦组的一般情况基本相当。使用与未使用恩替卡韦者的生存率分别为67%和23%,此外,年龄〉45岁和没有服用恩替卡韦是不良预后的两个独立相关因素。在年龄〉45岁的患者中使用恩替卡韦和未使用恩替卡韦者的存活率分别为50%和8%。结论:本研究证实了恩替卡韦对乙肝相关急性肝衰竭的治疗作用,我们建议所有乙型肝炎病毒引起的急性肝衰竭患者均应尽早开始恩替卡韦抗病毒治疗。  相似文献   

9.
幽门螺杆菌感染与门脉高压性胃病的发病关系   总被引:1,自引:0,他引:1  
为了解门脉高压性胃病 (portalhypertensivegastropathyPHG)与幽门螺杆菌 (HP)感染的关系 ,选门脉高压性胃病胃窦粘膜 30例 ,免疫组化SP法 (链霉菌抗生物素蛋白—过氧化酶法 ,Streplavidin Peroxidase,SP)抗HP抗体染色 ,并以慢性乙型肝炎并胃病 2 0例及非肝病胃病 2 1例胃窦粘膜作对照。结果显示 ,30例门脉高压性胃病阳性2 2例 ,占 73.3% ;2 0例慢乙肝组阳性 11例 ,占 5 5 % ;2 1例非肝病组阳性 11例 ,占 5 2 .38%。门脉高压组HP感染阳性率与慢乙肝组、非肝病组相比差异无显著性 (P >0 .0 5 )。可见HP感染虽不是门脉高压性胃病的发生原因 ,但在治疗中短期加用杀HP的药物是必要的。  相似文献   

10.
目的:观察新生儿体内母源性乙型肝炎表面抗体(抗-HBs)对乙型肝炎疫苗接种后抗体应答的远期影响。方法:2006年10月-2007年1月在南京大学医学院附属鼓楼医院产前检查并住院分娩的单胎足月妊娠妇女中,选择抗-HBs阳性孕妇32例,抗-HBs阴性孕妇32例,其新生儿均按0、1、6方案接种重组(酵母)乙型肝炎疫苗,检测两组儿童乙型肝炎疫苗第3针接种后2年血清抗-HBs浓度。结果:新生儿接种乙型肝炎疫苗第3针后2年,母源性抗-HBs阴性组与阳性组儿童抗-HBs阳性率分别为90.6%与87.5%,其抗-HBs几何平均浓度分别为73.48mIU/ml与75.49mIU/ml,两组间抗-HBs阳性率与GMC的差异均无统计学意义(P=1.000,P=0.778);6例母源性抗-HBs>1000mIU/ml儿童中1例抗-HBs转阴(16.7%),而母源性抗-HBs<1000mIU/ml组和母源性抗-HBs组的儿童抗-HBs转阴率分别仅为7.69%和11.1%,但差异无统计学意(P=0.811)。结论:新生儿目前按照0,1,6方案接种乙型肝炎疫苗,能够有效保护其抵抗乙型肝炎病毒的感染;母源性抗-HBs对新生儿接种乙型肝炎疫苗...  相似文献   

11.
Liver failure induced by hepatitis B virus (HBV) is a severe disease with a high mortality rate. Liver support treatment is a powerful method for treating liver failure and is a bridge to liver transplantation. Patients with similar liver function indices, however, have different outcomes following treatment, and no satisfying prediction parameters exist. In this study, we used ultraperformance liquid chromatography-mass spectrometry (UPLC-MS) to investigate plasma metabolites in groups of acute-on-chronic liver failure patients with different prognosis. An orthogonal partial least squares (OPLS) model, with satisfactory explanatory and predictive ability (R 2 Y?=?0.943, Q 2?=?0.913) was established using SIMCA-P?+?12.0. The model was based on samples collected just before the first artificial treatment for comparable model efficacy. The concordance statistics of our model was 0.968 (95% CI [0.951, 0.985]) which is superior to that of the MELD (the Model for End-stage Liver Diseases) score (0.737, 95% CI [0.578, 0.896]). Three groups of markers were identified: lysophosphatidylcholine, primary fatty acid amides and conjugated bile acids. Lysophosphatidylcholine and conjugated bile acids were protection factors for survival and primary fatty acid amides were risk factors. The cut-off point for the predictive value of our model was greater than or equal to 0.196, at which the model showed the best discrimination between the recovery and non-recovery groups, with a sensitivity of 95% and a specificity of 87%. This metabolomic model, based on plasma UPLC-MS profiles, provides not only excellent discrimination and prognostic ability for HBV-induced acute-on-chronic liver failure but also early and precise warning of possible liver transplantation.  相似文献   

12.
目的:分析肝移植术后肝脏淋巴回流淤滞(Intrahepatic lymphatic stasis,IHLS)的影响因素。方法:收集我院自2004~2012年期间行肝移植手术并经增强计算机断层扫描(Computed tomography,CT)和/或磁共振(Magnetic resonance imaging,MRI)确诊的IHLS病人,分析正常肝移植组IHLS阳性率与肝移植术后静脉并发症、胆道并发症、乙肝复发、肝癌复发、动脉并发症、移植排斥、药物性肝损害、转移瘤组IHLS阳性率的差异。结果:正常移植肝组术后IHLS的阳性率分别与术后胆道并发症、静脉并发症、乙肝复发组肝移植术后IHLS的阳性率差异有统计学意义(P0.05),与其他并发症组IHLS的阳性率差异无统计学意义(P0.05)。结论:肝移植术后静脉并发症、胆道并发症及乙肝复发可影响肝移植术后IHLS发生。  相似文献   

13.
Hepatitis B virus (HBV)-associated acute-on-chronic liver failure (ACLF) is a clinical syndrome of severe liver damage. HBV infection is affected by N6-methyladenosine (m6A) RNA modification. Here, we investigated whether methyltransferase-like 3 (METTL3)-mediated m6A methylation can affect ACLF. Human hepatic cells (THLE-2) were treated with lipopolysaccharide (LPS) to induce cell damage. Proliferation, apoptosis and m6A modification were measured by MTT assay, flow cytometry and Dot blot assay. Our results showed that HBV infection significantly enhanced the levels of m6A modification and elevated the expression of METTL3 and mature-miR-146a-5p in THLE-2 cells, which was repressed by cycloleucine (m6A inhibitor). METTL3 overexpression enhanced m6A modification and promoted mature-miR-146a-5p expression. METTL3 overexpression promoted HBV replication and apoptosis, enhanced the levels of pro-inflammatory cytokines, hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg), and repressed cell proliferation in THLE-2 cells, which attributed to repress miR-146a-5p maturation. Moreover, a severe liver failure mouse model was established by HBV infection to verify the impact of METTL3 knockdown on liver damage in vivo. HBV-infection led to a severe liver damage and increase of apoptosis in hepatic tissues of mice, which was abolished by METTL3 knockdown. METTL3 knockdown reduced METTL3 expression and impeded miR-146a-5p maturation in HBV-infected mice. In conclusion, this work demonstrates that METTL3 inhibition ameliorates liver damage in mouse with HBV-associated ACLF, which contributes to repress miR-146a-5p maturation. Thus, this article suggests a novel therapeutic avenue to prevent and treat HBV-associated ACLF.  相似文献   

14.
Toll-like receptors (TLRs) are a class of proteins that play key roles in innate immunity through recognition of microbial components. TLR3 is expressed abundantly in dendritic cells, and is responsible for recognizing viral pathogens and inducing interferon beta (IFN-β) production. Although TLR3 has been reported to be involved in several diseases caused by viral infections, its role in hepatitis B virus (HBV)-induced hepatitis is still largely unknown. We found that expression of TLR3 and IFN-β was decreased significantly in monocyte-derived dendritic cells (MoDCs) from patients with chronic hepatitis B (CHB, n = 40) or acute-on-chronic hepatitis B liver failure (ACHBLF, n = 60), compared with normal controls (n = 20). We observed a further decrease in TLR3 and IFN-β in ACHBLF compared to CHB patients. Compared with surviving patients, TLR3 and IFN-β expression was significantly lower in non-surviving ACHBLF patients, which strongly indicated a correlation between TLR3 signaling impairment in MoDCs and disease severity in ACHBLF patients. Further linear correlation analysis demonstrated significant correlations between expression of TLR3 signaling components (TLR3 and IFN-β) and disease severity markers (prothrombin activity and total bilirubin) for individual ACHBLF patients. To the best of our knowledge, this is the first study to show that MoDC impairment is correlated with severe liver damage in ACHBLF patients, which suggests the potential of TLR3/IFN-β expression in MoDCs as a diagnostic marker.  相似文献   

15.
Oxidative damage of albumin in advanced liver disease   总被引:1,自引:0,他引:1  
Albumin has a number of biological functions and the serum albumin level is related to prognosis in advanced liver disease. Oxidative stress is believed to play an important role in the pathogenesis of liver failure. The aim of the present study was to characterize oxidative modification of albumin in patients with various degrees of liver failure and to investigate implications for its binding function. Patients with liver cirrhosis (n=10), acute-on-chronic liver failure (n=8) and healthy controls (n=15) were included in the study. Three fractions of albumin were separated by HPLC according to the redox state of cysteine-34 and detected by fluorescence as well as UV absorption. Carbonyl groups were measured as a marker of oxidative modification in plasma proteins and, by western blotting, on albumin. Progressive oxidative modification of albumin was found with increasing severity of liver failure indicated by an increased content of carbonyl groups and oxidation of cysteine-34. Fluorescence properties of albumin were altered by oxidation and, in patients with acute-on-chronic liver failure, by high plasma levels of bilirubin. This alteration of albumin fluorescence by bilirubin provides evidence for a preferred binding of bilirubin to the fully reduced form of albumin.  相似文献   

16.
采用9种终末期肝病预后评分模型对乙型肝炎病毒相关性慢加急肝衰竭(hepatitis B virus-related acute-on-chronic liver failure,HBV-ACLF)患者进行预后评估,分析引起HBV-ACLF患者死亡的危险因素。连续收集2014年7月-2018年7月复旦大学附属华山医院确诊的HBV-ACLF患者,通过评估受试者工作特征曲线的曲线下面积(area under receiver operating characteristic curve,AUROC),判断目前9种终末期肝病预后评分模型预测HBV-ACLF患者预后的准确性。采用多因素Logistic回归分析,探讨HBV-ACLF患者死亡的危险因素。共纳入91例HBV-ACLF患者,死亡46例。COSSH-ACLFs评分对轻度、重度患者的短期和中期预后具有最佳预测能力(总体死亡率AUROC:28 d为 0.946,90 d为 0.920;按器官衰竭数量分级,0~1级:28 d为 0.900,90 d为 0.846;2~3级:28 d为 0.957,90 d为 0.917);确定COSSH-ACLFs评分的最佳临界点为 6.245,生存曲线分析显示评分>6.245 的患者生存率明显低于评分≤6.245 的患者(10.7% vs. 81.8%,P<0.000 1)。年龄、总胆红素、血小板计数、凝血系统衰竭、肝性脑病是HBV-ACLF患者死亡的独立危险因素。死亡组患者血小板计数显著低于生存组(P<0.002 2),血小板计数≤63×109/L与HBV-ACLF患者病情严重程度及预后显著相关。本研究证实COSSH-ACLFs评分模型预测HBV-ACLF患者预后的能力较其他评分模型更为准确,血小板计数与HBV-ACLF患者病情严重程度及预后显著相关。  相似文献   

17.
Excessive activation of innate immune response contributes to the pathogenesis of acute-on-chronic hepatitis B liver failure (ACLF-HBV). miR-146a was recently found to be implicated in the regulation of innate immunity. In this study, we explored the biological significance of a single-nucleotide polymorphism (rs2910164) within the miR-146a gene in the risk of acquiring ACLF-HBV. We completed a hospital-based case–control study including 717 cases of HBV-infected patients—251 cases of ACLF-HBV and 466 cases of chronic hepatitis B. Whole blood samples were collected for isolation of DNA and peripheral blood mononuclear cells (PBMCs). The association between genotypes and risk of ACLF-HBV was analyzed by multivariate unconditional logistic regression, with adjustment for sex and age. Our results showed that the GG homozygote was a protective genotype in terms of susceptibility to ACLF-HBV, with odds ratio?=?0.496, 95 % confidence interval?=?0.309–0.797, P?=?0.004 compared with CC+GC genotypes. The amount of mature miR-146a in PBMCs was significantly higher in the GG homozygote group than those in the CC and CG genotype groups of ACLF-HBV patients. The GG genotype group also represented lower serum level of TNF-α and higher survival rate (follow-up period?=?4 months). In conclusion, The GG genotype within the pre-miR-146a is reversely associated with susceptibility of ACLF-HBV in the studied Chinese population. This may be partially explained by the relatively higher amount of mature miR-146a and the lower serum level of TNF-α in this genotype group.  相似文献   

18.

Background and Aims

Previous work conducted by our group has shown that the accumulation of hepatic natural killer (NK) cells and the up-regulation of natural cytotoxicity receptors (NKP30 and NKP46) on NK cells from patients with hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) were correlated with disease progression in HBV-ACLF. The natural cytotoxicity receptors expressed on NK cells are believed to be probable candidates involved in the NK cell-mediated hepatocyte damage in HBV-ACLF. However, the underlying mechanisms remain to be elucidated. In the present study, we aimed to discover the role of NKP30-B7-H6 interaction in NK cells-mediated hepatocyte damage in HBV-ACLF.

Methods

Hepatic expressions of B7-H6 and interleukin-32 (IL-32) were examined by immunochemistry staining in samples from patients with HBV-ACLF or mild chronic hepatitis B (CHB). The cytotoxicity of NK-92 cell against target cells (Huh-7 and LO2) was evaluated by CCK8 assay. Expression of IL-32 in liver NK cell, T cells and NK-92 cell line was detected by the flow cytometric analysis. The effect of IL-32 on the apoptosis of Huh7 cells was evaluated using Annexin V/PI staining analysis.

Results

An enhancement of hepatic B7-H6 and IL-32 expression was associated with the severity of liver injury in HBV-ACLF. And there was a positive association between hepatic B7-H6 and IL-32 expression. Expressions of IL-32 in liver NK cells and T cells were increased in HBV-ACLF patients. In vitro NK-92 cells are highly capable of killing the high B7-H6 expressing Huh7 cells and B7-H6-tansfected hepatocyte line LO2 cells dependent on NKP30 and B7-H6 interaction. Furthermore, NK-92 cells exhibited elevated IL-32 expression when stimulated with anti-NKP30 antibodies or when co-cultured with Huh7 cells. IL-32 can induce the apoptosis of Huh7 cells in a dose-dependent manner.

Conclusion

Our results suggest that NKP30-B7-H6 interaction can aggravate hepatocyte damage, probably through up-regulation of IL-32 expression in HBV-ACLF.  相似文献   

19.
A 62-year-old man had chronic hepatitis B virus (HBV) infection and was diagnosed with liver cirrhosis. At the time of diagnosis the patient’s virologic markers were positive for hepatitis B surface antigen (HBsAg), antibody to hepatitis B e antigen (anti-HBe) and antibody to hepatitis B core antigen (anti-HBc), while antibody to hepatitis B surface antigen (anti-HBs) and HBV DNA were negative. Later the patient received chemotherapy for malignancy. However, this was interrupted due to elevated liver enzymes. At the same time HBV DNA became positive. Lamivudine (LMV) therapy was administered immediately. However, the levels of serum aminotransferase and total bilirubin (TB) were still rising. Finally the patient died of fulminant hepatic failure. A sequence revealed HBV genotype C (HBsAg subtype adw) with immune escape mutations, F8L, S34L, F41S, G44V, F93C, V96G, L110I, C149Y and F161Y. The high morbidity and mortality of this complication is one of the major obstacles to completing the standard treatment for malignancy in HBV carriers. Therefore, the relative risk of antiviral prophylactic failure should be further assessed and the optimal strategy for antiviral prophylaxis in HBsAg-positive patients with oncologic and hematologic malignancies undergoing chemotherapy should be revised.  相似文献   

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