慢性乙型肝炎病毒感染者心理健康状况调查分析

目的调查分析乙型肝炎病毒携带者、慢性乙型肝炎、乙型肝炎肝硬化患者的心理健康状况及特点。方法采用症状自评量表(SCL-90)对246例门诊自愿接受调查的乙型肝炎病毒携带者、慢性乙型肝炎及乙型肝炎肝硬化患者进行评定,按量表因子分进行比较分析。结果所有乙型肝炎病毒感染对象的各项因子分大多高于国内普通人群,特别是在躯体化、抑郁、焦虑、敌意等因子方面,以慢性乙型肝炎、乙型肝炎肝硬化患者尤其明显。各因子分值随疾病严重程度加重有升高趋势,且在精神病性一个因子得分上存在统计学差异。多因素分析表明,疾病类型、年龄、受教育程度是SCL-90因子分值的重要影响因素。结论慢性乙型肝炎病毒感染者的心理问题,随着病情的严重程度有逐渐加重的趋势,年龄和受教育程度对其产生一定的影响。     

慢性乙型肝炎多重病毒感染临床特征研究

目的慢性乙型肝炎多重病毒感染临床并不多见，可使肝炎的病程变得较为复杂，预后相对较差，国内外相关的文献报道较少。分析慢性乙型肝炎多重病毒感染的病原学类型并研究其临床特征。方法共有慢性乙型肝炎多重病毒感染88例，其中三重感染74例，四重感染14例；用日期随机法抽取同期单纯乙型肝炎100例作为对照组。结果乙型肝炎多重病毒感染患者中合并丁肝病毒（HDV）、巨细胞病毒（CMV）、甲肝病毒（HAV）与戊肝病毒（HEV）者较多，分别为84．1％、43．2％、33．0％、26．1％。多重病毒感染患者的肝功能损害明显较单纯感染者重，疗效差，住院时间长。结论与慢性乙型肝炎单纯感染相比，慢性乙型肝炎多重病毒感染肝功能损害严重，疗效较差。     

病毒性肝炎

重型病毒性肝炎并发低血糖临床分析；重型肝炎合并低氧血症患者静脉高氧疗法治疗前后细胞因子的变化；三种人工肝疗法对重型肝炎患者电解质的影响；慢性乙型肝炎病毒感染并发重型再生障碍性贫血的临床特征；性别因素对成人急性乙型肝炎早期病毒清除的影响。     

HLA、细胞因子与丙型肝炎发展的相关性研究进展

病毒性肝炎,尤其是慢性病毒性肝炎对人体的危害极大,丙型肝炎作为慢性肝炎之一其危害不亚于乙型肝炎,其主要原因是感染早期临床症状较轻,患者一般不会引起注意,一旦感染后极易慢性化且易转化成肝硬化和肝癌,预后较差。研究影响丙型肝炎转归的相关因素,例如人类白细胞抗原(HLA)等位基因的多态性和细胞因子对疾病的影响,有助于丙型肝炎患者早期病情的控制。     

慢性乙型肝炎重叠HAV与HEV感染的临床分析

目的研究慢性乙型肝炎患者重叠甲型肝炎与重叠戊型肝炎病毒的临床特点及其对病情转归的影响。方法采用ELISA法检测甲、乙、丙、戊型肝炎病毒血清标记物,选择慢性乙型肝炎重叠甲型肝炎52例与慢性乙型肝炎重叠戊型肝炎267例进行对比分析。结果慢性乙型肝炎重叠戊型肝炎患者较慢性乙型肝炎重叠甲型肝炎患者总胆红素水平高、重型肝炎发生率高、病死率高,两组白蛋白水平和平均住院日无明显差异。结论慢性乙型肝炎患者重叠戊型肝炎病毒感染较重叠甲型肝炎病毒感染病情更重、预后差。     

重型肝炎

慢性重型乙型肝炎转归相关因素及抗病毒治疗研究——吴云忠等（北京北京地坛医院肝炎一科100011）；《中华实验和临床病毒学杂志》2007，21（2）：120-122[目的：探讨慢性重型乙型肝炎转归的影响因素及抗病毒治疗对其转归的影响。方法：应用回顾性研究方法，     

慢性病毒性肝炎抗病毒治疗的新进展

慢性病毒性肝炎主要由乙型肝炎病毒及丙型肝炎病毒感染所致。慢性病毒性肝炎的治疗,主要包括抗病毒、免疫调节、抗炎护肝、抗纤维化和对症治疗等。经过数十年的探索,尤其近年不断涌现出的新的有效抗病毒药物,临床使用及应用循证医学观点评价治疗效果等因素的影响,慢性病毒性肝炎的治疗有不少新观点及新进展。2004年3月和2005年12月,由中华医学会肝病学分会和感染病学分会联合公布的“丙型肝炎防治指南”和“慢性乙型肝炎防治指南”,对于规范慢性病毒性肝炎的治疗有重要意义。1乙型病毒性肝炎1.1抗病毒治疗是慢性乙型肝炎治疗的关键有效的抗…     

乙肝病毒肝源细胞培养模型的研究进展

乙型肝炎病毒感染可以引发慢性病毒性肝炎、肝炎肝硬化,甚至是肝细胞癌。全球约有3.5亿人感染慢性乙型肝炎病毒。随着分子生物学和细胞培养技术在乙肝病毒研究中的发展与应用,研究者们建立起了多种细胞模型。本文简要综述肝源细胞模型在乙型肝炎病毒研究中的应用进展。     

灵肝片治疗慢性肝炎的双盲对照研究

迄今,慢性乙型肝炎的发病机理尚未阐明,有人认为乙型肝炎的慢性化与HBV在肝内的持续复制和患者受病毒感染影响后发生免疫紊乱有关。许多中药治疗慢性乙型肝炎的临床研究结果表明,中药对于抑制病毒复制和恢复肝功能有一定作用。我们采用中药组方(灵肝片)治疗慢性乙型肝炎,现报告如下。     

抗乙型肝炎病毒的免疫治疗

乙型肝炎病毒侵入人体后,易于形成持续性感染,并诱发各种慢性肝脏疾患。这种持续慢性感染状态,是由于被感染者机体免疫系统对乙型肝炎病毒的特异性耐受所造成。主要是由两个方面因素,一是机体免疫系统对乙型肝炎病毒识别、加工和递呈环节存在障碍;二是病毒感染使宿主细胞免疫信息传递以及病毒变异使得免疫攻击效应减弱或丧失。细胞免疫应答,在抗病毒感染、清除病毒过程中起关键作用。一般地说,乙型肝炎病毒感染的控制是Ⅰ类主要组织相容性抗原限制的细胞毒性T淋巴细胞（CTL）的杀伤作用,被认为是通过裂解、破坏病毒感染的靶细胞来…     

The immunology of hepatitis B

The hepatitis B virus (HBV) is an enveloped, hepatotrophic, oncogenic hepadnavirus that is noncytopathic for hepatocytes. HBV infection results in a variety of outcomes that are determined by the quality, quantity, and kinetics of the host innate and adaptive immune responses. Whether HBV infection is cleared or persists as a progressive or nonprogressive liver disease is determined by both viral and host factors. Replicative intermediates can persist in the liver under immunologic control after resolution of acute or chronic hepatitis B, conferring a risk for reactivation following a course of immunosuppression or chemotherapy.     

Association between metabolic factors and chronic hepatitis B virus infection

There are limited data regarding the relationship between chronic hepatitis B virus (HBV) infection and metabolic factors. This article aims to highlight the link of metabolic factors with hepatitis B surface antigen (HBsAg) serostatus, HBV load, and HBV-related hepatocellular carcinoma (HCC). Although HBsAg-positive serostatus was positively correlated with a high risk of metabolic syndrome in students, chronic HBV-infected individuals have high serum adiponectin levels. The androgen pathway in HBV carriers with a low body mass index is more triggered which leads to enhanced HBV replication. High HBV load was inversely associated with obesity in hepatitis B e antigen (HBeAg)-seropositive HBV carriers; while in HBeAg-seronegative HBV carriers, high HBV load was inversely related to hypertriglyceridemia rather than obesity. For overweight and obese HBV-infected patients, high HBV load was positively associated with serum adiponectin levels. Several large cohort studies have revealed a positive link of diabetes with incidence of HBV-related HCC. However, the association between incidence of HCC and metabolic factors other than diabetes is still inconclusive. More long-term prospective studies should elucidate the association of chronic HBV infection and its outcomes with metabolic factors in clinical practice.     

Improving clinical outcomes of chronic hepatitis B virus infection

Chronic hepatitis B virus (HBV) infection is a global health problem, leading to cirrhosis, hepatocellular carcinoma (HCC) and liver-related deaths. Universal hepatitis B vaccination is the most cost–effective way to eradicate HBV infection with the remarkable reduction of chronic carriage, neonatal fulminant hepatitis and childhood HCC. The introduction of highly effective antiviral agents, including lamivudine, adefovir dipivoxil, entecavir, telbivudine, tenofovir disoproxil fumarate and pegylated interferons further improve short-, medium- and long-term outcomes of chronic HBV infection, such as ALT normalization, HBV DNA suppression, HBeAg seroconversion, HBsAg seroclearance, fibrosis regression, reduction of cirrhosis, HCC, liver-related deaths and the need for liver transplantation. Above all, sustained and profound viral suppression is the key to improve the clinical outcomes of chronic hepatitis B.     

Role of viral factors in the natural course and therapy of chronic hepatitis B

Hepatitis B virus (HBV) infection is a global health problem that causes a wide spectrum of liver disease, including acute or fulminant hepatitis, inactive carrier state, chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC). The pathogenesis of hepatocyte damage associated with HBV is mainly through immune-mediated mechanisms. On the basis of the virus and host interactions, the natural history of HBV carriers who are infected in early life can be divided into four dynamic phases. The frequency, extent, and severity of hepatitis flares or acute exacerbation in the second immune clearance and/or fourth reactivation phase predict liver disease progression in HBV carriers. In the past decade, hepatitis B viral factors including serum HBV DNA level, genotype, and naturally occurring mutants predictive of clinical outcomes have been identified. The higher the serum HBV DNA level after the immune clearance phase, the higher the incidence of adverse outcomes over time. In addition, high viral load, genotype C, basal core promoter mutation, and pre-S deletion correlate with increased risk of cirrhosis and HCC development. As to the treatment of chronic hepatitis B, patients with high HBV DNA level and genotype C or D infection are shown to have a worse response to interferon therapy. In conclusion, serum HBV DNA level, genotype, and naturally occurring mutants are identified to influence liver disease progression and therapy of chronic hepatitis B. More investigations are needed to clarify the molecular mechanisms of the viral factors involved in the pathogenesis of each stage of liver disease and the response to antiviral treatments.     

慢性乙型肝炎病毒感染者家族隐匿性乙型肝炎病毒感染的调查

目的 了解慢性HBV感染者家族隐匿性HBV感染的发生率及其与HBV标志物、年龄和性别等的关系.方法 ELISA方法检测慢性HBV感染者家族成员的HBV血清学标志物,套式PCR法检测136例HBsAg阴性家族成员的血清HBV DNA,并将隐匿性HBV感染者和HBsAg、HBV DNA均阴性者分别作为试验组和对照组进行HBV标志物、年龄、性别和生物化学检测结果的比较.两组均数比较采用t检验.率的比较采用χ~2检验或Fisher确切概率法检验.结果 在52个慢性HBV感染者家族中共检测到92例HBsAg阳性者和136例HBsAg阴性者,其中15例为隐匿性HBV感染者,慢性HBV感染者家族HBsAg阳性率和隐匿性HBV感染的发生率分别为40.4%和11.0%,15例隐匿性HBV感染者中有7例抗-HBc阳性(χ~2=5.341,P=0.02),但隐匿性HBV感染的存在与年龄、性别等无关.结论 HBV感染存在家庭聚集现象,且在其家族中存在隐匿性HBV感染,并在抗-HBc阳性者中发生率较高.     

Baseline and On-Treatment Predictors for Outcome of Chronic Hepatitis B Treatment

Persistently high levels of hepatitis B virus (HBV) DNA in patients with chronic HBV infection have been clearly implicated in an increased risk of liver cirrhosis and hepatocellular carcinoma. Hence, the primary objective of antiviral treatment is profound and lasting suppression of HBV DNA levels to improve long-term patient outcomes. Analyses of various patient and treatment characteristics have identified baseline and on-treatment factors that may be helpful in achieving this goal. In this article, the available data on baseline and on-treatment predictors of treatment outcomes in patients with chronic hepatitis B treated with both (pegylated) interferon and nucleos(t)ide analogues are reviewed.     

Chronic hepatitis B and metabolic risk factors:A call for rigorous longitudinal studies

Long-term nucleos(t)ide analogue therapy in chronic hepatitis B virus(HBV)infection is effective in suppressing viral replication and reducing liver-related complications. However, HBV-related liver events can still occur in different patient sub-groups. There is emerging evidence that, similar to chronic hepatitis C virus infection, metabolic risk factors may play a role in the disease process of chronic HBV. While the mechanistic nature of metabolic-HBV interactions remains uncertain, studies in different HBV-infected populations have demonstrated that hepatic steatosis, increased body-mass index, diabetes, or a combination of different metabolic risk factors are associated with an increased risk of hepatocellular carcinoma and cirrhosis. The impact of metabolic risk factors is especially prominent in patients with quiescent virological activity,including on-treatment patients with effective viral suppression. As the proportion of on-treatment chronic HBV patients increases worldwide,longitudinal studies determining the relative risks of different metabolic parameters with respect to clinical outcomes are needed. Future studies should also determine if metabolic-directed interventions can improve disease outcomes in chronic HBV.     

Pregnancy and chronic hepatitis B virus infection

The combination of chronic hepatitis B virus (HBV) infection and pregnancy presents unique management questions. Aspects of care that need to be considered include effects of hepatitis B on pregnancy, effects of pregnancy itself on the course of hepatitis B infection, treatment of hepatitis B during pregnancy and prevention of mother-to-infant transmission. Chronic HBV infection is usually mild in pregnant women, but may flare shortly after delivery. Effect of HBV infection on pregnancy outcomes are generally favorable, but may depend on severity of liver disease. Mother-to-infant transmission can be minimized by current immunoprophylaxis strategies, however, high levels of viremia in mothers may be a factor in the small but reproducible failure rate of current immunoprophylaxis strategies. Use of antivirals during pregnancy needs to be individualized. Careful planning and management of pregnancy must be done among patients with chronic HBV infection.     

Natural history of chronic hepatitis B

Chronic hepatitis B virus (HBV) infection can cause chronic hepatitis, cirrhosis, liver failure, and hepatocellular carcinoma (HCC). Chronic hepatitis B is characterized by an early replicative phase with hepatitis B e antigen (HBeAg) positivity, high serum HBV-DNA levels and disease activity (HBeAgpositive chronic hepatitis), and a late inactive phase with anti-HBe seroconversion, low or undetectable serum HBV-DNA, and liver disease remission (inactive carrier state). Another form is characterized by active disease due to HBV variants not expressing HBeAg (HBeAg-negative chronic hepatitis). Both types of chronic hepatitis B can lead to cirrhosis and its complications. The incidence of cirrhosis is two to five per 100 person-years, but may be as high as eight to 10 in HBeAg-negative cases. The incidence of HCC varies geographically and increases with the duration and severity of liver disease (0.1 to 8 per 100 person-years). The prognosis is reasonably good in compensated cirrhosis, but very poor following decompensation. Viral and environmental factors influence the natural history of chronic hepatitis B and explain the heterogeneity of its clinical outcomes.     

Basal core-promoter mutant of hepatitis B virus and progression of liver disease in hepatitis B e antigen-negative chronic hepatitis B.

BACKGROUND/AIMS: The long-term outcomes in hepatitis B e antigen (HBeAg)-negative chronic hepatitis B are distinct from those in HBeAg-positive chronic hepatitis. However, the molecular virological factors that contribute to the progression of liver disease in this special clinical setting remain largely unknown. We thus investigated the association of hepatitis B virus (HBV) genotypes as well as precore/basal core-promoter mutations with the clinical and virological characteristics of patients with HBeAg-negative chronic hepatitis B in Taiwan. METHODS: HBV genotypes and sequences of precore and basal core-promoter regions of the HBV genome were determined in 174 HBeAg-negative chronic HBV infection patients including 62 inactive carriers and 112 with different stages of liver disease. RESULTS: HBV carriers with older age (> 50 years) (odds ratio, 9.09; 95% confidence interval (CI), 3.22-25, P < 0.001) and basal core-promoter mutant of HBV (odds ratio, 4.12; 95% CI, 1.41-12.03, P = 0.01) were associated with the development of liver cirrhosis and hepatocellular carcinoma (HCC). The gender-related risk factors associated with the development of liver cirrhosis and HCC were further analyzed, and basal core-promoter mutant was only associated with the development of liver cirrhosis and HCC in male carriers (odds ratio, 4.35; 95% CI, 1.30-14.52, P = 0.02). CONCLUSIONS: The risk of development of liver cirrhosis and HCC is significantly increased in patients with advanced age as well as with basal core-promoter mutant of HBV. In addition, basal core-promoter mutant might contribute to the gender difference of the progression of liver disease in HBeAg-negative chronic hepatitis B in Taiwan.