急性和慢性乙型肝炎临床特点的比较

近年来,成年人急性乙型肝炎的发病率有增多趋势.急性乙型肝炎在临床上有时与慢性乙型肝炎急性发作极为相似,难以鉴别.本文就我科自2003年起收治的急性乙型肝炎患者进行回顾性研究,并与同期住院的慢性乙型肝炎患者进行对照,现将观察结果报道如下:     

慢性乙型肝炎免疫治疗现状

乙型肝炎是严重危害人类健康的疾病。感染乙肝病毒后的转归与机体的免疫状态密切相关。从免疫学的观点看,治疗乙肝的关键是恢复慢性HBV感染患者体内有效的T细胞反应。已有研究证实机体免疫系统可以通过非细胞破坏性机制清除cccDNA,故乙肝的免疫调节治疗正受到人们的广泛关注。     

慢性乙型肝炎的辨证难点与突破方向

慢性乙型肝炎是一个＂年轻＂的临床诊断,自1965年Blumberg发现＂澳大利亚抗原＂、1974年正式确立乙型肝炎诊断以来,仅仅有30多年的历史。     

慢性乙型肝炎低病毒血症的研究现状和挑战

慢性乙型肝炎治疗过程中持续存在的低病毒血症（LLV）会进一步促进耐药突变、肝纤维化进展甚至是肝细胞癌发生,严重影响患者预后。希望通过组织本期重点号,阐述LLV发生的可能机制、分析其临床结局,从而辅助调整个体化治疗方案,以期为该类患者的诊疗提供参考。     

慢性乙型肝炎患者生存质量研究现状

本文就慢性乙型肝炎患者生存质量的现状、测评量表及影响因素和干预措施等方面进行综述,为提高该人群的生存质量提供依据,并指出制定特异性量表的重要性。     

慢性乙型肝炎的治愈现状

慢性乙型肝炎（chronic hepatitis B, CHB）是一种广泛的全球感染性疾病,是肝细胞癌和肝衰竭的主要原因。目前可以通过接种乙型肝炎疫苗降低CHB的新发感染率,主要的治疗方法是通过聚乙二醇化干扰素α和核苷（酸）类似物抑制病毒,延缓CHB患者的疾病进展,但不能治愈CHB。如何清除稳定的DNA中间体共价闭合环状DNA,以及如何恢复肝脏微环境中疲惫的免疫系统是目前面临的挑战。为此肝病学者们不断探索新的靶标和药物,研究通过针对HBV生活周期不同阶段的药物联合疗法实现持久功能性治愈。本文将对目前CHB的多种治疗策略以及正在研发的新靶标和新药物进行回顾。     

拉米夫定和华蟾素单用或联用对乙型肝炎患者血清标志物的影响

2002年4月以来,我们采取拉米夫定、华蟾素联合用药方式,治疗慢性乙型肝炎42例,以期达到协同增效的目的.     

拉米夫定联合其他药物治疗慢性乙型肝炎的现状和展望

拉米夫定是目前世界公认对慢性乙型肝炎抗病毒治疗的有效药物,有资料显示,经拉米夫定治疗的患者肝癌发生率也降低。但并不能根治慢性肝炎,主要的问题是持续应答率较低,停药后复发率高;长期治疗后发生病毒耐药突变导致药物敏感性下降。治疗HIV/AIDS的实践证实,拉米夫定联合治疗能有效地提高疗效和减少耐药,因此美国食品药品管理局(FDA)在1995年批准拉米夫定单药治疗的适应证后,又分别于1997年和2000年先后批准了拉米夫定联合其他药物的二联和三联治疗的适应证。因此,拉米夫定或其他核苷类似物联合抗病毒治疗是有理论和实践根据的,联合用…     

慢性乙型肝炎临床研究注册现状分析

目的:基于临床试验注册资料,分析中国慢性乙型肝炎(CHB)的临床研究现状。方法:检索建库起至2020年12月31日在中国临床试验注册中心(http://www.chictr.org.cn/index.aspx)注册的有关CHB临床研究,并进行挖掘分析。结果:共检索临床研究1 282项,符合纳入标准的研究165项,包括干预性研究78项、观察性研究64项、病因学/相关因素研究16项、基础科学研究4项、预后研究1项、流行病学研究1项、诊断试验1项。结论:近年来中国慢性乙型肝炎的临床研究逐渐增多,研究以干预性研究为主。研究中干预措施可以分为针对“病毒因素为主”的抗病毒疗法和针对“宿主因素为主”的干扰素治疗、免疫疗法、粪菌移植治疗、中西医结合治疗等。临床研究致力于抗病毒方案的优化及治疗方案的多元化,中医药在其中发挥着越来越重要的作用。     

HBeAg阴性慢性乙型肝炎研究现状

虽然乙型肝炎疫苗的广泛应用已经降低了乙型肝炎病毒(HBV)感染的流行趋势,但不可否认的是HBV感染依然是全球性面临的重大健康问题,世界范围内约有20亿人曾经感染过乙肝病毒,其中3.5亿为慢性HBV感染者,每年约有100万人死于HBV感染所致的肝衰竭、肝硬化和原发性肝癌[1].     

Emerging Patterns off Hepatitis B Chronic Liver Disease in Australia

Summary: Emerging patterns of hepatitis B chronic liver disease in Australia. G. W. McCaughan, C. Parsons and N. D. Gallagher, Aust. N.Z. J. Med., 1979, 9, pp. 359–364.
Until now, the hepatitis B virus has been thought to play a minor role in the aetiology of chronic liver disease in Australia. This is a report of 21 patients with cirrhosis and/or primary hepatocellular carcinoma with hepatitis B antigenaemia. Primary hepatocellular carcinoma occurred in six patients, five of whom had underlying cirrhosis. The disease occurred mainly in non-Australian born males, and was not often associated with a previous history of hepatitis. The death of 16 patients within 12 months of presentation is in contrast to previous concepts of the benign nature of hepatitis B associated cirrhosis.     

Hepatitis B outbreak following a mass-casualty incident, Australia

On 16 April 2009, a boat carrying 47 Afghan asylum seekers and 2 Indonesian crew exploded in Australian waters, resulting in mass casualties. Of these casualties, 23 persons who suffered significant burns were transferred to Royal Perth Hospital, Perth, Western Australia. One patient was subsequently shown to be a hepatitis B virus (HBV) carrier at the time of the explosion. Over the following months, 3 other patients received a diagnosis of acute hepatitis B, and an additional 4 patients showed serological evidence of recent HBV infection, including 1 patient who was transferred to another Australian city. Molecular typing determined that the strains from the HBV carrier and the acute and recent case patients formed a closely related cluster, and the investigation suggested that transmission occurred at or around the time of the boat explosion. This is the first report of confirmed transmission of HBV following a disaster, and it reinforces the importance of postexposure prophylaxis for HBV in mass casualty situations.     

Hepatitis B status in migrants and refugees: increasing health burden in Western Australia

Background: In light of increasing migration from endemic countries with chronic hepatitis B (CHB), this study describes the changing epidemiology of CHB patients born outside Australia referred to a tertiary hospital in Western Australia. It aims to stratify risk and progression to cirrhosis and hepatocellular carcinoma according to viral factors and to provide an indication of the growing burden of disease and current and future treatment costs. Methods: Demographic, serological and biochemical data were obtained from patients with CHB between July 2002 and December 2008. Hepatitis B virus DNA quantification was performed to assess baseline viral loads in the patients. Total cost estimates for surveillance and treatment are based on probabilities of the population anticipated to be at a given stage of the disease in a given year. Results: There is a progressive increase in referrals (n = 478) with the majority coming from Asia (57%) and Africa (35%). The mean age of Africans is 11 years less than that of Asians, with a lower proportion of Africans having hepatitis B virus DNA > 2000 IU/mL compared with Asians (36.7% vs 54.3%). Approximately 50% of CHB patients referred are at risk of cirrhosis and hepatocellular carcinoma unless treated. Without treatment, a substantial increase in cost over 10 years (from $401 460 to $2 027 078) is estimated at 400%. Conclusion: This study highlights the increasing burden of CHB in Western Australia, from people born in endemic countries, in particular, the direct costs of treatment. It will help to develop strategies that can be tailored to Western Australia with appropriate allocation of resources.     

Hepatitis C virus genotypes in Australia

The relative distribution of Australian hepatitis C virus (HCV) genotypes was determined for 500 isolates. Genotyping was performed using a commercial reverse phase hybridization assay after amplification of the 5' untranslated region of HCV by the polymerase chain reaction. Australian isolates comprised, predominantly, genotype 1 (55%) and genotype 3 (38%) with genotype 2 accounting for only 7%. Genotype 3a was the most common subtype. When the major risk groups of injecting drug users or transfusion-acquired hepatitis C were compared, there was a significantly higher incidence of genotype 1b in the transfusion-acquired group ( P < 0.03). When the age of the patients was analysed, genotype 3a was more prevalent in the 21–40-year age group than the 41–60-year age group ( P <0.05). There was no significant difference in genotype distribution between males and females. HCV genotypes 1, 2 and 3 are most often found in developed countries but the relatively high prevalence of genotype 3a in Australia is unusual.     

Hepatitis B antigen and antibody in active chronic hepatitis and other liver diseases in Australia

In a multicenter cooperative study, sera from 85 patients with active chronic hepatitis (ACH) were examined for the presence of hepatitis B (Australia) antigen (HBAg) by radioimmunoassay (RIA) and antibody to HBAg (anti-HBAg) by RIA and passive hemagglutination (PHA), the most sensitive currently available techniques. In addition, sera from 83 patients with other liver diseases, 98 other hospital patients, and 67 healthy controls were tested. HBAg was detected in 3 of the 85 patients (four percent) with ACH. In a further 3 patients (four percent) anti-HBAg was detected. Thus, 6 patients with ACH (seven percent) had evidence of present or prior infection with the hepatitis B virus (HBV). HBAg was also detected in 7 of the patients with other liver diseases, 2 of the other hospital patients, and none of the healthy controls. Anti-HBAg was detected in 17 of the non-ACH subjects. These results indicate that neither persistent nor prior self-limited infection with HBV is a major factor in the pathogenesis of ACH in Australia.W.G.E. Cooksley and I.R. Mackay were both in receipt of grants from the National Health and Medical Research Council of Australia.     

Hepatitis B: 50 years after the discovery of Australia antigen

It is an honour to be invited to recount the progress in our understanding and management of hepatitis B 50 years after the discovery of Australia antigen (Au Ag). During this half century, we have gone from identifying the causative agent – hepatitis B virus (HBV), understanding its biology and the disease it causes, to having vaccines that can prevent HBV infection and antiviral therapy that can suppress HBV replication and prevent progression of HBV‐related liver disease. As a result of the progress, prevalence of HBV infection and morbidity and mortality from chronic HBV infection has declined.     

Australia Antigen and Posttransfusion Hepatitis

Abstract. The incidence of posttransfusion hepatitis reported in Copenhagen was studied for 2 consecutive years. The 2 years were comparable in every respect, including the number of transfusions (21,000 per year). In the first year no screening of transfusion blood was made, while in the second year all units of blood were systematically screened for Au antigen by a counterelectrophoresis method. During that year, 49 Au antigen-positive units were detected and refused.
The number of cases of transfusion hepatitis officially registered during the 2 years was 9 and 8, respectively. Detailed diagnostic studies revealed that the probable number of cases classifiable as transfusion hepatitis was 8 and 6 in the 2 years. Thus, in the present study screening of transfusion blood for Au antigen has not resulted in an obvious reduction in the incidence of transfusion hepatitis. Three patients were repeatedly examined for more than 6 months after transfusion of a unit of Au antigenaemic blood, but no case or hepatitis or Au antigenaemia was found. Our findings may be related to the fact that cases of acute and chronic hepatitis are unusual among Au antigenaemic Danish blood donors. Further studies are necessary to elucidate the correlation between donor Au antigenaemia, donor liver disease and hepatitis infectivity of donor blood.