乙型/丙型肝炎病毒相关性肝细胞癌450例分析

目的比较乙型/丙型肝炎病毒(HBV/HCV)相关性肝细胞癌(HCC)的特点,探讨HCC发生的相关因素。方法收集2005年1月～2009年7月济南市传染病医院450例确诊的HCC住院患者病史及血清学资料,建立数据库,应用SPSS16.0软件进行统计分析。结果450例HCC患者HBV、HCV、HBV合并HCV感染分别为422、17例和11例。422例HBV感染者平均年龄(53.85±10.00)岁,高发年龄为50～59岁,男女比例为7.79∶1;17例HCV感染者平均年龄(60.18±5.47)岁,高发年龄为60～69岁,男女比例为2.40∶1。HCV相关性HCC(C-HCC)患者的发病年龄高于HBV相关性HCC(B-HCC)患者;B-HCC男性患者比例高于C-HCC;高病毒载量及长期肝炎发作是HCC形成的相关因素;C-HCC患者中2型糖尿病比例高于B-HCC患者。结论HBV感染所致的肝炎较HCV所致的肝炎更容易发生HCC。年龄大、男性、肝炎史长、肝硬化是HBV/HCV相关性HCC的主要相关因素。     

乙型肝炎病毒感染合并丙型肝炎病毒感染直接抗病毒药物治疗的描述性研究

目的 分析乙型肝炎病毒（hepatitis B virus,HBV）合并丙型肝炎病毒（hepatitis C virus,HCV）感染者的流行病学特征及直接抗病毒药物（direct-acting antiviral agents,DAA）抗HCV后HBV再激活的发生和预后。方法 收集2008年10月至2020年5月首都医科大学附属北京地坛医院HCV/HBV合并感染并接受抗HCV治疗的患者进行回顾性分析,分析共感染者的感染途径、是否存在肝硬化及肝细胞癌（hepatocellular carcinoma,HCC）,比较患者治疗前后乙型肝炎病毒表面抗原（hepatitis B virus surface antigen,HBsAg）、丙氨酸氨基转移酶（alaninetransminase,ALT）、天门冬氨酸氨基转移酶（aspirate transaminase,AST）、血清总胆红素（total bilirubin,TBil）、血清直接胆红素（direct bilirubin,DBil）、血清白蛋白（albumin,ALB）的变化情况。统计DAA抗HCV的治疗效果及HBV再激活情况。结果 ...     

细胞自噬在慢性肝炎病毒感染中的作用

一、慢性肝炎病毒 (一)乙型肝炎病毒 HBV感染呈全球流行,据世界卫生组织报道,全球约20亿人曾感染过HBV,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、肝硬化和肝细胞癌(Hepatocellular carcinoma,HCC)[1].我国1～59岁普通人群的HBsAg携带率为7.18％[2].据此推算,我国现有的慢性HBV感染者约9 300万例,其中慢性乙型肝炎患者约2 000万例[3].我国每年死于与乙肝相关肝病的约30万例.HBV慢性感染不仅难以治愈,造成患者病情的反复发作,且与HCC的发生密切相关[4].     

HBV和HCV重叠感染的研究进展

乙型肝炎病毒（HBV）和丙型肝炎病毒（HCV）感染是目前全球慢性肝病的主要原因。据世界卫生组织（WHO）估计全球HBV和HCV慢性感染者分别超过3．5亿和1．7亿。由于具有共同的传播途径,所以HBV和HCV重叠感染现象的发生相当普遍,特别是在两种病毒都流行的地区,可达1％～15％。2004年东欧一项研究显示,在随机选择的2200健康个体中发现HBV／HCV重叠感染率为0．68％。     

本刊常用英文缩写词汇

正甲型肝炎病毒(hepatitis A virus,HAV)乙型肝炎病毒(hepatitis B virus,HBV)丙型肝炎病毒(hepatitis C virus,HCV)慢性乙型肝炎(chronic hepatitis B,CHB)慢性丙型肝炎(chronic hepatitis C,CHC)肝细胞肝癌(hepatocellular carcinoma,HCC)原发性肝癌(primary hepatocellular carcinoma,PHC)人类免疫缺陷病毒(human immunodeficiency virus,HIV)     

病毒性肝炎流行病学进展

病毒性肝炎是一个严重的公共卫生问题,全球每年超过100万人死于病毒性肝炎.其感染人数是艾滋病人数的10倍以上[1].全球估计有57％的肝硬化病例和78％的肝细胞癌(HCC)病例与乙型肝炎病毒(HBV)或丙型肝炎病毒(HCV)感染有关.全世界约有20亿人已感染HBV,其中3.5～4亿人为慢性HBV感染者,每年约50～70万人死于与HBV感染相关的疾病.约有1.3～1.7亿人为慢性HCV感染,每年约有35万人死于HCV感染相关疾病[2].2010年5月,世界卫生组织(WHO)第63届世界卫生大会通过一项议案,呼吁采取综合措施来预防和控制病毒性肝炎.尽管目前甲型肝炎(甲肝)和乙型肝炎(乙肝)有有效的预防方法,但在发展中国家,多数慢性乙肝和丙型肝炎(丙肝)患者尚未得到有效的治疗[3].     

慢性乙型肝炎的治疗:进展、问题和对策

持续乙型肝炎病毒(HBV)感染是慢性肝炎、肝硬化、肝衰竭和肝细胞癌(HCC)的主要病因。据报道慢性乙型肝炎(CHB)患者每年有014％～14．2％进展为肝硬化．在HBV相关性肝硬化中每年有4％～9．5％发生肝功能失代偿,年死亡率为4％～10％；男性慢性HBV感染者发生HCC的危险性为非HBV感染人群的102倍。     

丙型肝炎病毒感染导致负性调节因子与T细胞功能的失调

丙型肝炎病毒（hepatitis C virus,HCV）严重威胁着人类健康,全世界约有1.7亿～2.0亿HCV感染者,其中我国占4000万以上,HCV感染率约3.2%。由于HCV能够躲避宿主免疫,约80%的HCV感染者为慢性持续感染,这种持续感染与肝硬化、肝癌的发生高度相关,已成为肝移植的首要原因。目前,HCV持续感染的机制尚不明确。     

酒精合并病毒性肝损伤与肝癌的关系

病毒性肝炎和酒精均是肝细胞癌(肝癌)致病的主要病因, 慢性乙型肝炎病毒(hepatitis Bvirus, HBV)和丙型肝炎病毒(hepatitis C virus,HCV)感染引起肝癌的危险性为正常人10倍以上, 饮酒引起肝癌危险性近2倍, 病毒性肝炎伴饮酒危险性进一步增大. 病毒和酒精协同作用的机制尚未完全清楚, 在多数患者, 两种因素均先通过肝硬化再进展为肝癌. 预防肝炎病毒感染和控制饮酒是预防肝癌的最好手段, 普及乙型肝炎疫苗接种已取得非常好的成绩. 对慢性HBV和HCV感染者应抗病毒治疗, 早期戒酒对预防肝癌的肯定有益, 但尚没有足够证据支持戒酒可减低肝硬化向肝癌发展的风险.     

非酒精性脂肪性肝病与乙型肝炎病毒既往感染者肝癌发生关系的研究

目的乙型肝炎表面抗原(HBsAg)清除并不能消除乙型肝炎病毒(HBV)感染患者的肝细胞癌(HCC)风险, 本研究旨在探讨非酒精性脂肪性肝病(NAFLD)在HBV既往感染者(HBsAg阴性、抗-HBc阳性)HCC发生中的作用。方法本研究是回顾性调查研究, 纳入2015年至2017年在南方医院住院并首次诊断为HCC的患者共1 605例。将HBV现症感染(HBsAg阳性、抗-HBc阳性)基础上发生HCC的患者作为参照, 采用多因素Logistic回归模型分析NAFLD与HBV既往感染者发生HCC之间的关系。结果在HBsAg和抗-HCV均阴性的HCC患者中, HBV既往感染者占比达86.7%。与HBV现症感染基础上发生HCC的患者相比, HBV既往感染基础上发生HCC的患者NAFLD患病率更高(19.7%比8.5%, P < 0.001)。校正性别、年龄、高血压、丙氨酸转氨酶、肝硬化后, HBV既往感染基础上发生HCC的患者更可能患有NAFLD(OR = 2.29, 95%CI:1.40～3.74)。且这种现象只在非肝硬化(OR = 5.26, 95%CI:2.53～10.96)、年龄≥...     

Dual chronic hepatitis B virus and hepatitis C virus infection

Dual hepatitis B virus (HBV) and hepatitis C virus (HCV) infection are common in HBV or HCV endemic areas. However, several clinical and pathogenetic issues remain unresolved. First, clinical and in vitro studies suggest the interactions between two viruses. The dynamics of the interaction in untreated setting versus treated setting and its influence on the long-term outcomes await further studies. A key issue regarding viral interactions is whether modulation of infection occurs in the same dually infected individual hepatocyte of the liver. Clarifying this issue may help to understand the reciprocal interference between HCV and HBV and provide clues for future immunopathogenetic studies. Second, the prevalence and clinical significance of coexisting occult HBV infection in patients with chronic HCV infection need further investigations. Third, combination therapy of peginterferon alfa-2a and ribavirin appears to be just as effective and safe for the treatment of hepatitis B surface antigen (HBsAg)-positive patients chronically infected with active chronic hepatitis C as it is in patients with HCV monoinfection. Nevertheless, one-third of dually infected patients with nondetectable serum HBV DNA-level pretreatment developed HBV reactivation posttreatment. How to prevent and treat this reactivation should be clarified. Furthermore, about 10% of the dually infected patients lost HBsAg. Underlying mechanisms await further investigations. Finally, the optimal treatment strategies for dually infected patients with hepatitis B e antigen-positive chronic hepatitis B should be identified in future clinical trials.     

HBV/HCV重叠感染的抗病毒治疗

从全球范围看,乙型肝炎病毒(hepatitis B virus,HBV)和丙型肝炎病毒(hepatitis C virus,HCV)重叠感染估计约有700-2000万人口感染.重叠感染和单一HBV或HCV感染比较,更易发展为肝硬化、肝细胞癌甚至肝衰竭的比例也高,HBV和HCV重叠感染可有四种不同的临床模式,即HCV活动...     

Vietnamese community screening for hepatitis B virus and hepatitis C virus

Summary. Asian Americans represent an important cohort at high risk for viral hepatitis. To determine the prevalence of Hepatitis B virus (HBV) and Hepatitis C virus (HCV) infection and HBV vaccination in a Vietnamese community, a total of 322 Vietnamese subjects from a local doctor’s office and annual Vietnamese Health Fair were included in this study. Demographic and clinical data were collected. 2.2% of the screened cohort tested positive for anti‐HCV and 9.3% tested positive for HBsAg. Unlike HBV‐positive subjects, HCV‐positive subjects had significantly higher liver enzymes (P = 0.0045 and P = 0.0332, respectively). The HBV‐positive group was more likely to report jaundice (P = 0.0138) and a family history of HBV (P = 0.0115) compared to HBV‐negative subjects. Forty‐eight patients (15.5%) reported a family history of liver disease (HBV, HCV, HCC, cirrhosis, other). Of this 48, 68.8% reported no personal history of HBV vaccination and 77.1% reported no family history of vaccination for HBV. Among the 183 subjects without a family history of liver disease, 156 (85.2%) reported no personal history of vaccination and 168 (91.8%) reported no family history of vaccination. HBV vaccination rates in those reporting a family history of liver disease were significantly higher (P = 0.020). There was a high prevalence of HBV infection in this community screening. Nevertheless, the rate for HBV vaccination was low. The low prevalence of abnormal liver enzymes in HBV‐positive subjects emphasizes the need for screening to be triggered by risk factors and not by abnormal liver enzymes.     

Hepatitis B virus and hepatitis D virus replication in HBsAg-positive fulminant hepatitis

Hepatitis B virus DNA and hepatitis D virus RNA, the most sensitive markers of hepatitis B and hepatitis D virus replication, were sought by molecular hybridization with radioactive probes in serial serum samples from 29 consecutive patients with HBsAg-positive fulminant hepatitis. Nineteen patients had evidence of hepatitis D virus infection, as assessed by the presence in serum of delta antigen, anti-delta antibodies, or both. Hepatitis B virus DNA was found in only two patients: one was a chronic HBsAg carrier with hepatitis D virus superinfection and the other had fulminant hepatitis caused by hepatitis B and hepatitis D coinfection. Hepatitis D virus RNA was detected in three patients: two with hepatitis B and hepatitis D coinfection and also in the HBsAg carrier with positive hepatitis B virus DNA and hepatitis D virus superinfection. None of 10 patients with hepatitis B virus infection alone had detectable viral nucleic acids in serum. Overall, viral nucleic acids were detected in the sera of 4 of the 29 patients (14%). Hepatitis D virus antigenemia did not indicate hepatitis D virus replication because hepatitis D virus RNA was not detected in 9 of 12 patients with hepatitis D virus antigen in their sera. The low frequency of viral replication found in fulminant hepatitis B or D may explain the low recurrence rate of viral hepatitis in patients with fulminant hepatitis who have received liver transplantations.     

Adefovir combined with hepatitis C virus treatment may prevent hepatitis B reactivation after hepatitis C virus eradication in hepatitis B and C virus carriers

This observation reports that a hepatitis B virus (HBV) reactivation, as the result of hepatitis C virus (HCV) eradication on a dominant HCV coinfected HBV/HCV patient, was subsequently prevented by treating both viral infections together. This finding raises the question as to whether preemptive HBV treatment should be prescribed along with HCV treatment to prevent HBV from being reactive after HCV eradication in coinfected HBV/HCV patients.