血液透析患者肝炎感染的危险因素和对策探讨

目的研究血液透析患并发肝炎病毒感染的危险因素及预防对策。方法采用临床资料回顾调查方法，选156例2003年1月1日-2004年8月1日接受透析治疗的患，入选标准：在半年内接受检查乙肝和丙肝病毒感染指标的透析患。感染指标通过E1LSA检测。感染标准：HBsAg阳性为乙肝病毒感染，抗HCV阳性为丙型肝炎病毒感染。结果156例患中HBsAg阳性13例，感染率8．3％，抗HCV阳性31例，感染率19．9％；经过半年血透后检测：治疗前没有被乙肝病毒或丙肝病毒感染的血透患没有一例发生乙肝或丙肝病毒的感染，但是有肝炎病毒感染的患也没有发生转阴。结论输血量、透析疗程、消毒隔离措施等是发生肝炎病毒感染的相关危险因素，因而通过减少输血、加强患的登记管理、严格消毒隔离及使用一次性透析器等措施可有效预防肝炎病毒感染的发生。     

术前乙型肝炎病毒感染状态与原发性肝癌预后的相关性分析

目的： 探讨术前乙型肝炎病毒（hepatitis B virus，HBV）感染状态与肝癌切除术后预后的关系。方法： 选择2014年7月至2015年6月复旦大学附属中山医院收治的行根治性切除的肝细胞癌患者910例，收集术前乙肝两对半和HBV-DNA的结果，结合临床病理信息和随访资料，阐明肝癌患者乙肝感染状态和其对患者预后的影响。结果： 95.1%的肝癌手术患者存在乙型肝炎病毒感染，其中以"小三阳"者最为多见，占54.2%。HBV-DNA的阳性患者术后无瘤生存率及总生存率显著低于阴性患者（P<0.05）。HBV-DNA阳性组和阴性组的肝硬化程度、甲胎蛋白（alpha-fetoprotein，AFP）水平、肿瘤大小以及血管侵犯差异均有统计学意义（P<0.001）。结论： 完善乙肝血清学标志物的检测，有利于肝癌的防治以及改善患者预后。     

血液透析患者乙肝合并丙肝病毒标志物检测分析

目的：调查血液透析患者乙肝重叠感染丙肝的情况，探讨乙肝和丙肝感染之间的相互关系。方法：对436例血液透析患者乙肝阳性血清进行了HCV标志物的检测。结果：发现436例乙肝感染的病例中有25例患者受到过丙肝病，毒感染，感染率为5．7％，说明乙肝与丙肝重叠感染在血液透析乙肝患者中分布面较广，这与透析时间、输血有关。结论：乙肝病毒对丙肝病毒复制有抑制作用，临床对血液透析乙肝患者的治疗过程中，考虑对丙肝病毒感染的控制是有必要的。     

肝细胞肝癌发病及术后复发与乙肝病毒的相关性研究进展

乙型肝炎病毒的感染是国人肝细胞肝癌发生的主要病因之一。流行病学资料显示已经受乙肝病毒感染的患者,肝细胞肝癌发生的危险性将提高100倍。由慢性乙型肝炎逐步发展成肝硬化,到最后发生癌变是最常见的“三部曲”发病模式。近年来乙肝病毒（HBV）与肝癌的相关性已得到了广泛的关注,现就乙肝病毒及相关组分在肝细胞性肝癌的发生以及术后复发的进程中的作用及其机制作一综述。     

原发性肝癌甲胎蛋白阳性与乙肝病毒标志物感染血清学的关系

目的：探讨原发性肝癌患者血清甲胎蛋白阳性与乙型肝炎病毒感染发生的关系。方法：采用化学发光免疫分析和ELISA法分别检测90例原发性肝癌患者、40例健康对照组进行了血清甲胎蛋白、乙型肝炎病毒血清五项标志物检测。结果：90例原发性肝癌患者中有87例乙肝五项标志阳性，乙型肝炎病毒总感染率为96．7％。乙型肝炎病毒总出现率：HBsAg（＋）为92．2％，HBeAg（＋）为17．8％，HBsAb（＋）为4．4％，HBeAb（＋）为57．8％，HBcAb（＋）为65．5％；5项指标全为阴性者占3．3％，明显高于健康对照组47．5％（19／40）（P〈0．01）和乙型肝炎病毒总感染率（52．5％）（P〈0．01）。肝癌组乙型肝炎病毒血清标志物感染模式，以HBsAg、抗-HBe和抗-HBC阳性模式多见，为40％。表明该模式的乙肝患者为原发性肝癌的高危人群。结论：乙型肝炎病毒与原发性肝癌之间的关系非常明确，乙型肝炎病毒感染不仅是肝癌发生的一个重要的危险因素，而且表明肝癌患者常伴有乙型肝炎病毒的复制活跃。因此，积极预防和控制乙型肝炎病毒感染流行，是减少原发性肝癌发生的关键所在。     

原发性肝癌患者HCV感染的血清学调查

原发性肝癌患者ＨＣＶ感染的血清学调查刘力勇（辽宁省临床检验中心，沈阳１１００１５）金旭红（辽宁省人民医院）原发性肝细菌癌（ＨＣＣ）是我国较常见的恶性肿瘤之一，其发病因素也比较复杂，有黄曲霉菌、理化因素和肝炎病毒等。在肝炎病毒有乙肝、丙肝和丁肝病毒可导...     

血液透析患者乙肝、丙肝病毒感染情况分析

目的：了解血液透析患者乙肝、丙肝病毒感染情况。方法：用酶联免疫方法,对８５６例血液透析患者,进行 肝表面抗原（ＨＢｓＡｇ）、丙肝病毒抗体（抗－ＨＣＶ）检测,并与非血透组进行比较,同时对是否有输血史、输血量、透析时间、透析器复用情况进行观察。结果Ｌ血透患者乙肝、丙肝病毒感同于非血透组。随透析时间的延长,乙肝、丙肝病毒的感染增加,并与透析器的复用有关。血液透析患者输血组丙肝病毒感染,明显高于非输血组,     

凋亡抑制蛋白XIAP在肝细胞癌中的表达及其对肝细胞癌肝移植患者预后的影响

目的：研究凋亡抑制蛋白XIAP在肝细胞癌中的表达并探讨其对肝细胞癌肝移植患者预后的影响。方法：用免疫组化方法检测组织芯片中192例肝细胞癌及癌旁组织中XIAP的表达,分析其与其他临床病理因素的相关性及对肝细胞癌肝移植患者预后的影响。结果：XIAP在肝细胞癌组织中的阳性表达率高达89.6%,显著高于癌旁组织（45.8%,P=0.000）。以XI-AP表达对肝细胞癌患者肝移植术后生存情况进行分层分析显示,XIAP阳性组3年总体生存率明显低于阴性组（P=0.021）,复发率显著高于阴性组（P=0.001）。Cox多因素分析提示XIAP是影响肝细胞癌肝移植术后患者总体生存率的独立预后因素。结论：XIAP在肝细胞癌中阳性表达率较高,XIAP的表达水平是肝细胞癌肝移植患者预后的独立相关因素。     

HBV、HCV感染与原发性肝细胞癌关系的对照研究

目的探讨乙型肝炎病毒(HBV)、丙型肝炎病毒(HCV)感染者罹患原发性肝细胞癌(PHC)的流行病学特点及其相关性。方法对70例有乙型病毒性肝炎肝硬化史(B组,54例)及丙型病毒性肝炎肝硬化史(C组,16例)的PHC患者的好发年龄、肿瘤分化程度及大体病理类型进行回顾性对比研究。结果与HCV感染的PHC患者比较,HBV感染的PHC患者的年龄较低[(54.86±9.82)vs(62.88±6.90)岁,P<0.01];大肝癌发生率较高(90.9%vs53.8%,P<0.01)。70例患者中获得病理结果者B组为28例,C组为16例;经秩和检验,HBV感染的PHC患者肿瘤分化程度(高分化60.7%,中分化39.3%,低分化0)高于HCV感染的PHC者(高分化37.5%,中分化25.0%,低分化37.5%)(P<0.05)。结论患乙型病毒性肝炎和丙型病毒性肝炎后导致肝硬化背景下的PHC在流行病学及病理基础方面存在差异,反映出不同病毒感染后PHC的发生、发展的不同特征。     

乙型肝炎病毒阳性分组与谷丙转氨酶的关系探讨

乙型肝炎（下称乙肝）病毒（HBV）感染是一种世界性传染病，我国是高流行区，50％～70％的人群受过乙肝病毒的感染，其中约有1亿人口为乙型肝炎病毒表面抗原（HBsAg）携带者。根据1980年全国调查表明，我国现有肝炎患者2000万人中60％以上为慢性肝炎患者。乙型肝炎病毒又与肝硬化以及原发性肝细胞癌密切相关，我国同时也是肝癌高发国家，因此用基因诊断方法对确定病原及诊断十分必要。     

Present status of hepatitis virus-associated hepatocellular carcinoma in Nagasaki Prefecture, Japan: a cross-sectional study of 1019 patients

The present study was designed to determine the frequency of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection in patients with hepatocellular carcinoma (HCC) in Nagasaki Prefecture, Japan. We examined the clinical features of 1019 patients with HCC who visited our hospitals between January and December 1999. The ratio of men to women was 709 : 310, and the peak incidence of HCC was in the seventh decade of life in both men and women. In the majority of the patients, HCC showed association with HCV infection (74%) compared with HBV infection (17%). HBV-associated HCC was more common in young patients, while HCV-associated HCC was more common in patients with a history as a "daily drinker", or with a history of blood transfusion, liver cirrhosis, and persistently high serum transaminases before the diagnosis of HCC. HCC was initially suspected by ultrasonography or computed tomography in 776 of the 874 patients for whom there was a history of mode of detection of HCC (89%). Tumor size at the time of diagnosis of HCC in patients who had been regularly followed up for liver diseases at our hospitals was significantly smaller than that in patients who were not followed up regularly before the diagnosis (P < 0.01). Our results indicate that the proportions of patients with HBV or with HCV infection among HCC patients in Nagasaki Prefecture are similar to those found in a nationwide survey in Japan, and there are some differences between the clinical manifestations of HBV- and HCV-associated HCC. Our results emphasize the importance of close follow-up for the high-risk group (i.e. those with HBV- or HCV-associated chronic liver diseases) for the early detection of HCC. Received: July 18, 2001 / Accepted: September 17, 2001     

血友病A患者血制品治疗后HBV和HCV感染指标分析

目的对血友病A患者替代治疗后血液传播乙型、丙型肝炎病毒(HBV、HCV)的感染指标进行检测。方法对经本院确诊的35例血友病A患者采用酶联免疫吸附法(ELISA)检测抗-HCV、HBV六项指标。结果 35例血友病A患者的抗-HCV阳性率为88.6%,输血次数和输注血液制品为主的种类与患者抗-HCV阳性率有相关性(P<0.01)。HBV六项指标检查,其中5例患者抗-HBe阳性(占14.3%),明显低于抗-HCV阳性率。结论血友病A患者替代治疗输血次数越多,感染风险越大,而较少输注以冷沉淀为主的血液制品的患者,其感染风险相对较小,且目前HCV感染率明显高于HBV感染率。     

丙型肝炎病毒患者抗病毒干预持续应答后发生肝细胞肝癌的临床特征

[目的]研究丙型肝炎病毒(HCV)直接抗病毒药物(DAA)抗病毒干预获得持续病毒学应答(SVR)后发生肝细胞肝癌(HCC)患者的临床特征.[方法]纳入本院130例HCV感染患者作为研究对象,所有患者均接受HCV抗病毒治疗,记录SVR情况.出院后随访记录HCC发生率.根据是否发生HCC,将获得SVR的患者分为观察组(发生...     

北京地区乙型肝炎病毒基因型及基因亚型的分布和临床意义

目的：调查北京地区乙型肝炎病毒（HBV）基因型及基因亚型的分布情况和临床意义。方法：应用型特异性引物聚合酶链反应法,对北京地区850份HBV感染者血清进行基因型、基因亚型检测,包括慢性乙型肝炎660例,肝硬化85例,肝癌105例。结果：B型、C型、BC混合型分布在不同类型乙肝病毒感染者中分布差异有显著性,肝硬化,肝癌患者C型所占比例明显高于慢性乙型肝炎患者。HBeAg阳性和阴性感染者中,HBV基因型分布差异无显著性。慢性肝炎、肝硬化及肝癌组中,均以C2和Ba亚型占优势。结论：在北京地区HBV感染者中,以Ba和C2亚型为主,C基因型感染者更易于发展为肝硬化、肝癌。     

Effects of alcohol consumption on viral hepatitis B and C

The liver is the main target organ for hepatitis viruses and the vital organ for alcohol metabolism. These two factors of viral hepatitis and alcohol abuse in combination can exert dual harmful actions, leading to enhanced damage to the liver. Epidemiological studies have revealed a higher prevalence of hepatitis C virus (HCV) infection among alcoholics than the general population. The interaction of alcohol with viral hepatitis [e.g., hepatitis B virus (HBV), HCV] and the underlying mechanisms are not fully understood. The effects of alcohol on viral hepatitis include promoted viral replication, weakened immune response, and increased oxidative stress. Clinically, alcohol abuse is correlated with an increased risk of developing end-stage liver cirrhosis and hepatocellular carcinoma in patients with chronic hepatitis B and C, suggesting that the combination of alcohol and HBV/HCV lead to more severe liver damage. The influence of mild to moderate alcohol drinking on the HBV-induced liver fibrosis, cirrhosis, and hepatocellular carcinoma among patients infected with HBV remains unclear. Unlike HBV infected patients, no safe level of alcohol intake has been established for patients with HCV. Even light to moderate alcohol use can exert a synergistic effect with viral hepatitis, leading to the rapid progression of liver disease. Furthermore, interferon-based therapy is less effective in alcohol drinkers than in control patients, even after abstinence from alcohol for a period of time. Therefore, abstaining from alcohol is highly recommended to protect the liver, especially in individuals with HBV/HCV infection, to improve the clinical efficacy of antiviral treatment and prevent the rapid progression of chronic viral hepatitis.     

Hepatitis B virus related hepatocellular carcinoma is the predominant cause of liver cancer in Bangladesh

ObjectiveTo investigate the etiology and other factor in development of hepatocellular carcinoma (HCC) in Bangladesh.MethodData from past studies were compared with our data to assess the etiology and other factor in development of HCC. Mainly four studies were compared which were done in different time. Ultrasonography was principle modality of primary diagnosis. Fine needle aspiration cytology was done in all cases to have tissue diagnosis.ResultsPrevious studies demonstrate hepatitis B in at least 46.9% cases. Recent studies demonstrate at least 61% association of HCC with hepatitis B infection. Our data which include 39 patients (M: F = 29: 10, Age 22–75 years, mean 51 year) demonstrate HBsAg positivity was present in 16 (41%), Anti HCV positivity in 2 (5%), both negativity in 8 (20.5%) and secondary carcinoma in 13 (33.3%) cases. If only primary HCC is considered then hepatitis B virus (HBV) related HCC constituted 61.5%. Alpha feto-protein was > 350 ng/mL in 11 out of 26 cases (42.3%).ConclusionsThough the study populations are small, they reflect that the prevalence of HBV related HCC correlates with the existing prevalence of HBsAg positivity in general population. Also the etiology has not changed over years and prevalence of hepatitis B related HCC is more or less a static as compared with previous studies.     

Hepatitis and transfusions.

Hepatitis B virus (HBV) and Hepatitis C virus (HCV) are major causes of liver disease. Chronic infection with these viruses often leads to chronic liver disease, including cirrhosis or primary hepatocellular carcinoma (HCC). Concern is growing among patients and health care workers about possible transmission of bloodborne pathogens during medical procedures. This fear has primarily been focused on nosocomial transmission of human immunodeficiency virus (HIV), but other bloodborne infectious agents may also be transmitted during procedures. Chief among these are the hepatitis viruses, particularly HBVand HCV, both of which are significantly more widespread than HIV Circumstantial evidence suggests that hemodialysis, per se, is an important risk factor for infection with HCV.     

乙型肝炎病毒和丙型肝炎病毒感染对肾移植受者长期预后影响

目的：研究乙型肝炎病毒和（或）丙型肝炎病毒感染对肾移植受者的长期预后的影响。方法：比较术前乙型肝炎病毒表面抗原（HBsAg）阳性或（和）丙型肝炎病毒抗体（抗-HBV）阳性与HBsAg和抗-HCV均阴性肾移植术患者的预后,用Kaplan—Meier法统计生存率。结果：肝炎病毒阴性受者的生存率和肾存活率分别为：1年94％和92．3％;3年88．6％和86．5％;5年83％和79．6％;10年69．9％和54％;肝炎病毒阳性受者的生存率和肾存活率分别为：1年98％和95．9％;3年91．3％和89．3％;5年79％和80．8％;10年64．7％和64．7％,阳性和阴性者相比生存率无明显差别。1999年前免疫抑制剂以环孢素A（CsA）、硫唑嘌呤（Aza）和激素为主,肝炎病毒阳性者5年和10年人生存率低于阴性患者,移植肾生存率无差别。肝炎病毒阳性受者死亡8例,4例死因为肝功能衰竭或肝硬化。1999年后吗替麦考酚酯（MMF）及他克莫司（FK506）应用于抗排斥治疗,肝炎病毒阳性和阴性受者移植肾和患者生存率均无差异,29例阳性者仅1例死亡,原因为移植肾失功后尿毒症。结论：在以CsA和A2a为主要免疫抑制剂的年代,肝相关并发症是肝炎病毒阳性肾移植受者重要死因,但肝炎病毒阳性与阴性者相比生存率、肾活率无明显差别。新型免疫抑制剂的应用和移植前后正确处理,可能改善乙型或丙型肝炎病毒感染肾移植受者预后。     

乙型肝炎病毒前C区(1896)和BCP区(1762/1764)变异对肝癌发病率的影响

目的探讨乙型肝炎病毒(HBV)前C区(1896)和BCP区(1762/1764)变异对肝癌发病率的影响。方法对520例HBV感染(慢性乙肝)患者进行HBV前C区(1896)和BCP区(1762/1764)变异检测,并观察其继发肝癌情况。结果 520例慢性乙肝患者HBV前C区(1896)变异肝癌发病率为8.3%,BCP区(1762/1764)变异肝癌发病率为30.0%,前C区(1896)和BCP区(1762/1764)同时变异肝癌发病率为10.9%,变异者合计肝癌发病率为22.9%;前C区(1896)和BCP区(1762/1764)均未发生变异(野生型)肝癌发病率为1.1%。变异者肝癌发病率显著高于未发生变异者(P<0.01)。结论 HBV前C区(1896)和BCP区(1762/1764)变异可能与肝癌的发病有关,应加强对此类患者HBV基因变异的检测。     

Pathological characterization of occult hepatitis B virus infection in hepatitis C virus-associated or non-alcoholic steatohepatitis-related hepatocellular carcinoma

Occult hepatitis B virus (HBV) infection, by definition, is a state in which infection with this virus does not manifest with the conventional diagnostic laboratory criteria reserved for the obvious form of HBV infection. As a result, occult HBV infection is commonly a surprise finding discovered accidently during the evaluation of other apparent liver diseases, such as hepatitis C virus (HCV) infection or non-alcoholic fatty liver disease and, more importantly, their evolution into life-threatening hepatocellular carcinoma. As infection with HCV and occult HBV is rarely considered when assessing these more obvious conditions, and in an attempt to offer a better understanding of this phenomenon, this study attempted to shed some light onto the uniqueness of occult HBV infection by addressing the natural history of HBV and HCV infections, as well as non-alcoholic fatty liver disease. This was carried out by taking into account the exclusive integration process undertaken by the HBV genome into infected host hepatocytes, with consideration given to conditions which afford reactivation of the occult infection and stress on the molecular mechanisms that underlie occult HBV infection. Finally, the clinical outcome of occult HBV infection and its relation to hepatocellular carcinoma is analyzed.