200例输血前患者四项感染指标的检测结果分析

目的探讨200例输血前患者四项感染指标检测结果。方法 2011年8月至2013年2月选择住院进行输血治疗的200例患者,输血前都进行了甲型肝炎病毒(HAV)、乙型肝炎病毒(HBV)、丙型肝炎病毒(HCV)、艾滋病病毒(HIV)的检测与临床资料的调查。结果 200例患者检出HAV、HBV、HCV、HIV病毒感染阳性率分别为1.0%、9.0%、4.0%、1.0%,对比差异具有统计学意义(P<0.05)。非条件Logistic回归分析结果显示文化程度、输血次数、体质量指数与感染有明显相关性(P<0.05)。结论本院输血前患者四项感染指标检测阳性率比较高,需要积极根据感染危险因素加强预防与管理。     

甲乙丙乙戊乙肝炎病毒重叠感染的临床研究

我国是肝炎多发国家,各型肝炎病毒的重叠感染在临床上十分常见,为了了解甲(HAV)、丙(HCV)、戊(HEV)型肝炎病毒重叠于乙肝病毒(HBV)感染时的临床特点及对疾病转归的影响,特设对照组进行分析研究,现报告如下: 1 病例与方法 1.1 病例 均为1990年4月～1995年12月我科住院的病人,其中HAV、HBV感染     

某市2500例孕晚期妇女肝炎病毒感染现状的调查

目的了解宜昌市2500例孕晚期妇女肝炎病毒感染情况。方法选取2011年6月至2013年9月宜昌市2500例孕晚期妇女作为研究对象,采用酶联免疫吸附试验(ELISA)法检测甲型肝炎病毒(HAV)、乙型肝炎病毒(HBV)、丙型肝炎病毒(HCV)、戊型肝炎病毒(HEV)血清学标志物,比较分析各年龄段抗体及血清学标志物检测结果。结果所选孕晚期妇女中共检测出HBs Ag阳性185例(7.4%),抗HAV IgM阳性5例(0.2%),抗HCV阳性8例(0.3%),抗HEV Ig M阳性11例(0.4%),抗HEV Ig G阳性587例(23.5%)。结论孕晚期妇女肝炎病毒感染情况与年龄存在一定的相关性,监测肝炎病毒感染血清标志物有助于准确诊断病毒性肝炎类型,为针对性治疗提供参考。     

500例儿童甲型、乙型肝炎病毒双重感染分析

甲型肝炎病毒（HAV）与乙型肝炎病毒（HBV）的双重感染在儿童中比较少见.为了解莆田沿海地区儿童HAV和HBV双重感染的情况,本资料收集本院1998年以来的500例儿童甲型肝炎患者血清,同时检测乙肝病毒标志物,现就结果报道如下.     

医院内乙型肝炎与丙型肝炎病毒重叠感染及防治对策

随着丙型肝炎病毒抗体(抗—HCV)特异性诊断方法的建立,目前对丙型肝炎的研究已取得了很大进展。由于丙型肝炎病毒 (HCV)主要经血或血制品传播,因此,医院内乙型肝炎病人重叠HCV感染尤为临床重视。为了解乙肝病人医院内罹意HCV感染的途径以及HCV对肝病的影响,同时找出重叠感染的防治对策,本文检测165例乙肝病人的抗—HCV,现报告如下。     

孕妇乙型肝炎病毒DNA含量及胎儿窘迫与宫内感染的关系

目的　探讨乙型肝炎病毒 (HBV)DNA含量及胎儿窘迫与宫内感染的影响。方法　用荧光定量PCR法检测 16 9例乙肝病毒表面抗原 (HBsAg)阳性携带者孕妇血清中HBVDNA含量 ,随访观察胎儿窘迫和胎儿HBV宫内感染情况 ,并采用logistic多因素回归分析对胎儿HBV宫内感染 ,筛选胎儿HBV宫内感染的危险因素。结果　 (1)HBVDNA阳性孕妇的宫内感染率为 12 6 4 % ,HBVDNA阴性孕妇为 0 ,两者差异有统计学意义 (P <0 0 1) ;(2 )HBVDNA阳性孕妇的胎儿窘迫发生率为 2 7 5 9% ,HBVDNA阴性孕妇为 12 2 0 % ,两者差异有统计学意义 (P <0 0 1)。 (3)logistic多因素回归模型选入 3个胎儿HBV宫内感染的危险因素 :HBVDNA含量、胎儿窘迫、孕妇年龄 ,而HBeAg被排除在回归模型之外。 结论　估计宫内感染危险性高低 ,HBVDNA较HBeAg更可靠 ;HBVDNA含量可作为孕妇HBsAg阳性孕妇孕期使用乙肝免疫球蛋白 (HBIG)的指标 ;发生胎儿窘迫的和高龄的HBsAg阳性孕妇是宫内感染的高危人群。     

程序性死亡受体-1在慢性病毒性肝炎中的研究进展

摘要：乙型肝炎病毒（HBV）和丙型肝炎病毒(HCV)感染是导致慢性活动性肝炎、肝硬化和肝细胞癌的主要原因。近年来研究发现程序性死亡受体（programmed death-1 PD-1）负性调节病毒特异反应性T细胞的功能,被认为是HBV和HCV肝炎病毒持续感染的决定性因素,在慢性病毒性(HBV和HCV)性肝炎发病中扮演着重要角色。本文就程序性死亡受体（PD-1）在慢性病毒性肝炎中的研究进展进行综述。     

545例肝病患者甲、乙、丙三型肝炎感染的血清学分析

丙型肝炎病毒(HCV)是引起输血后肝炎的病原体之一,近年来各地相继对HCV感染病例及病毒重叠感染进行了研究,发现乙型肝炎病毒(HBV)感染率明显高于HCV,慢性肝炎仍以HBV感染为主,HCV感染在肝炎的慢性化和肝硬化的发病过程中起重要作用。HBV与HCV重叠感染对肝癌的发生似有相加作用。为了解本地区各类肝病中HCV的感染情况及甲、乙、丙三型肝炎的重叠感染,本对545例肝病患的血清学检测作一分析,报告如下。     

血清抗—HCV在乙肝病毒感染者中的检测

新近几年病毒性肝炎的研究有很大进展,尤其是非甲非乙型肝炎,已正式命名为丙型病毒性肝炎(HC)和戊型病毒性肝炎(HE)。我国是乙型病毒性肝炎(HB)的高发区,为了了解乙型肝炎病毒(HBV)感染者中丙型肝炎病毒(HCV)混合感染的状况,作者于1991～1992年对41例住院乙肝病毒感染者进行了血清抗—HCV的检测,结果报告于后。     

238例病毒性肝炎患者HCV和HAV、HBV重叠感染的临床分析

对238例各型病毒性肝炎患者检测了血清丙型肝炎病毒抗体（抗-HCV），对HCV与甲型肝炎病毒（HAV）、乙型肝炎病毒（HBV）重叠感染患者的部分临床资料进行了分析，现报道如下。材料与方法一、研究对象238例各型肝炎系本院1993年1月至1994年12月住院患者。男195例，女43例，年龄13～62岁。二、研究方法（1）血清抗一HCV检测采用ELISA方法，试剂由上海科华公司提供。（2）血清抗一HAVIgM及血清HBV标志均采用ELISA法检测。结果一、各型肝炎患者抗一HCV和抗一HAV－IgM、HBVM的检测238例病毒性肝炎患者抗一HCV阳性31例，阳性率…     

海洛因依赖者肝功能损害与各型肝炎病毒感染标志及其相关临床因素

目的··:了解海洛因依赖者肝功能损害与各型肝炎病毒感染标志及其它有关临床因素的相关关系。方法··:将198例海洛因依赖者肝功能丙氨酸转氨酶 (ALT)检查结果与各型肝炎病毒感染标志、梅毒检测的结果及临床特点通过Linear多因素回归模型进行回顾性分析、比较。结果··:海洛因依赖者ALT的变化与抗 -HCV、梅毒测定结果和HB sAg的阳性结果呈显著正相关 ,而与抗 -HBe的阳性结果呈显著负相关 ,而ALT的变化与抗 -HAV、HBeAg、抗 -HBc和抗 -HBs及临床特点未显示出显著的相关关系。结论··:海洛因依赖者ALT的高低依次取决于抗 -HCV、抗-HBe、梅毒测定结果和HBsAg,抗 -HCV是引起ALT变化的主要因素 ,其次是抗 -HBe。海洛因依赖者中HCV较HBV更易引起其ALT变化 ,对于抗 -HCV、抗 -HBe阳性的海洛因依赖者尤其应该注意其肝功能的损害。     

海洛因依赖者肝功能损害与各型肝炎病毒感染标志及其？…

目的：了解海洛因依赖者肝功能损害与各型肝炎病毒感染标志及其它有关临床因素的相关关系。方法：将１９８例海洛因依赖者肝功能丙氨酸转氨酶（ＡＬＴ）检查结果与各型肝炎病毒感染标志、梅毒检测的结果及临床特点通过Ｌｉｎｅａｒ多因素回归模型进行回顾性分析、比较。结果：海洛因依赖者ＬＡＴ的变化与抗－ＨＣＶ、梅毒测定结果和ＨＢ－ｓＡｇ的阳性结果呈显著正相关,而与抗－ＨＢｅ的阳性结果呈显著负相关,而ＡＬＴ的变化与抗－     

The prevalence of viral hepatitis (HAV, HBV and HCV) in the Christchurch community

AIM: To determine the prevalence of hepatitis A (HAV), hepatitis B (HBV) and hepatitis C (HCV) in adults randomly selected from the Christchurch community. METHODS: A list of names was randomly generated from the Christchurch electoral roll and subjects were sequentially contacted and invited to participate. A blood sample was taken and tested for hepatitis A (IgG anti-HAV antibody), hepatitis B (HBsAg and anti-HBc) and HCV (anti-HCV antibody) using Abbott Elisa kits. Subjects positive for HBsAg were also tested for HBeAg/HBV DNA. Those positive for anti-HBc were tested for anti-HBs. HCV antibody positive samples were tested for HCV RNA using PCR. RESULTS: 1064 subjects (30.3% of those invited) participated in the study. The prevalence of HAV antibodies was 27.9%, and increased with age. The overall prevalence of HBV markers was 42/1064 (4.2%), and of these 0.3% were HBsAg positive and 3.9% were considered immune. No gender or ethnic differences in these proportions were observed. The seroprevalence of HVC antibody was 3/1064 (0.3%), two of whom were also PCR positive for HCV RNA. CONCLUSION: In the Christchurch community there was a high prevalence of antibodies to HAV, which increased with age. The prevalence of HBsAg and antibody to HCV were both low at 0.3%.     

Patterns of hepatocellular carcinoma development in hepatitis B virus and hepatitis C virus related cirrhosis.

To compare incidence, risk factors and morphologic pattern of hepatocellular carcinoma (HCC) development in hepatitis B virus (HBV) and hepatitis C virus (HCV) related cirrhosis, 401 patients were followed prospectively by periodic ultrasound examination for 14-189 months (mean: 84.8+/-36.7). During follow-up, 77 (19.2%) patients developed HCC, with 5 and 10 year cumulative incidence of 10 and 27.5%, respectively. The risk of HCC was significantly higher in HBV and HCV co-infected patients (P=0.014) compared to those with single HBsAg or anti-HCV (antibodies to hepatitis C virus) positivity. In anti-HCV positive cases the annual risk of HCC increased from 2% in the first 5 year period to 4% in the third 5 year period, while it decreased from 2 to 0% in the same time periods in the HBsAg positive group. By Cox's regression, age above 59 years (P=0.001), male sex (P=0.09), longer duration (P=0.04) and more advanced stage (P=0.01) of cirrhosis, lower platelets count (P=0.001) and higher ALT levels were significant risk factors for HCC in anti-HCV positive patients, while only high alpha-fetoprotein (AFP) levels during follow-up (P=0.04) was a significant risk factor for HCC in HBsAg positive cases. The pattern of HCC was nodular in 63 (81.8%) patients and infiltrating in 14 (18.2%), and the former type was associated with older age (P=0.0001), longer duration (P=0.002) and more advanced stage (P=0.0001) of cirrhosis but not with the viral etiology of disease. In contrast, development of infiltrating HCC was unrelated to age and disease duration and stage, and was associated with male sex (P=0.01), HBV infection (P=0.06) and HBV and HCV co-infection (P=0.0001). Our results indicate different incidence profile, risk factors and patterns of morphogenesis of HCC development in HBV and HCV associated cirrhosis, suggesting different mechanisms of carcinogenesis.     

乙型和丙型肝炎病毒双重感染肝组织病毒标志物的检测

为观察乙型肝炎和丙型肝炎双重感染的尸体肝组织中两种病毒核酸及抗原的分布，对１５例ＨＢＶ与ＨＣＶ双重感染的尸检肝组织用免疫组织化学法检测ＨＢｓＡｇ、ＨＢｃＡｇ和ＨＣＡｇ，Ｄｉｇｏｘｉｇｅｎｉｎ标记的探针原位杂交法分别检测ＨＢＶ ＤＮＡ和ＨＣＶ ＲＮＡ。结果：ＨＢｓＡｇ、ＨＢｃＡｇ、ＨＢＶ ＤＮＡ、ＨＣＡｇ和ＨＣＶ ＲＮＡ的阳性数分别为１２／１５（８０．０％）、１０／１５（６６．７％）、９／１５（６０     

Hepatitis and human immunodeficiency virus co-infection among injection drug users in Los Angeles County, California

This study examined the prevalence of hepatitis A (HAV), B (HBV), C (HCV), and Human Immunodeficiency Virus (HIV) co-infection among Injection Drug Users (IDUs) in Los Angeles County, California, and predictors of multiple infections in this population. Six hundred seventy-nine IDUs were recruited from October 2002 through June 2004. Participants completed questionnaires to elicit demographic, drug and sex risk information, and were tested for hepatitis A, B, C and HIV.A linear regression model predicting the total number of infections (0 to 4 possible) was constructed. Significant associations were found between HAV and HBV infection, HAV and HCV infection, and HBV and HCV infection. Predictors of total co-infections included age of first injection, lifetime years in jail, and Hispanic ethnicity. Latinos had the highest proportion of HAV and HBV co-infection with HCV. The total number of co-infections, especially those co-infected with all three of the hepatitis infections, was unexpectedly high.     

Role of silent hepatitis B virus in chronic hepatitis B surface antigen(-) liver disease.

Despite a number of studies documenting hepatitis B virus (HBV) infection in the absence of hepatitis B surface antigen (HBsAg) a causal relationship between silent HBV infection and liver disease remain difficult to establish. In particular, both the prevalence and clinical significance of this observation are poorly understood. Why is HBV replication apparently so low in these patients? A number of studies have tried to elucidate the mechanism of HBsAg negative infections, and considerable data documenting HBV infectivity or reinfection in the absence of detectable HBsAg support the hypothesis that in some of these cases, HBV is undergoing low-level replication in the liver and this, in several situations including: (1) chronic liver disease, alcoholic liver disease, hepatocellular carcinoma; (2) viral reactivation following cancer chemotherapy or immunosuppression and (3) transmission via transfusion or from human serum to chimpanzees. In a recent study including 50 patients with chronic liver disease of unknown etiology we could detect serum HBV DNA by nested polymerase chain reaction (PCR) in 15/50 patients (50% at the cirrhosis stage) in the absence of HBsAg; in the liver of the 15 patients both HBcAg and/or HBsAg can be detected at very low-level. Viral host factors allowing HBV persistence in the absence of HBsAg can depend on several mechanisms. Coinfections with HCV can explain only a proportion of HBsAg(-) HBV infections. Secondly, HBV mutations in the core promotor region leading to a minimal viral replication, or mutations in the HBsAg-encoding region might explain the absence of serological recognition. Finally, it is possible that in some cases host immune mechanisms can maintain HBV infection in a latent state until transmission to another individual who subsequently develops a more active infection especially when immunosuppressive therapy is employed. Existence of HBsAg(-) HBV infections should be taken into account by the use of sensitive PCR tests for prevention of viral transmission in the settings of blood donations and organ transplants.     

戊型病毒性肝炎32例临床分析

目的 了解戊型病毒性肝炎在五型病毒性肝炎中的构成比及其临床特点。方法 应用ELISA法和PCR法对1996－1999年诊治338例病毒性肝炎病人进行了甲、乙、丙、丁、戊型肝炎病原体检测和临床特点的统计分析。结果 共检出戊型病毒性肝炎32例,占受检人数的8．2％。其中单纯HIE、HEV＋HAV、HEV＋HBV、HEV＋HAV＋HBV、HEV＋HCV感染率分别占46．9％、18．8％、15．6％、9．4％、9．4％。临床分型主要是急性黄胆型,其次是急性无黄胆型及瘀胆型。戊型病毒性肝炎主要症状为：纳差、厌油（93．8％）,乏力（81．3％）,发热、头痛（71．9％）,恶心、呕吐、黄胆（59．4％）,肝肿大（53．1％）,腹胀（37．5％）,可有心肌损害（12．5％）,ALT几乎均有升高（96．9％）。结论 HEV可单纯感染,也可与HAV、HBV、HCV混合感染,总混合感染率为53．1％,混合感染较单纯感染病情重、黄胆深,且病情恢复慢。     

Occult hepatitis B virus infection in dialysis patients: a multicentre survey

BACKGROUND: The epidemiology and clinical significance of occult hepatitis B virus infection (serum hepatitis B surface antigen-negative patients with detectable hepatitis B virus viraemia in serum) remains controversial with only limited information about its prevalence in patients on long-term dialysis. AIM: To address the epidemiology of occult HBV infection in a large cohort of dialysis patients. METHODS: We screened a large cohort (n = 585) of Italian chronic dialysis patients; from this population, a group of hepatitis B virus surface antigen seronegative patients (n = 213) was tested by Amplicor hepatitis B virus Monitor Test to detect hepatitis B virus viraemia (hepatitis B virus-DNA) in serum. RESULTS: Occult hepatitis B virus infection was absent (zero of 213 = 0%). Persistent hepatitis B virus surface antigen carriage was less frequent than anti-hepatitis B virus core antibody (anti-hepatitis B core antigen) seropositive status in this study group [1.88% (11 of 585) vs. 36% (216 of 585), P = 0.0001]. No dialysis patients seropositive for anti-hepatitis B core antibody in serum (zero of 123 = 0%) had detectable hepatitis B virus-DNA by polymerase chain reaction technology. No significant association between abnormal biochemical liver tests and serum anti-hepatitis B core antibody was noted in our population. Nominal logistic regression analysis demonstrated an independent and significant relationship between anti-HCV antibody and anti-hepatitis B virus core antibody in serum (Wald chi-square 16.06, P = 0.0001). The rate of seropositive patients for anti-hepatitis B virus core antibody was higher among study patients than controls with normal renal function [36.9% (216 of 585) vs. 21.4% (59 of 275), P = 0.0001]; this difference partially persisted after correction for demographic parameters, and viral markers. CONCLUSION: In conclusion, occult hepatitis B virus was absent in our study group. Anti-hepatitis B core antibody was significantly related to presence of anti-HCV antibody supporting shared modes of transmission. Clinical studies based on molecular biology techniques provided with higher sensitivity are planned.     

Magnitude and quality of antibody response to a combination hepatitis A and hepatitis B vaccine.

Interference between antibodies generated by a combination hepatitis A and B vaccine was investigated by evaluating the quantity and quality of anti-hepatitis A virus (HAV) and anti-hepatitis B surface antigen (HBs) antibodies generated by Twinrix (Hepatitis A Inactivated and Hepatitis B (Recombinant) Vaccine). The magnitude of the immune response was determined by a retrospective analysis of eight clinical trials, completed during stepwise development of Twinrix. The functionality of anti-HAV was evaluated by comparison of routine ELISA results with neutralization assays and was further characterized by defining the epitope-specificity of binding. Functionality of the anti-HBs response was not tested because a validated assay was not developed at the time this study was conducted. Results of all analyses demonstrated that the combination vaccine induced high antibody titers against hepatitis A and B and a functional anti-HAV response, with no evidence of immune interference to either viral antigen.