某地区HIV、HCV、TP感染与HBV感染情况调查

目的 探讨成都地区乙型肝炎病毒(HBV)感染与HIV、丙型肝炎病毒(HCV)和梅毒(TP)感染及其相互合并感染的关系,为预防、控制和治疗相关疾病提供参考.方法 对近期半年内该院门诊、住院及体检者HBsAg、抗HIV抗体、抗HCV抗体和抗TP抗体检测结果进行回顾性分析,分析HBsAg阴、阳性结果与其他各项检测结果之间的关系.结果 HBsAg阳性者合并抗HIV抗体阳性率明显高于HBsAg阴性者(P<0.01),HBsAg阴性者TP感染率更高(P<0.01),HBV感染情况与合并抗HCV抗体阳性没有相关性(P>0.05);双重感染与HBV感染相关(P<0.05),以HCV/TP重叠感染与HBV感染相关性最为明显(P<0.05),HIV/HCV重叠感染和HIV/TP重叠感染均与HBV感染无明显相关性(P>0.05);未见HCV、HIV、TP三重感染.结论 HIV感染与HBV感染明显相关,HCV/TP重叠感染与HBV感染也有相关性.     

病毒性肝炎病毒类型与病情关系的研究

对121例病毒性肝炎进行病毒标志的研究,并分析其影响预后因素.结果发现单纯HBV感染60例(49.6%),混合感染共61例(50.4%),其中HBV与HCV33例(27.3%)、HBV与HDV12例(9.9%)、HAV与HBV4例(3.3%)、HAV、HBV、HCV4例(3.3%)、HBV、HCV、HDV8例(6.6%).混合感染的病情重、病死率高.血清TB越多、PTA越低,其病死率越高,而AFP升高者预后较好.     

80例肝硬化乙肝病毒感染标志检测分析

随着对乙肝病毒(HBV)感染标志的实验室检测技术迅速进展,发现HBV感染与肝硬化的关系密切。本文就近年住院的80例肝硬化(失代偿期)患者的HBV感染标志进行分析。一.血清HBV感染标志检测方法: 乙肝病毒表面抗原(HBsAg)用R-PHA法;乙肝病毒表面抗体(抗-HBs)和乙肝病毒核心抗体(抗-HBc)用SP-RIA法;乙肝病毒e抗原(HB-eAg)、乙肝病毒e抗体(抗-HBe)和乙肝病毒核心抗体-IgM(抗-HBc-IgM)用ELISA法。二.检测结果: 1.80例肝硬化HBV感染标志检测结果,详见附表。     

单独抗-HBs阳性的丁型肝炎1例

丁型肝炎病毒(HDV)是一种缺陷核糖核酸病毒,只有在HBsAg的存在下才能复制,乙型肝炎病毒(HBV)起一种辅助作用.由于HDV感染时患者多存在HBV感染,故HBV感染的有无,一般来说是诊断HDV感染的前提.     

乙肝病毒宫内感染机制及危险因素的研究进展

宫内感染是指分娩前乙型肝炎病毒(HBV)通过胎盘生殖细胞或外周血单核细胞(PBMC)等方式,使胎儿携带HBV的过程.许多研究者在引产胎儿的肝、肾、胰、脾、胎盘等组织中均检出乙肝病毒基因(HBV DNA).为探索更有效的HBV宫内感染阻断策略,本文综述了乙肝病毒宫内感染机制及危险因素的研究进展.     

乙型与其它型肝炎病毒重叠感染对乙肝标志物的影响

目的探讨乙型肝炎病毒(HBV)与其它型肝炎病毒重叠感染对血清中乙型肝炎病毒标志物的影响.方法采用酶联免疫吸附试验(ELISA)方法,检测了HBV感染者血清中各型肝炎病毒抗体和HBV标志物,选取其中已确诊为重叠感染者49例作为实验组,并从已确诊为单一HBV感染者中随机抽取68例作为对照组.结果重叠感染组血清HBsAg、抗-HBcIgG、抗-HBcIgM等阳性率均明显低于对照组(P＜0.05),而抗-HBs阳性率则明显高于对照组(P＜0.05).其中丙型或戊型肝炎与HBV重叠感染时,HBeAg阳性率明显低于对照组(P＜0.05).结论其它型肝炎病毒与HBV重叠感染后,病毒间存在相互干扰作用,丙型及戊型肝炎病毒与HBV重叠感染时在一定程度上可抑制HBV复制.     

乙型肝炎病毒感染HepG2细胞模型的构建

目的:构建乙型肝炎病毒(HBV)感染的细胞模型.方法:将携带1.2拷贝HBV基因的重组腺病毒感染HEK293细胞进行包装、扩增并分离纯化.将扩增得到的HBV感染HepG2细胞,用ELISA法检测感染后第4天培养上清中的HBsAg,Real-time RT-PCR检测HBV mRNA.结果:ELISA检测结果显示,HepG2细胞感染HBV后上清液中HBsAg呈阳性.Real-time RT-PCR可以检测到HBV mRNA.结论:HBV能在HepG2细胞中表达复制和表达.HBV感染的HepG2细胞模型构建成功.     

温州地区乙型肝炎病毒基因型分布调查及意义

目的 调查乙型肝炎病毒(HBV)感染者的HBV基因型分布,探讨HBV基因型与临床的相关性.方法 用SP-nPCR法检测469例HBV感染者的HBV基因型.用荧光定量PCR法检测HBV DNA载量,用ELISA法检测HBV血清学标志物.结果 469份标本分出基因型430例,HBV基因型分布为:A型2.6%(11,430),B型34.9%(150/430),C型49-8%(214/430),B/C型12.8%(55/430),未检出D、E、F基因型;无症状携带者(ASC)和慢性乙肝患者(CH)以C、B基因型为主,肝硬化(LC)和肝癌(HCC)以C基因型占绝对优势.基因型分布与性别无关.30岁以下人群感染以B基因型为主.30岁以上则以C基因型为优势.结论 SP-nPCR法适用于慢性HBV感染者(病人和携带者)的基因分型和流行病学调查.HBV感染以C、B基因型为主,存在B,C混合基因型和A基因型.C基因型感染与肝硬化和肝细胞癌相关.     

HBV感染型与非HBV感染型肝细胞癌VEGF与CD34的表达及其肿瘤血管生成关系的研究

目的探讨HBV感染型与非HBV感染型肝细胞癌VEGF与CD34的表达及其与肿瘤血管生成关系。方法回顾性分析收治并确诊的82例肝细胞肝癌患者临床资料,根据HBV感染与否分为HBV感染型组、非HBV感染型组,通过免疫组化方法检测两组VEGF、CD_(34)阳性表达的差异,同时记录两组微血管密度值(MVD)情况。结果 HBV感染型组VEGF、CD_(34)阳性表达率分别为74.4%、51.2%,显著高于非HBV感染型组的38.5%、25.6%,差异具有统计学意义(P0.05);HBV感染型组MVD计数水平显著高于非HBV感染型组,具差异有统计学意义(P0.05)。结论 HBV感染型肝癌较非HBV感染型肝癌VEGF、CD34阳性表达高,MVD计数也较高,VEGF、CD_(34)高表达促进肿瘤血管生成,值得临床选择。     

铁路机车乘务员乙型肝炎病毒感染血清学调查

目的 了解铁路机车乘务员乙型肝炎(下称乙肝)病毒(HBV)感染情况.方法 对某铁路局3个机务段的全部机车乘务员进行HBV感染的血清学调查,按编码盲法进行检验,采用Excel建立数据库,计算各特征别的阳性率.结果 机车乘务员的HBV感染率为69.32%,HBV表面抗体(抗-HBs)阳性52.79%,HBV表面抗原(HBsAg)阳性10.96%.结论 该局机车乘务员的HBV感染率69.32%,抗-HBs阳性52.79%,这也与中国1985年以来推广接种乙肝疫苗后产生抗-HBs有关;HBsAg阳性10.96%,高于全国平均水平.     

Viral hepatitis in Israel. Transfusion-associated hepatitis

Follow-up of 1,754 transfused persons and 1,659 nontransfused patients at two hospitals in Israel revealed 13 cases of icteric hepatitis, all among transfusion recipients. Factors influencing attack rate were number of units administered and age (but not sex) of the recipient. Interview of 47 donors to cases and 248 donors to non-cases indicated an increased risk to patients receiving blood from individuals with a past history of jaundice, from those with a history of transfusion, and from persons born in North Africa.     

Transmission of serologically silent hepatitis B virus along with hepatitis C virus in two cases of posttransfusion hepatitis

The polymerase chain reaction (PCR) was used to investigate the presence of hepatitis B virus (HBV)-related DNA sequences in blood from three blood donors and two transfusion recipients who developed posttransfusion non-A, non-B hepatitis (NANBH). In the first case, the sole donor was positive for antibody to hepatitis B surface (HBs) and core (HBc) antigens and had elevated alanine aminotransferase (ALT) levels, while the recipient had no HBV serologic markers. Both the donor and the recipient had serologic markers of hepatitis C virus (HCV) and were found positive for HBV DNA and HCV RNA sequences by PCR. The second case involved two donors and one recipient. Serologic tests for conventional HBV markers were negative in all three individuals, but one of the donors had elevated ALT. HBV DNA sequences were detected by PCR in the serum of the recipient and of the donor with high ALT, but not in the serum of the donor with normal ALT. Anti-HCV was detected in the serum of the recipient and of the suspect donor but not in that of the donor with normal ALT. The sequences amplified in the S region and determined after cloning of PCR products for both donor-recipient pairs were indistinguishable from each other and identical to the sequence of the major HBV subtype of adw in the first case and ayw in the second case. Furthermore, for the second case, an identical single-point mutation was found in both the donor and the recipient. These data confirm the transmission of conserved HBV sequences together with HCV in posttransfusion NANBH.(ABSTRACT TRUNCATED AT 250 WORDS)     

Drug-induced hepatitis

AIM: To improve diagnosis and treatment of drug-induced hepatitis: to specify drugs with hepatotoxic effect, clinical variants of drug-induced hepatic diseases, management of drug-induced hepatitis (DIH). MATERIALS AND METHODS: Of 2300 examinees with hepatic lesions, 62 were diagnosed to have DIH. Measurements were made of serum levels of bilirubin and its fractions, total protein, some protein fractions, markers of hepatitis A, B, C, activity of aminotransferases (AlAT and AsAT), alkaline phosphatase (AP), glutamate dehydrogenase (GlDG), sorbitol dehydrogenase (SDG), gamma-glutamate transpeptidase (GGTP), choline esterase (CE). Timolveronal test was made. On demand, tests were made for CEA, AFP; device examinations were made: ultrasound investigation, computed tomography of the abdominal organs, endoscopic retrograde pancreatography, laparoscopy with hepatic biopsy, transcutaneous hepatic biopsy, laparotomy with cholecystocholangiography. RESULTS: A direct relationship of hepatitis with drugs intake was revealed in all the patients. Development of drug-induced intrahepatic cholestasis in patients on long-term treatment with anticancer drugs was accompanied with affection of cellular organellas and progressive destruction of small interlobular ducts provoking intrahepatic cholestasis and depletion of natural glutathione. CONCLUSION: Correction of intrahepatic cholestasis and deficiency of endogenic glutathione is successfully carried out with heptral.