HIV/HCV合并感染患者的抗HCV治疗

一、背景 据WHO估计，全球HIV感染者已超过4000万。由于HIV与丙型肝炎病毒（HCV）有共同的传播途径，因而有大量的HIV感染者合并感染HCV。目前的研究显示，约有1／4～1／3的HIV感染者合并HCV感染，据此估计，全球约有近1000万的HIV／HCV合并感染者。HCV感染及相关的肝脏疾病（终末期肝衰竭和肝癌）已成为影响HIV感染人群发病率和死亡率的重要因素。     

艾滋病絮谈(七十四)

1丙型肝炎与艾滋病混合感染特点 全球丙型肝炎病毒（HCV）感染者约2亿；艾滋病毒（HIV）感染者约3500万。在HIV感染者中约1／3混合HCV感染。     

有偿献血员中艾滋病病毒、乙型肝炎和丙型肝炎病毒感染状况的研究

目的：探讨有偿献血员艾滋病病毒（HIV）、丙型肝炎（丙肝）病毒（HCV）、乙型肝炎（乙肝）病毒（HBV）感染的特点，方法：71份HIV阳性献血员及89份HIV阴性献血员的血清，经酶联免疫吸附试验（ELISA）检测HCV抗体（抗－HCV）及HBV血清学标志物，比较两组人群的HCV、HBV及HCV／HBV感染情况，结果：HIV阳性献血员的抗－HCIV阳性率为70．49％，乙肝血清学标志物，比较两组人群的HCV、HBV及HCV／HBV感染情况。结果：HIV阳性献血员的抗－HCV阳性率为70．49％，地病毒表面抗原（HBsAg）与抗体（抗－HBs）、乙肝病毒e抗原（HBeAg）与抗体（抗－HBe)、乙肝病毒核心抗体（抗－HBc）和HBV的阳性率分别为8．20％、29．51％、3．28％、44．26％，11．48％、47．54％、1．12％、47．19％、6．74％、47．19％。经统计学分析，两组人群的HCV、HCV／HBV感染率的差异有显著的统计学意义，而HBV血清学标志物则无显著性差异。结论：与HIV阴性献血员相比，HIV阳性献血员的HCV感染率很高，而HBV血清学标志物则无显著性差异，对献血员进行HBV检测而未检测HIV、HCV造成的选择偏倚，可能是中国中部一些省份HIV感染者HCV感染率高而HBV感染并不相应增高这一现象的原因之一。     

隐匿性HBV和HCV感染的分子诊断（上）

乙型肝炎病毒（HBV）和丙型肝炎病毒（HCV）分别属于嗜肝DNA病毒科及黄病毒科，均能引起慢性肝脏疾病，全球约有5．5—6亿人口因感染HBV或HCV而危及生命。尽管两种病毒分子组成、复制过程及结构蛋白功能不尽相同，HBV及HCV仍具有许多共同特点。两者均有明确的嗜肝性、能在淋巴系统内感染并复制；     

HIV／HBV合并感染的抗病毒治疗

全球有3．7亿-4亿的乙型肝炎病毒（HBV）携带者，由于其与人类免疫缺陷病毒（human immunodeficiency virus，HIV）有共同的传播途径，即血液传播、性传播和母婴垂直传播，因而有部分患者合并HIV感染。在欧洲，约8％的HBsAg阳性患者合并HIV感染。性传播和／或静脉注射毒品是最为普遍的传播方式。在HIV感染者中，HBV感染引起的肝脏损害是影响病情进展和死亡的重要因素。     

恩替卡韦抗HIV活性的探讨

目前全球大约有4亿人长期感染乙型肝炎病毒（HBV），同时有近4千万人感染人类免疫缺陷病毒（HIV）。由于HⅣ与HBV有共同的传播途径，所以经常可以观察到HIV／HBV合并感染的病例。有报告指出在发达国家6％-9％的HIV感染者同时感染HBV。此外，已证实HIV感染可加速乙肝病毒相关肝病的病程。     

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％。     

绍兴县吸毒人群HIV HBV HCV和梅毒感染状况的调查

绍兴县自1999年发现首例艾滋病病毒（HIV）感染者以来，近几年HIV感染者增长幅度惊人，HIV感染者主要集中在吸毒人群。为进一步了解绍兴县吸毒人群的HIV、乙型肝炎病毒（HBV）、丙型肝炎病毒（HCV）和梅毒的感染状况，吸毒方式和高危因素，于2005年对绍兴县戒毒所收容的吸毒人员开展调查，报告如下。     

慢性乙型肝炎的治疗目标、终点和策略

慢性乙型肝炎是一种流行性、进展性传染病。全球乙型肝炎病毒（HBV）感染者约为3．5亿人，我国是HBV感染的高流行地区。根据2002年全国HBV感染者血清流行病学调查．乙型肝炎表面抗原（HBsAg）流行率为9．09％，约1．2亿人，其中慢性乙型肝炎患者约为3000万人，如无正确治疗．慢性乙型肝炎患者5年后约10%-20％可发展为肝硬化．20％-23％可发展为失代偿期肝硬化．6％～15％可发展为肝细胞性肝癌（HCC）。而5年存活率，代偿期肝硬化为55％，失代偿期肝硬化为14％。每年死于乙型肝炎相关性肝病者约30万人。此外．母亲为HBV携带者可通过垂直传播使婴儿受染，婴儿时期感染HBV者90％以上将成为慢性HBV携带者．随着年龄的增长，可反复发作肝炎．     

1 201名劳教人员HIV HBV HCV及梅毒检测结果分析

为掌握劳教场所吸毒类高危人群艾滋病病毒（HIV）、乙型肝炎病毒（HBV）、丙型肝炎病毒（HCV）及梅毒的感染状况及特点，以便采取有效的预防和干预措施，对我所2002～2004年新收容的吸毒类劳教人员进行检测，对结果分析如下。     

Autoimmune hepatitis caused by acute hepatitis due to hepatitis A virus

We describe the case of a 27-year-old man who presented acute hepatitis due to hepatitis A virus infection. Over the following weeks he consistently presented elevated transaminase levels and jaundice. Antinuclear and anti-smooth muscle antibodies, hypergammaglobulinemia and periportal necrosis were detected in the liver biopsy. The patient was diagnosed with autoimmune hepatitis and responded well to treatment with immunosuppressive drugs. This case, as well as other published reports, suggest that in certain individuals, acute hepatitis A may be the decisive factor leading to autoimmune hepatitis.     

Economics of chronic hepatitis B and hepatitis C

Although not all patients develop progressive liver disease, chronic hepatitis B and chronic hepatitis C infections cause substantial morbidity and mortality worldwide. To address this need, many new antiviral treatments have become available over the past 10 years. While safety, efficacy, and therapeutic indications have been well established for these agents, the economics of antiviral treatment have become increasingly a focus of discussion for physicians, policymakers, and health payers. In this paper, we will elucidate some economic principles using examples from the treatment of hepatitis B and C. In particular, we will examine the considerations in estimating drug costs, methods for performing economic analyses and lastly summarize published cost-effectiveness analyses for antiviral treatments of chronic hepatitis B and chronic hepatitis C. This review should help clinicians understand economic issues regarding new drugs and answer questions about whether the clinical benefit provided by a medication justifies its expense.     

Autoimmune hepatitis versus viral hepatitis C

Abstract: Numerous viruses are capable of inducing the syndrome of chronic hepatitis. Among them are the hepatitis B, C and D viruses. Out of the most common agents of chronic hepatitis, the hepatitis C virus has been found to be strikingly associated with autoimmune diseases and serological markers of autoimmunity. Conversely, the syndrome of genuine autoimmune hepatitis lacks evidence of previous or ongoing virus infection and is diagnosed by additionally excluding metabolic, toxic, and genetic causes of chronic hepatitis, and by the response to immunosuppressive treatment. This review article summarizes the current knowledge of hepatotropic virus-induced autoimmunity. It focuses on the present molecular and immunological definitions, the clinical and molecular distinction between autoimmune hepatitis and chronic viral hepatitis and the implications for the safe and efficacious therapy of these disease entities.     

Isoniazid-rifampin-induced hepatitis in hepatitis B carriers

From January 1984-December 1987, 1783 patients received combination therapy of isoniazid, rifampin, and ethambutol for the control of tuberculosis. Forty-two developed symptomatic hepatitis during the period of treatment. Fifteen were hepatitis B virus carriers, and the remaining 27 were noncarriers. The peak serum transaminase and bilirubin levels were higher in carriers. Seven carriers died of fulminant or subacute hepatic failure, and only 1 noncarrier died. Eleven carriers had detectable serum hepatitis B virus deoxyribonucleic acid during the acute stage of hepatitis. The roles of isoniazid-rifampin combination therapy and hepatitis B virus in the adverse outcomes of carriers were discussed.