慢性肝病者乙型和丙型肝炎病毒重叠感染的研究

对２１３例老年慢性肝病患者的乙型肝炎病毒（ＨＢＶ）和丙型肝炎病毒（ＨＣＶ）血清标志物检测发现：ＨＢＶ感染占７３．２４％、ＨＢＶ和ＨＣＶ重叠感染占重叠感染点１５．４９％、ＨＣＶ感染占７．０４％、其它占４．２６％；ＨＢＶ阴性者ＨＣＶ检出率高于ＨＢＶ阳性者，肝癌和肝硬化患者较慢性肝炎患者高；ＨＢＶ和ＨＣＶ重叠感染患者的血清血蛋白下降显著，γ－球蛋白升高明显，肝硬化并腹水和上消化道出血者了多。结果表明，老     

输血后乙型和丙型肝炎病毒感染的前瞻性调查

目的 了解输血所致ＨＢＶ和ＨＣＶ感染现状及ＨＢｓＡｇ抗ＨＣＶ和ＡＬＴ筛检供血的效果。方法 对１３８例输血者输血前，后１，３，６，９个月血清标本及其供血检测ＨＢｓＡｇ，抗ＨＢｓ，抗ＨＢｃ，抗ＨＣＶ和ＡＬＴ，并对部分血清标本用ＰＣＲ及巢式ＲＴ－ＰＣＲ法检测ＨＢＶＤＮＡ和ＨＣＶＲＮＡ，结果和结论 输血后ＨＢＶ和ＨＣＶ感染率分别为１．４％（２／１３８）和３４．８％（４８／１３８），输血后乙型和丙型肝炎发生     

乙型和丙型肝炎病毒感染与肝细胞癌

为探讨乙型和丙型肝炎病毒（ＨＢＶ和ＨＣＶ）感染与肝细胞癌（肝癌）发生的关系，采用ＥＬＩＳＡ和聚合酶链反应（ＰＣＲ）对沈阳地区１１７例肝癌、１０７例肝硬化和４５例血液透析患者血清进行了ＨＢＶ和ＨＣＶ血清标志及ＨＢＶＤＮＡ和ＨＣＶＲＮＡ检测，并采用限制性片段长度多态性对其中７３例ＨＣＶＲＮＡ阳性血清进行了ＨＣＶ基因分型。结果，肝癌组ＨＢＶ感染率（６０７％）显著高于ＨＣＶ感染率（３３３％，Ｐ＜００１），肝硬化组ＨＢＶ感染率（４３９％）明显高于ＨＣＶ感染率（２９０％，Ｐ＜００５）；血液透析组ＨＢＶ和ＨＣＶ重叠感染率（２６７％）明显高于肝硬化组（１０３％，Ｐ＜００５）；各组均以ＨＣＶⅡ型为主（６５２％～８００％），ＨＣＶⅢ型次之（２００％～３１４％）。结果提示：沈阳地区肝癌的诱发因素仍以ＨＢＶ为主，血液透析患者ＨＢＶ和ＨＣＶ重叠感染的机会更大，ＨＣＶⅡ型感染在本地区ＨＣＶ相关性肝癌和肝硬化的发生中可能起主要作用。     

重叠乙型和丙型肝炎病毒感染的临床与病理分析

目的 观察HBV和HCV重叠感染的临床与病理,探讨HBV和HCV相互作用的特点.方法 收集226例慢性肝病患者的血清学指标,实时荧光定量PCR法测定HBV DNA和HCVRNA,ELISA检测HBV血清标志物、抗-HCV抗体.行肝穿刺活组织病理检查、免疫组织化学HBsAg、HBcAg和原位杂交HBV DNA、HCV RNA检测.计数资料比较采用X2检验或Fisher确切率检验.结果 HBV和HCV重叠感染的重度慢性肝炎患者比例为62.50%,高于HBV或HCV单独感染者的27.05%和30.56%(X2=14.70,P＜0.01).HBV感染组的血ALT、AST、TBil、DBil和Alb高于HBV和HCV重叠感染组和HCV感染组,差异均有统计学意义(X2=8.52,P＜0.05).重叠感染组和HBV感染组的血HBsAg与肝内HBsAg一致率比较,差异均有统计学意义(X2=15.60,P＜0.01).HBV和HCV重叠感染组血清HBV DNA阳性率为12.5%,低于HBV单独感染组的87.7%(X2=17.66,P＜0.01);而HBV和HCV重叠感染组HCV RNA阳性率为75.0%,低于HCV单独感染组的80.6%,差异无统计学意义(P＞0.05).结论 HBV和HCV重叠感染导致的肝损伤更明显.     

乙型和丙型肝炎病毒重叠感染的临床分析

对20例乙型和丙型肝炎病毒重叠感染患者进行临床分析,表明重叠感染与单纯乙型肝炎病毒感染两者主要生化指标 ALT 和血胆红素无显著性差异,重叠感染丙型肝炎病毒对乙型肝炎病毒并无抑制现象,重叠感染的慢性肝炎好转治愈率比单纯乙型肝炎,病毒感染者低(P<0.01);重症肝炎重叠感染者预后差;肝硬化重叠感染者好转率比单纯乙型肝炎病毒感染者低,但两者相比无显著性差异(P>0.15)。     

广西桂中地区艾滋病患者乙型和丙型肝炎病毒感染调查研究

目的了解广西桂中地区人类免疫缺陷病毒(HIV)/艾滋病(AIDS)患者合并乙型肝炎病毒(HBV)、丙型肝炎病毒(HCV)感染的情况。方法调查分析我院2007-01～2009-12确诊的2 342例AIDS患者临床资料。结果 HIV/HBV、HIV/HCV、HIV/HBV/HCV共感染率分别为16.8%、22.5%、2.5%,其中吸毒和性传播者HIV/HCV感染率分别为74.7%和8.0%、HIV/HBV感染率分别为15.6%和17.2%、HIV/HBV/HCV感染率分别为7.8%和1.0%。结论广西桂中地区HIV/HBV共感染在性传播和吸毒传播者中差异无统计学意义,HIV/HCV、HIV/HBV/HCV共感染差异有统计学意义,应采取措施控制其传播。     

慢性乙丙型肝炎重叠感染后血清病毒标志物的变化

目的为了探讨病毒之间的干扰现象，作者对慢性乙丙型病毒性肝炎重叠感染患者的血清肝炎病毒标志物的变化进行研究。方法１９９２年１月＿１９９４年１０月连续在我院住院确诊的慢性乙丙型病毒性肝炎重叠感染患者６０例，同期连续收住院的单纯慢性乙型肝炎患者１１０例作为对照组，比较两组患者入院时的血清乙型肝炎病毒标志物，并对观察组中２０例患者进行了随访，随访期０．５＿３年。结果入院时观察组ＨＢｅＡｇ和抗＿ＨＢｃＩｇＭ阳性率较对照组显著减少（１９／６０对５２／１０６，８／６０对２９／１１０，Ｐ＜０．０５），ＨＢｓＡｇ阴性率和抗＿ＨＢｅ阳性率显著增高（１０／／６０对５／１１０，Ｐ＜０．０１；３８／６０对４８／１０６，Ｐ＜０．０５）。观察组２０例随访发现，ＨＢＶ＿ＤＮＡ阳性及ＨＢＶ＿ＤＮＡ，ＨＣＶ＿ＲＮＡ二项同时阳性例数都比入院时明显减少（４／２０对１０／２０，Ｐ＜０．０５；１／２０对７／２０，Ｐ＜０．０５）。结论慢性乙丙型病毒性肝炎重叠感染时存在病毒干扰现象     

隐匿性丙型肝炎病毒感染与慢性丙型肝炎的比较分析

目的:比较隐匿性丙型肝炎病毒(HCV)感染者与慢性丙型肝炎(CHC)患者的特点.方法:选择51例隐匿性HCV感染者和52例未经治疗的CHC患者,两组患者的年龄、性别、肝功能异常的持续时间相匹配,分别比较两组患者的肝功能指标和外周血单个核细胞(PBMCs)中的丙型肝炎病毒核酸(HCV RNA)含量.结果:CHC患者的天门冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)、甲胎蛋白(AFP)显著高于隐匿性HCV感染者(P<0.01),而胆固醇(Ch)和甘油三酯(TG)则显著低于后者(P<0.01),γ谷氨酰转肽酶(GGT)在两组感染者中差异无显著性意义(P>0.05);CHC患者的PBMCs中HCV RNA平均含量显著高于隐匿性HCV感染者(P<0.01).结论:隐匿性HCV感染者病情严重程度不如CHC患者,这可能与其PBMCs中的病毒载量高低相关.     

丙型肝炎病毒感染与肝癌

丙型肝炎病毒感染与肝癌余竹元，郑宁（上海医科大学肝癌研究所上海２０００３２）肝癌（ｈｅｐａｔｏｃｅｌｌｕｌａｒｃａｒｃｉｎｏｍａ，ＨＣＣ）居我国癌症死亡的第三位，除已知的乙肝病毒（ＨＢＶ），黄曲霉毒素及饮水污染为重要的致癌因素外，近年来丙型肝炎病毒（...     

丙型肝炎病毒感染与肾脏疾病

丙型肝炎病毒感染与肾脏疾病姚小丹，黎磊石自从丙型肝炎病毒（ＨＣＶ）的存在被证实且被认定为非甲非乙型肝炎的主要病原体以来，ＨＣＶ感染引起了临床医学界的广泛重视。在肾脏病学领域，ＨＣＶ感染与晚期肾脏疾病（ＥＳＲＤ）及某些类型的肾小球疾病之间的联系已成为近...     

Hepatitis type C virus infection in patients with type B chronic liver disease

Anti-c100-3 (Ortho) was determined in the sera of 152 patients with HBs antigen-positive chronic liver diseases to assess coinfection of hepatitis B virus (HBV) and hepatitis C virus (HCV). Eleven patients (7.2%) were positive for anti-c100-3. Anti-CP-9 (Okamoto) and HCV-RNA (RT-PCR) were also examined in these 11 patients. Anti-CP-9 was detected in 7 patients and HCV-RNA was detected in all 11 patients. Four of the 11 anti-c100-3-positive patients were positive for HBe antigen (HBeAg) and others were negative. In 8 of the 11 patients, HCV was suspected to be superinfected by blood transfusion. In HBeAgpositive patients, serum glutamic pyruvic transaminase (SGPT) was elevated in relation to active replication of HBV shown by DNA-polymerase activity. The histological findings showed chronic active hepatitis, with or without cirrhosis. On the other hand, in HBeAg-negative patients, SGPT fluctuated without evidence of active replication of HBV. Active inflammation in the liver was observed in 3 of 5 HBeAg-negative patients by liver biopsy. These findings suggest that HBV might play an important role in chronic active inflammation in HBeAg-positive patients coinfected with HCV, and that HCV might be responsible for continuous inflammation in HBeAg-negative patients coinfected with HCV.     

Hepatitis type C virus infection in patients with type B chronic liver disease.

Anti-c100-3 (Ortho) was determined in the sera of 152 patients with HBs antigen-positive chronic liver diseases to assess coinfection of hepatitis B virus (HBV) and hepatitis C virus (HCV). Eleven patients (7.2%) were positive for anti-c100-3. Anti-CP-9 (Okamoto) and HCV-RNA (RT-PCR) were also examined in these 11 patients. Anti-CP-9 was detected in 7 patients and HCV-RNA was detected in all 11 patients. Four of the 11 anti-c100-3-positive patients were positive for HBe antigen (HBeAg) and others were negative. In 8 of the 11 patients, HCV was suspected to be superinfected by blood transfusion. In HBeAg-positive patients, serum glutamic pyruvic transaminase (SGPT) was elevated in relation to active replication of HBV shown by DNA-polymerase activity. The histological findings showed chronic active hepatitis, with or without cirrhosis. On the other hand, in HBeAg-negative patients, SGPT fluctuated without evidence of active replication of HBV. Active inflammation in the liver was observed in 3 of 5 HBeAg-negative patients by liver biopsy. These findings suggest that HBV might play an important role in chronic active inflammation in HBeAg-positive patients coinfected with HCV, and that HCV might be responsible for continuous inflammation in HBeAg-negative patients coinfected with HCV.     

Hepatitis B virus infection and chronic liver disease in Taiwan.

Three hundred and eighty-five patients mostly with chronic liver diseases and 729 apparently healthy adults were studied for hepatitis B surface antigen (HBsAg) with reversed passive hemagglutination and antibody (anti-HBs) with passive hemagglutination. In healthy adults around 15% was HBsAg positive and in 45% was anti-HBs positive, estimating hepatitis B virus (HBV) infection in nearly two thirds of the population. The infection already occurred before adulthood. The prevalences of HBsAg were invariably over 80% in chronic hepatitis, cirrhosis and hepatocellular carcinoma (hepatoma) indicating an intimate relationship to HBV. On the contrary, the positive rates of anti-HBs in these diseases were far lower than those in healthy people and patients with other diseases, this is similar to the situation in chronic HBsAg carriers. The prevalence of HBsAg in hepatoma patients was unusually high, being 82.7% in contrast to 11.9% in patients with other malignancies. Not only hepatoma patients with cirrhosis but also those without cirrhosis were found to have high prevalence of HBsAg. The fact indicates an even more intimate relationship between hepatoma and HBV.     

Virus replication and liver disease in chronic hepatitis B virus infection

Recent studies on the natural history of chronic hepatitis B virus infection have provided evidence for a close temporal relationship between the phase of active virus replication and development of liver lesions. To assess the role that virus replication plays in this phase in determining the severity of the liver disease, we studied serum levels of virus-specific DNA-polymerase activity and hepatitis B_e antigen/antibody status in 48 chronic carriers of the hepatitis B surface antigen found positive for the hepatitis B core antigen in the liver. There was a remarkably evident inverse correlation between virus replication activity and liver disease activity, patients with minimal histological changes having the highest DNA-polymerase levels (mean±sd: 3879±2557 cpm) and those with severe chronic active hepatitis the lowest enzyme levels (419±246 cpm), while cases of chronic persistent hepatitis and of mild chronic active hepatitis had intermediate levels. Serum hepatitis B_e antigen was detected in 31/32 patients with milder liver lesions and in 11/16 with severe liver lesions; the remaining five cases were anti-HB_e-positive despite the presence of the core antigen in the liver. Serum levels of virus replication markers closely correlated with the distribution pattern of the core antigen in the liver. These findings indicate that in chronic hepatitis B the severity of liver disease is not directly related to levels of virus replication, thus suggesting a predominant role of host immune mechanisms.     

Hepatitis C virus infection in chronic liver disease in Bombay.

To find out the prevalence of antibody of hepatitis C virus (anti-HCV) in patients with chronic liver disease in Bombay, sera from 126 patients (93 men, 33 women; aged 9-70 years, mean 39.7) with chronic liver disease (cirrhosis 103, cirrhosis with hepatocellular carcinoma 3, chronic active hepatitis 20) were tested for HBsAg and anti-HCV antibody. HBsAg positive sera were tested for anti-delta antibody and IgM anti-HBc. All the tests were carried out by ELISA. Of 126 patients, 51 (40.5%) were HBsAg positive, 49 (38.8%) alcoholic and 21 (16.6%) anti-HCV positive. The prevalence of anti-HCV in HBsAg positive, alcoholic and cryptogenic (HBV negative and no alcohol) liver disease patients was 13.7%, 14.7% and 20.5% respectively. Of 21 anti-HCV antibody positive patients, 8 (38%) had received blood transfusions previously. HCV is present in 15-20% of patients with chronic liver disease in Bombay.     

Hepatitis C virus infection in patients with nonalcoholic chronic liver disease

STUDY OBJECTIVE: To determine the prevalence and meaning of antibodies to the hepatitis C virus (HCV) in patients with nonalcoholic chronic liver diseases. DESIGN: Cross-sectional study. SETTING: The liver unit of a referral-based university hospital. PATIENTS: Three hundred and forty-six consecutive patients, including 137 with cryptogenic chronic liver disease, 156 with chronic hepatitis B, 47 with primary biliary cirrhosis, and 8 with persistently abnormal aminotransferase serum levels and normal liver histology. Among patients with cryptogenic liver disease, 41 received blood transfusions before discovery of liver disease and 18 had circulating nonorgan-specific autoantibodies. For comparison, 1495 apparently healthy volunteer blood donors were included in the study. LABORATORY INVESTIGATIONS: The presence of anti-HCV antibodies (anti-HCV) was determined by a recently developed enzyme-linked immunoassay. MEASUREMENTS AND MAIN RESULTS: In patients with cryptogenic liver disease, the prevalence of anti-HCV was 82% (95% CI, 76% to 89%), being higher (P = 0.02) in patients with histories of blood transfusion than in those with unknown sources of exposure. Antibodies to HCV were not detected in patients with antinuclear antibodies at high titer. Among patients with chronic hepatitis B, anti-HCV were found in 11% (CI, 5% to 18%) of those with hepatitis B virus (HBV)-associated DNA in serum and in 29% (CI, 17% to 43%) of those with undetectable HBV replication (P less than 0.05). The prevalence of anti-HCV in blood donors was 1.2% (CI, 1.1% to 1.3%). CONCLUSIONS: Our results indicate that HCV infection probably plays an important etiologic role in cryptogenic liver disease and, in some patients, in chronic hepatitis B. Determining whether anti-HCV are present appears to be useful for differentiating viral from autoimmune chronic liver diseases.     

Hepatitis C infection and nonalcoholic fatty liver disease

In hepatitis C virus (HCV) infection, significant hepatic steatosis or superimposed nonalcoholic steatohepatitis is associated with disease severity and poor response to antiviral therapy. Nonalcoholic fatty liver disease (NAFLD) and HCV are common causes of chronic liver disease in Western countries and are strongly linked to concurrent obesity, insulin resistance, and the metabolic syndrome. With the escalating prevalence of obesity in North America, insulin resistance and the metabolic syndrome are major public health problems that have a significant impact on morbidity and mortality associated with NAFLD and HCV. This article focuses on the current understanding of the interplay between host and viral factors that are involved in the interaction between NAFLD and HCV.     

Hepatitis E autochthonous infection in chronic liver disease

Hepatitis E virus is endemic in many parts of the developing world and causes a self-limiting hepatitis in young adults, except in pregnant women and patients with chronic liver disease, where the mortality is high. Locally acquired hepatitis E is increasingly recognized in the developed world. It is caused by hepatitis E virus genotype 3, affects the middle-aged and the elderly, and may be a zoonotic infection from pigs. We present a case of locally acquired hepatitis E infection in a patient with previously undiagnosed cirrhosis, which resulted in subacute liver failure and death. We describe our attempt to trace this infection to a free-range pig farm adjacent to the patient's place of employment. Hepatitis E infection should be considered in the differential diagnosis in patients with decompensated chronic liver disease whatever their age or travel history. When found, the prognosis may be poor.     

Hepatitis B and C infection and liver disease trends among human immunodeficiency virus-infected individuals

AIM:To examine trends in and correlates of liver disease and viral hepatitis in an human immunodeficiency virus (HIV)-infected cohort. METHODS:The multi-site adult/adolescent spectrum of HIV-related diseases (ASD) followed 29 490 HIVinfected individuals receiving medical care in 11 U.S. metropolitan areas for an average of 2.4 years,and a total of 69 487 person-years,between 1998 and 2004. ASD collected data on the presentation,treatment,and outcomes of HIV,including liver disease,hepatitis screening,and he...