HEV重叠感染对乙肝患者血清生化指标及标志物的影响

各型肝炎病毒重叠戊型肝炎病毒感染临床上并不少见。为此我们对我院住院的单纯戊肝及乙、戊重叠感染者126例进行对比研究，并与同期住院的单纯HBV感染者58例进行比较，观察HBV重叠HEV感染后，其血清生化指标的变化及对HBV复制是否产生影响，现报道如下。     

重型肝炎中HEV感染的临床意义

为探讨重型戊肝的临床表现及转归，对75例重型肝炎中的13例戊肝病毒（HEV）感染者进行临床分析。以单纯乙肝病毒（HBV）感染20例为对照组，比较其与单纯HEV，HEV合并HBV感染的重型肝炎在临床表现，实验室检查，预后等方面的差异。结果显示，重型肝炎的HEV感染率为17．3％（13／75），HEV与HBV重叠感染率为8．0％（6／75），在临床表现方面各组差异无显著性意义（P＞0．05）。HEV合并HBV感染组SB，PT及死亡率明显高于单纯HEV组及单纯HBV组，差异有显著性差异（P＜0．05）。肝炎病毒重叠感染是影响戊型重型肝炎预后的重要因素。     

慢性乙型肝炎重叠戊型肝炎病毒感染致重型肝炎的临床分析

为了探讨慢性乙型肝炎病毒(HBV)感染者重叠戊型肝炎病毒(HEV)感染发展为重型肝炎后的临床特征,我们对2005年1-7月住院的慢性乙型肝炎重叠HEV感染的48例重型肝炎患者和单纯慢性HBV重型肝炎50例进行分析.结果报告如下.     

戊型肝炎病毒与甲乙丙型肝炎病毒重叠感染的研究

本文对419例病毒性肝炎患者进行抗-HEV-IgM/IgG及其它病毒标志物检测。结果:HEV感染者112例(26.2％);其中单纯HEV感染者30例,两种以上肝炎病毒重叠感染占73.2％;43.75％为HBV和HEV重叠感染,HAV和HEV合并感染占急性肝炎的40.58％。在重型肝炎中HEV感染率占57.89％,均为HBV和HEV重叠感染,病死率达72.73％。16.67％的单纯HEV感染者为慢性肝炎和肝硬变。结果表明,本地区戊型肝炎以散发为主,重叠感染多见。HBV与HEV重叠感染和HAV与HEV重叠感染是较常见的感染模式。在HBV感染的基础上重叠HEV感染是肝炎重症化的重要原因。HEV感染有导致慢性化的可能性。     

戊型肝炎149例临床分析

目的　了解戊型肝炎的临床特点。方法　回顾性总结分析14 9例戊型肝炎临床资料。结果　①14 9例戊型肝炎中,单纯性戊型肝炎41例,平均年龄47.3 2±16.10岁;乙型与戊型肝炎重叠感染95例,平均年龄40 .17±14 .15岁(P <0 .0 5 ) ;②乙、戊型肝炎重叠感染者较单纯戊型肝炎者,虽然ALT和TBIL无显著差异(P >0 .0 5 ) ,但ALB明显降低,且病程长、并发症多(P <0 .0 5和P <0 .0 1) ;③全部病例中好转118例;死亡8例,其中乙、戊型肝炎重叠感染6例;④2 1例检测了血清甲胎蛋白,2 0～40 0ng/ml 11例,>40 0ng/ml 3例。结论　戊型肝炎临床上以成年人多见。HBV感染者容易感染HEV ,且致临床病程延长,并发症多,预后差。良性肝病患者AFP也可明显升高。     

戊型肝炎及重叠乙型肝炎感染患者丙氨酸转氨酶变化

目的　观察戊型肝炎及重叠乙型肝炎感染患者丙氨酸转氨酶 (ALT)变化。方法　将戊型肝炎抗体阳性及重叠乙型肝炎感染患者 2 73例分为 5组。A组 12 7例 ,为戊型肝炎病毒 (HEV) IgG阳性 ;B组 9例 ,为HEV IgM阳性 ;C组 64例 ,为HEV IgM和HEV IgG均阳性 ;D组 3 2例 ,为HEV IgM和HEV IgG均阳性并重叠乙型肝炎感染 ;E组 41例 ,为HEV IgG阳性并重叠乙型肝炎感染。另选戊型肝炎抗体阴性的非乙型肝炎患者 5 0 0例作为对照组。用速率法测定各组ALT值。结果　各组ALT异常增高百分率及异常增高者ALT值分别为 :A组 2 1例 ( 16.5 %) ,ALT( 183± 89)U /L ;B组 3例 ,ALT( 2 0 3± 112 )U /L ;C组 16例 ( 2 5 .8%) ,ALT( 2 17± 119)U/L ;D组 11例 ( 3 4.4%) ,ALT( 2 3 4± 12 8)U/L ;E组 13例 ( 3 1.7%) ,ALT( 2 10± 98)U/L ;对照组 5 1例 ( 10 .2 %) ,ALT( 112± 68)U/L。戊型肝炎抗体阳性各组ALT异常增高率与对照组间差异有显著性 (P <0 .0 5 ) ,戊型肝炎抗体阳性各组ALT异常增高者ALT值与对照组间差异有显著性 (P <0 .0 5 )。结论　戊型肝炎抗体阳性组ALT异常增高率和增高者ALT值均较对照组有明显增高 ,HEV IgM阳性或重叠乙型肝炎感染较单纯HEV IgG阳性者 ,ALT增高明显     

慢性乙型肝炎与急性戊型肝炎重叠感染机制研究进展

我国为乙型肝炎病毒（HBV）和戊型肝炎病毒（HEV）感染的高发区之一,约有1.25亿人口为HBV的慢性感染者。1999年庄辉等[1]对我国11个城市1 819例急性病毒性肝炎的病原学研究发现,其中HBV感染率为24.8%,HEV感染率为8.6%。近年的大量研究报告显示慢性乙型肝炎重叠急性戊型肝炎是慢性乙型肝炎病情加重的重要因素。     

北京地区慢性重型肝炎的病原学特点

目的 了解北京地区慢性重型肝炎（下称慢重肝）的病原学特点。方法 11例患者的选择均符合2000年9月西安“病毒性肝炎防治方案”慢性重型肝炎诊断标准。所有病人均抽血做甲、乙、丙、丁、戊型肝炎病原学检查。结果 111例慢重肝患者中,HBV感染者108例（97．30％）,HEV感染者22例（19．82％）,HAV感染者4例（3．60％）,甲－戊型肝炎病毒血清标志物均阴性者3例（2．7％）。单纯乙肝病毒感染者83例（74．77％）,其中HBV DNA阳性率18．07％（15／83）,HBeAg阳性率57．83％（48／83）。乙、戊重叠感染者21例（18．92％）,乙、甲重叠感染者3例（2．70％）,乙、甲、戊三重感染者1例（0．90％）。结论 （1）HBV感染是慢重肝最多见原因。其中乙肝病毒复制指标HBV DNA、HBeAg的阳性率均不很高,二者同时阳性者更少,说明其在慢重肝的发生中不起决定性作用。（2）HBV与其它肝炎病毒的重叠感染在慢重肝中占一定比例。尤其是乙、戊重叠最多。单纯HEV感染诱发重型肝炎者不多见,而在中、重度慢性乙肝或肝硬化基础上再感染HEV,易发展为慢重肝。HBV与HAV重叠较少见,本组与HCV或HDV重叠发生慢重肝者未见。（3）还有3例慢重肝甲－戊肝病原学指标均阴性（可除外药物、酒精、中毒等原因所致慢重肝）,提示仍有一部分慢重肝病因未明,有待进一步研究。     

慢性乙型肝炎重叠感染HEV 58例分析

1996年3月～1998年3月我院收治58例慢性乙型肝炎重叠感染戊型肝炎病毒(HEV)者,现报告如下。 资料与方法 一、临床资料 58例慢性乙型肝炎重叠HEV感染者中男性45例,女性13例,年龄19～62岁,平均58.8±8.9岁。随机抽取同期住院慢性乙型肝炎及急性戊型肝炎各58例作对照,三组年龄、性别无显著差异。诊断符合1995年北京第五次全国传染病寄生虫     

慢性乙型肝炎重叠HAV与HEV感染的临床分析

目的研究慢性乙型肝炎患者重叠甲型肝炎与重叠戊型肝炎病毒的临床特点及其对病情转归的影响。方法采用ELISA法检测甲、乙、丙、戊型肝炎病毒血清标记物,选择慢性乙型肝炎重叠甲型肝炎52例与慢性乙型肝炎重叠戊型肝炎267例进行对比分析。结果慢性乙型肝炎重叠戊型肝炎患者较慢性乙型肝炎重叠甲型肝炎患者总胆红素水平高、重型肝炎发生率高、病死率高,两组白蛋白水平和平均住院日无明显差异。结论慢性乙型肝炎患者重叠戊型肝炎病毒感染较重叠甲型肝炎病毒感染病情更重、预后差。     

Lower Hepatitis G Virus Infection Prevalence Compared to Hepatitis B and C Virus Infection Prevalences

To more accurately determine the seroprevalence of hepatitis G virus (HGV) infection, we surveyed antibody to HGV (anti-E2) by enzyme-linked immunosorbent assay (ELISA) and HGV RNA by nested polymerase chain reaction (PCR) in 298 residents of a hepatitis C virus (HCV)-endemic area of Japan and in 225 hemodialysis patients. We then compared these findings with known HCV and hepatitis B virus (HBV) infection prevalences. Anti-E2 and HGV RNA prevalences were 32 (10.7%) and 5 (1.7%) in the residents and 24 (10.7%) and 10 (4.4%) in the hemodialysis patients, respectively. Anti-E2 and HGV RNA concurrence was found in two of the hemodialysis patients. Total HGV marker (anti-E2 and/or HGV RNA) prevalences [37 (12.4%) in residents and 32 (14.2%) in hemodialysis patients], were significantly lower than the prevalences of antibody to HCV (anti-HCV) by ELISA [59 (19.8%) and 96 (42.7%)], and antibody to hepatitis B core antigen (anti-HBc) by radioimmunoassay (RIA) [87 (29.2%) and 101 (44.9%)] (P < 0.05). The anti-HCV prevalence in subjects with total HGV marker was significantly higher than in those without total HGV marker. There was no significant difference in anti-HBc prevalence between those with and without total HGV marker. The viremic rate was highest in HCV infection (HCV RNA by PCR/anti-HCV) (83.2%), with HGV infection (HGV RNA/total HGV marker) (21.7%) intermediate, and HBV infection (hepatitis B surface antigen by RIA/anti-HBc) (5.3%) lowest (P < 0.05). These findings indicate that HGV infection was less endemic than HCV and HBV. HGV was eliminated naturally more frequently than HCV infection and less frequently than HBV infection.     

Hepatitis B Virus Gene in Liver Tissue Promotes Hepatocellular Carcinoma Development in Chronic Hepatitis C Patients

The hepatitis B virus (HBV) gene has been detected in hepatocellular carcinoma (HCC) tissue negative for the hepatitis B surface antigen and positive for the hepatitis C virus (HCV) antibody, but the precise role of the HBV gene in hepatocarcinogenesis has yet to be clarified. We studied the HBV gene in liver tissue several years before the emergence of HCC. Eleven patients diagnosed with HCV-positive chronic liver disease and who developed HCC were assigned to group A. HBV DNA was detected in 8 of the 11 patients (73%). Twenty-five patients, who did not develop HCC, were selected as group B. Six of the group B patients were classified as DNA-positive (24%). The HBV DNA in liver tissue was found to be significantly related to HCC development (P < 0.01). Thus, the presence of the HBV gene in patients with chronic HCV associated-liver injury appears to promote hepatocarcinogenesis, although prospective studies are needed to confirm this result.     

Previous or Occult Hepatitis B Virus Infection in Hepatitis C Virus-Associated Hepatocellular Carcinoma Without Hepatic Fibrosis

We investigated the role of hepatitis B virus infection in development of hepatocellular carcinoma in hepatitis C virus-infected patients without hepatic fibrosis. Of 253 patients, 8 lacked hepatic fibrosis (group 1); group 2 included the remaining 245 patients. Clinicopathologic findings were compared between the groups. Hepatitis B x gene was sought in cancers and adjoining noncancerous liver. Group 1 showed better liver function parameters and milder active hepatitis than group 2. The proportion of patients with anti-hepatitis B virus antibody tended to be higher in group 1 than in group 2. The proportion of patients with hepatitis B x RNA in cancers was significantly higher in group 1 than in group 2. All group 1 patients had previous or occult hepatitis B virus infection. Previous or occult hepatitis B virus infection may be critical in development of hepatocellular carcinomas in hepatitis C virus-infected patients without hepatic fibrosis.     

拉米夫定治疗慢性乙肝病毒感染病人的疗效分析

目的：观察拉米夫定（Lamivudine）治疗慢性乙肝病毒（HBV）感染病人的疗效及影响因素。方法：60例慢性HBV感染病人予拉米夫定（100mg qd）治疗12个月。疗效评估包括血清HBV病毒学、血清HBV免疫学、血清生化学应答率。结果：治疗12个月后，HBV DNA PCR荧光定量检测总的血清HBV DNA转阴率为57.89％，HBeAg/抗-HBe血清转换率为6.25％，ALT复常率为68.89％。其中，（1）血清ALT异常、HBeAg阳性组病人的荧光定量检测HBV DNA转阴率为55.56％，HBeAg/抗-HBe血清转换率为8.33％，ALT恢复正常率为63.89％；完全应答率为8.33％，部分应答率为75.00％，无应答率为16.67％。（2）ALT正常、HBeAg阳性组的12例病人中，仅有4例病人的血清HBV DNA转阴，无1例发生HBeAg/抗-HBe血清转换。（3）ALT异常、HBeAb阳性组的9例病人中，8例病人的HBV DNA转阴同时伴ALT复常。结论：本组病例分析结果表明，拉米夫定可以有效地抑制血清HBV的复制，改善肝功能。机体免疫状况对拉米夫定抗病毒治疗有较大影响，治疗前ALT水平是预测疗效的重要指标。对ALT异常的慢性HBV感染病人，HBeAg阴性者似乎比HBeAg阳性者有更好的治疗反应，可能更适合用拉米夫定治疗。病人对拉米夫定普遍耐受性良好。     

Hepatitis B Virus Genomes of Chronic Hepatitis Patients Do Not Contain Specific Mutations Related to Acute Exacerbation

To determine the specific viral variants associated with acute exacerbation of chronic hepatitis from hepatitis B virus (HBV) infection, we analyzed the complete nucleotide sequences of the HBV genome in serial serum samples from two chronic active hepatitis patients who seroconverted from HBeAg to anti-HBe. HBV DNA was amplified by polymerase chain reaction (PCR) and sequenced. A 1896 precore stop codon mutant (G to A at nt 1896) coexisting with the wild sequence was found in both patients prior to seroconversion from HBeAg to anti-HBe. Core promoter mutations at nucleotide positions 1762 (A to T) and 1764 (G to A) were found in both patients throughout the observation period. Mutations were observed in the HBV genome of the two patients at different time points, and there was no correlation between the mutations and liver disease or DNA polymerase levels. The nucleotide divergence rate and the composition of quasispecies in the HBV sequence at the time of acute exacerbation were almost the same as were found at other time points. These results suggest that acute exacerbation does not appear to be caused by a characteristic HBV species. The multiple factors that cause generalized HBV replication activation may contribute to acute exacerbation.     

Occult Hepatitis B Virus Infection in Hemodialysis Patients: A Concept for Consideration

Hemodialysis patients potentially have an increased risk of infection with parenterally transmitted viral agents due to an impaired host immune response and multiple transfusion requirements. Viral hepatitis is considered as a problem for hemodialysis patients because 1.9% of all deaths among this population are related to the consequence of viral hepatitis. Hepatitis B virus (HBV) is one of the most important causes of transmitted infections by the parenteral route in hemodialysis patients. Occult HBV infection is characterized by presence of HBV infection without detectable hepatitis B surface antigen (HBsAg), which harbors potential risk of HBV transmission through hemodialysis. There are conflicting reports on the prevalence of occult HBV infection (OBI) in hemodialysis patients. Considering the importance of occult HBV infection in hemodialysis patients and the growing evidence on this subject, the purpose of this review is to provide comprehensive information on OBI prevalence in hemodialysis patients and highlight the most important points in this issue.     

Significance of Prior Hepatitis B Virus Infection in the Development of Hepatocellular Carcinoma in Patients with Chronic Hepatitis C

To clarify the clinical significance of prior hepatitis B virus (HBV) infection in the development of C-viral hepatocellular carcinoma (HCC), we conducted two studies: (1) Two hundred thirty-four patients with C-viral HCC and 320 patients with C-viral chronic liver disease without HCC admitted to our hospital between 1990 and 1994 were analyzed for the association of hepatitis B core antibody (HBcAb) positivity with HCC by multivariate logistic regression analysis, and this revealed HBcAb positivity as an independent risk factor for development of HCC adjusted for age and sex. (2) Four hundred fifty-nine patients with biopsy-proven hepatitis C virus-related chronic liver disease between 1986 and 1998 were enrolled in the cohort study and followed for the development of HCC. During an average follow-up of 6.6 ± 3.3 years, HCC developed in 63 patients, 37 of 160 patients positive for HBcAb and 26 of 299 patients negative for HBcAb. Multivariate Cox proportional regression analysis showed that the incidence of HCC increased by age, advanced stage of liver fibrosis, mean alanine aminotransferase value of more than 80 IU/liter, and positivity of HBcAb. Sustained virological responders after interferon therapy revealed a reduced risk for HCC development. In conclusion, prior HBV infection was shown to be one of the independent risk factors for development of HCC in C-viral chronic liver disease.     

HBV特异性T细胞治疗慢性乙型肝炎的研究

为寻求一种治疗慢性乙型肝炎的新方法,应用ＨＢＶ特异性Ｔ细胞输注治疗慢性乙型肝炎９例,结果显示,在疗程结束后,患者的ＨＢｓＡｇ,ＨＢｅＡｇＨＢＶＤＮＡ的含量均有所下降,其中ＨＢｅＡｇ下降较明显,Ｐ〈０．０１,２例ＨＢｃＡｇ阳性患者,ＨＢｃＡｇ阴转,ＣＤ＾＋３,ＣＤ＾＋４,ＣＤ＾＋４／ＣＤ＾＋８ＮＫ活性上升,ＣＤ＾＋８,ｓＩＬ－２Ｒ较治疗前后所回复,表明特异性Ｔ细胞治疗慢性乙型肝炎有一定疗效,远期疗效