散发性戊型肝炎病毒对慢性乙型肝炎患者临床特点的影响

目的:观察散发性戊型肝炎病毒对慢性乙型肝炎患者肝功能指标、病情严重程度和预后的影响.方法:比较分析86例慢性乙型肝炎重叠戊型肝炎病毒感染者和152例慢性乙型肝炎患者的血清总胆红素(TBil)、丙氨酸转氨酶(ALT)、谷氨酸转肽酶(GGT)、碱性磷酸酶(AKP)及凝血酶原时间(PT)的水平;病情的严重程度:住院时间、肝硬化发生率、重型肝炎的发生率及病死率.结果:重叠感染者的TBil、ALT、GGT、AKP、PT的水平,住院时间,肝硬化发生率,重型肝炎发生率及病死率与慢性乙型肝炎组比较差异均有显著性意义(P＜0.05～0.01).结论:散发性戊型肝炎与慢性乙型肝炎重叠感染,能使乙型肝炎患者病情加重、肝内淤胆明显、预后不良.     

戊型肝炎与慢性乙型肝炎重叠戊型肝炎病毒感染的临床特征比较

目的分析比较戊型肝炎与慢性乙型肝炎重叠戊型肝炎病毒感染患者的临床特征,并初步探索戊型肝炎慢性化问题。方法对66例戊型肝炎与37例慢性乙型肝炎重叠戊型肝炎病毒感染患者的临床资料进行回顾性分析比较及统计。结果慢性乙型肝炎重叠戊型肝炎病毒感染患者较戊型肝炎患者丙氨酸氨基转移酶(ALT)、天门冬酸氨基转移酶(AST)、总胆红素(TBIL)、直接胆红素(DBIL)升高水平及发生率无显著差异,而在白蛋白(A)、白蛋白/球蛋白(A/G)及凝血酶原活动度(PTA)降低与肝纤维化系列各项指标增高方面更突出,消化道症状更重。结论慢性乙型肝炎重叠戊型肝炎病毒感染后肝功能损害更严重,凝血酶原时间长,慢性肝病特征常见,但单纯戊型肝炎患者慢性化问题也值得重视。     

甲、戊型肝炎与乙型肝炎重叠感染的临床特征

目的分析甲、乙及戊、乙型肝炎病毒重叠感染的临床特征。方法选择甲、乙及戊、乙型肝炎重叠感染病例各52例对比分析。结果戊、乙型肝炎重叠感染较甲、乙型肝炎重叠感染黄疸重,PTA低,白蛋白低。结论慢性乙型肝炎患者应尽量预防和避免重叠感染甲、戊型肝炎病毒。     

仲景退黄法联合西药治疗病毒性肝炎重度黄疸39例

1 临床资料 60例病人均为住院患者,诊断符合1995年全国第5次传染病学术会议修定的《病毒性肝炎防治方案》中的诊断标准(试行)。将患者随机分为两组:治疗组39例,男36例,女3例;年龄16～58岁,平均36岁;其中甲型肝炎5例,乙型肝炎27例,戊型肝炎4例,甲、乙型肝炎病毒重叠感染3例。对照组30例,男29例,女1例;年龄6～63岁,平均32.1岁;其中甲型肝炎3例,乙型肝炎22例,戊型肝炎2例,甲、乙型肝炎病毒重叠感染1例,戊,乙型肝炎病毒重叠感染2例。 2 治疗方法     

戊型肝炎102例临床分析

目的 了解戊型肝炎的临床特点。方法 回顾性分析102例戊型肝炎患者的临床资料。结果 在102例戊型肝炎中，单纯戊型肝炎77例，乙型与戊型重叠感染11例，重型肝炎14例；春季发病率高（P〈0．05）；乙、戊型肝炎病毒重叠感染者较单纯戊型肝炎发生重型肝炎的几率高（P〈0．01）；大于60岁者发生重型肝炎的几率高（P〈0．05）；大于60岁的患者临床症状及黄疸持续时间较青壮年者长。结论 戊型肝炎临床上以青壮年多见，老年患者黄疸持续时间长。乙、戊型肝炎病毒重叠感染及老年患者发生重型肝炎的几率高。     

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.     

中西医结合治疗老年病毒性黄疸型肝炎58例

我们于1993年1月～1998年6月用中西医结合方法治疗老年病毒性黄疸型肝炎58例,现报道如下。 1 一般资料 102例住院患者,年龄均≥60岁,诊断均符合1995年全国传染病与寄生虫病学术会议制定的诊断标准,随机分为治疗组与对照组。治疗组58例,男47人,女11人,年龄65±4岁,其中急性肝炎者17例(甲型肝炎者3例,戊型肝炎者7例,甲、乙、戊型肝炎病毒重叠感染者1例,非甲～戊型肝炎者6例)。慢性肝炎者41例(乙型肝炎者37例,甲、乙、丁型肝炎病毒重叠感染者3例,乙、丙型肝炎病毒重叠感染者1例)。     

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。     

参麦和复方丹参注射液治疗重度黄疸病毒性肝炎33例

1 资料与方法 1.1 病例选择 将1998年3月～2000年3月住院的重度黄疸(血清总胆红素≥171.1μmol/L)病毒性肝炎患者60例,采用1995年第5次全国传染病寄生虫病学术会议修订的病毒性肝炎分型与诊断标准,随机分为治疗组和对照组。治疗组33例,男31例,女2例,其中急性肝炎3例,慢性肝炎重度19例,慢性重型肝炎11例;病原类型为乙型肝炎24例,戊型肝炎3例,乙丁塑、乙丁戊型重叠感染各2例,乙丙型、乙戊型重叠感染各1例。对照组27例,男25例,女2例,其中急性肝炎4例,慢性肝炎重度14例,慢性重型肝炎9例;病原类型为乙型肝炎18例,戊型肝炎3例,甲型肝炎1例,乙甲型重叠感染3例,乙丁型、乙戊型重叠感染各1例。 1.2 治疗方法 对照组采用常规保肝疗法,即每日静滴肝安、     

333例散发性肝炎临床分析

1 临床资料1.1 一般资料 333例各类型散发性病毒性肝炎患儿中,男268例,女65例,年龄从2岁～14岁。临床诊断符合1995年5月北京第5次全国传染病寄生虫病学术会议讨论的标准。其中甲型肝炎159例,乙型肝炎98例,丙型肝炎20例,戊型肝炎15例,甲、乙型肝炎病毒重叠感染20例,乙戊型肝炎病毒重叠感染10例,乙、丙型肝炎病毒重叠感染11例。3例患儿有输血浆史或肌注入血丙种球蛋白史。1.2 症状与体征 333例患者均系散发起病,均有不同程度的     

慢性乙型肝炎重叠戊型肝炎病毒感染的研究

目的了解慢性乙型肝炎重叠戊型肝炎病毒(HEV)感染的临床特点、乙型肝炎病毒(HBV)复制指标、肝功能损伤程度及预后。方法收集慢性乙型肝炎患者和慢性乙型肝炎重叠HEV感染(重叠感染组)各115例,两组病情(轻、中、重度)和HBV DNA定量相同,对两组患者进行临床分析,慢性乙型肝炎组中74例和重叠感染组中的51例患者,在B超引导下做肝活组织检查；应用酶联免疫吸附试验和聚合酶链反应分别检测两组患者HBV标志物,HBV DNA及抗HEV lgM。结果重叠感染组重型肝炎57例,发生率49．6%,死亡29例,病死率25．2%；慢性乙型肝炎组重型肝炎5例,发生率4．4%,死亡2例,病死率1．7%,两组比较,x~2值分别为58．80和27．01,P值均＜0．01,差异有统计学意义。血清HBV DNA≥10~4患者：重叠感染组占83．7%(36/43),单纯慢性乙型肝炎组占97．1%(67/69),x~2=4．73,P＜0．05；重叠感染组总胆红素平均(495．0±217．0)μmol/L、丙氨酸氨基转移酶平均(967．0±395．0) U/L,单纯慢性乙型肝炎组总胆红素平均(216．0±195．0)μmol/L和丙氨酸氨基转移酶平均(373．0±212．0)U/L,两组比较,t值分别为10．20和14．52,P值均＜0．01,差异有统计学意义；肝组织炎症G3和G4重叠感染组33例,占64．7%,单纯慢性乙型肝炎组25例,占33．8%,x~2=12．46,P＜0．01,差异有统计学意义。结论重叠感染组肝功能损害严重,肝组织炎症程度高,HBV DNA水平低,病死率高,预后差。     

慢性乙型肝炎患者重叠戊型肝炎病毒感染的临床与病理学研究

目的：观察重叠戊型肝炎病毒（HEV）感染对慢性乙型肝炎（CHB）肝脏损害及HBV复制的影响。方法：应用ELISA法对122例CHB患者血清进行了抗－HEV IgkM,IgG检测,同时应用肝穿刺活检、荧光定量PCR及免疫组化等技术对重叠与未重叠HEV感染者分别进行了ALT、总胆红素（TBil)、凝血酶原活动度（PTA）、白蛋白／球蛋白（A／G）、电泳γ球蛋白（γ－EP）水平、肝脏病理学、血清HBeAg及肝组织HBcAg阳性率、血清及肝组织中HBV DNA含量对比。具有可比性的重叠（7例）与未重叠HEV感染者（14例）1年后做第2次肝穿活检并做病理学比较;HBeAg阴性重叠HEV感染者8例做HEV感染急性期、恢复期血清HBeAg定性、HBV DNA含量对比。结果：重叠HEV感染者21例（17．2％）。重叠HEV感染者较未重叠感染者ALT、TBil增高,PTA降低（P＜0．05）,但A／G、γ－EP水平未见显著差别（P＞0．05）;血清HBeAg及肝组织HBcAg阳性率、血清及肝组织HBV DNA含量低（P＜0．05）;肝组织炎症活动度重（P＜0．05）,但纤维化程度未见明显差别（P＞0．05）。两组患者1年前肝组织炎症活动度及纤维化程度无显著差别,1年后仍无显著差别（P＞0．05）。HEV感染恢复期血清HBeAg阳性率、HBV DNA含量高于急性期（P＜0．05）。结论：重叠HEV感染可加重CHB肝组织炎症活动度;对HBV复制具有短暂抑制作用。     

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     

Impact of acute hepatitis C virus superinfection in patients with chronic hepatitis B virus infection

BACKGROUND & AIMS: Superinfection in patients with chronic hepatitis B virus (HBV) infection is not uncommon. Acute hepatitis delta virus (HDV) superinfection is associated with severe and/or progressive liver disease. The natural course following acute hepatitis C virus (HCV) superinfection has not been well studied. The aim of this study was to investigate the impact of acute HCV superinfection. METHODS: The clinical features during acute phase and long-term outcomes of acute HCV superinfection were studied and compared with a cohort of acute HDV superinfection and a matched control group of active chronic hepatitis B. RESULTS: Acute HCV superinfection typically occurs as acute icteric hepatitis. The severity is similar to acute HDV superinfection in that hepatic decompensation developed in 34% of patients, hepatitis failure occurred in 11%, and 10% died. During a follow-up period of 1-21 years, patients with acute HCV superinfection had a significantly higher cumulated incidence of cirrhosis (48% at 10 years) and hepatocellular carcinoma (14% at 10 years, 21% at 15 years, and 32% at 20 years) than acute HDV superinfection or active chronic hepatitis B. Hepatitis B surface antigen (HBsAg) seroclearance occurred earlier in HCV superinfected patients. Continuing hepatitis after HBsAg seroclearance was observed only in HCV superinfected patients. CONCLUSIONS: Acute HCV superinfection in patients with chronic HBV infection is clinically severe during its acute phase. The long-term prognosis following acute HCV superinfection is much worse than that following HDV superinfection or active hepatitis B in terms of continuing hepatitis activity after HBsAg loss and the development of cirrhosis or hepatocellular carcinoma.     

Superinfection with hepatitis C virus in patients with symptomatic chronic hepatitis B.

11/323 patients (3.4%) with symptomatic chronic hepatitis B were positive for antibody to hepatitis C virus (anti-HCV). The positive rate of anti-HCV in patients with serum alanine aminotransferase (ALT) levels greater than 200 U/l (n = 219) did not exceed that of the patients with ALT less than or equal to 200 U/l (n = 104) (2.7% vs. 4.8%). Of the 219 patients who were positive for hepatitis B e antigen (HBeAg) and/or hepatitis B virus-DNA (HBV-DNA), 5 (2.3%) had anti-HCV, while 6/104 patients (5.8%) who were positive for antibody to HBeAg (anti-HBe) had anti-HCV (p greater than 0.1). In contrast to the anti-HCV-negative patients, the patients with anti-HCV had a higher percentage of cirrhosis in their liver histological findings (36.4% vs 5.4%, p less than 0.005). In conclusion, the prevalence of HCV superinfection in symptomatic chronic hepatitis B patients is low and HCV superinfection is not an important factor in acute exacerbation of chronic hepatitis B. However, the superinfection with HCV may exacerbate the existing liver disease and accelerate its progression.     

Hepatitis E virus superinfection impairs long-term outcome in hospitalized patients with hepatitis B virus-related decompensated liver cirrhosis

Introduction and objectivesHepatitis E virus (HEV) superinfection is a common excerbating event in patients with chronic hepatitis B, but the impact on the long-term prognosis is not clear. This study investigates the specific role of HEV superinfection in the long-term outcome of hepatitis B virus (HBV) patients with liver cirrhosis.Patients and methodsA retrospective, observational cohort study was conducted using clinical, laboratory, and survival data collected from patients suffering from hepatitis B cirrhosis with or without HEV superinfection. Disease progression and mortality rates were analyzed.ResultsAfter a two-year follow-up, HEV superinfection was identified in 27 of 811 patients. The transplantation-free mortality was significantly increased (51.9% vs. 14.3%, p< 0.001) in HEV superinfection compared to that in hepatitis B cirrhosis patients without HEV superinfection. Logistic regression analysis demonstrated that elderly people were independent host risk factors for hepatitis B cirrhosis patients with HEV superinfection before and after propensity score matching (PSM). Moreover, HEV superinfection was a risk factor for patients with hepatitis B cirrhosis with new acute decompensation (AD) and acute-on-chronic liver failure (ACLF) during hospitalization. A multivariate Cox proportional hazards regression model demonstrated that acute HEV co-infection is associated with two-year mortality (hazard ratio [HR]: 2.49; 95% CI: 1.40–4.43; p= 0.002; and HR: 5.79; 95% CI: 1.87–17.87; p= 0.002) in patients with hepatitis B cirrhosis before and after PSM.ConclusionsElder patients with hepatitis B cirrhosis are susceptible to HEV superinfection, accelerating disease progression and increasing long-term mortality in hospitalized patients with HBV-related decompensated liver cirrhosis.     

Natural course of patients with chronic type B hepatitis following acute hepatitis delta virus superinfection

A 6-96-month prospective follow-up study on the natural course of chronic type B hepatitis after contracting acute hepatitis delta virus (HDV) superinfection was conducted in 30 patients with clear-cut onset of acute HDV superinfection (HDV group). Thirty patients with acute exacerbation without evidence of HDV infection, and well matched in terms of age, sex and hepatitis B e antigen/antibody status, served as the control group. The clinical and biochemical presentations tended to be more severe in the HDV group. More patients in the HDV group had persistent abnormal liver biochemical tests (69% vs 47%) and progressed to chronic active hepatitis (46% vs 20%) or cirrhosis (9.4%/year vs 5.2%/year), but the differences were not significant statistically. The results suggest that HDV superinfection induces slow progression of liver disease. However, in the early stage, the impact of HDV superinfection is not particularly different from that of the acute exacerbation unrelated to HDV in patients with chronic type B hepatitis.     

Hepatitis B virus replication in acute hepatitis B, acute hepatitis B virus-hepatitis delta virus coinfection and acute hepatitis delta superinfection

To evaluate the effect of hepatitis delta virus on the level of replication of hepatitis B virus and to assess the clinical significance that such an effect might have on the final outcome of the infection, the serological profile of hepatitis B virus DNA was investigated in 153 patients with acute or chronic hepatitis B virus infection with or without associated delta infection. Serum hepatitis B virus DNA was detected in 57% of patients with acute hepatitis B, 67% of those with acute hepatitis B virus-hepatitis delta virus coinfection and 25% of HBsAg carriers with hepatitis delta virus superinfection during the first week after the onset of symptoms. Patients with acute hepatitis B and those with acute hepatitis B virus-hepatitis delta virus coinfection did not differ significantly with respect to the serological profile of hepatitis B virus DNA and final clinical outcome. Within the group of HBsAg carriers with hepatitis delta virus superinfection, all patients who were initially negative for hepatitis B virus DNA developed chronic hepatitis delta virus infection, whereas 3 of the 4 patients with active hepatitis B virus infection at the time of superinfection showed transient inhibition of hepatitis B virus replication followed by termination of hepatitis delta virus infection in two patients. Therefore, although delta virus may inhibit the replication of hepatitis B virus among chronic HBsAg carriers, this effect is not readily apparent among patients with hepatitis B virus-hepatitis delta virus coinfection.