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.     

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。     

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。     

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。     

戊型肝炎重叠其他肝病的临床特征

目的调查2007至2017年我院收治重叠其他肝病戊型肝炎患者的流行病学临床特征。方法收集2007至2017年我院收治重叠其他肝病戊型肝炎患者的临床资料,总结分析其临床特征。结果 2007至2017年我科共收治重叠其他肝病戊型肝炎患者109例,男、女病例数分别为93、16,男女比为5.8∶1。发病年龄主要集中在40岁以上中老年人群,其中40～59岁60例,60岁以上31例。发病高峰为第一季度,1、2月份发病人数最多,均为20例,其次为3月16例,4月15例。与女性患者相比,男性患者TBil、ALT较高。与单纯戊型肝炎患者相比,重叠其他肝病戊型肝炎患者的TBil、ALT、AST更高、凝血酶原时间(PT)延长、凝血酶原活动度(PTA)降低、胆碱酯酶(CHE)降低、住院时间更长,差异有统计学意义。经治疗,87例患者好转,22例患者死亡,病死率为20.2%(22/109),其中男性20例、女性2例,14例合并慢性HBV感染。结论重叠其他肝病戊型肝炎发病人群主要集中在40岁以上中老年男性,发病月份主要集中于第一季度,与单纯戊型肝炎相比,重叠其他肝病戊型肝炎患者肝损伤更重,病死率高。     

慢性乙型肝炎重叠急性戊型肝炎3种血清细胞因子表达及意义

目的分析慢性乙型肝炎重叠急性戊型肝炎患者血清γ-干扰素（IFN-γ）、白细胞介素-2（IL-2）、白细胞介素-10（IL-10）的表达及临床意义。方法采用酶联免疫吸附试验（ELISA）测定慢性乙型肝炎重叠急性戊型肝炎患者（重叠组）、急性戊型肝炎患者（AHE组）、慢性乙型肝炎患者（CHB组）和健康体检者（对照组）的血清IFN-γ、IL-2、IL-10水平;分别采用实时荧光PCR和ELISA方法测定重叠组和CHB组的乙肝病毒（HBV）基因定量（HBV DNA）和HBV血清标记物;同时检测重叠组、AHE组和CHB组的主要肝功能指标。结果 重叠组IFN-γ高于CHB组和对照组,IL-10低于CHB组和对照组,IL-2高于CHB组（P〈0.05）;CHB组IL-10高于其他3组（P〈0.05）。重叠组丙氨酸氨基转移酶（ALT）、门冬氨酸氨基转移酶（AST）、血清总胆红素（TBIL）高于CHB组,胆碱酯酶（CHE）、白蛋白（ALB）、凝血酶原活动度（PTA）低于CHB组（P〈0.05）。重叠组乙型肝炎e抗原（HBeAg）和HBV DNA阴性率高于CHB组（P=0.00）。重叠组组中HBV-DNA阴性者IFN-γ、IL-2水平高于HBV-DNA阳性者,IL-10水平低于HBV DNA阳性者（P〈0.01）。结论 IFN-γ、IL-2、IL-10参与慢性乙型肝炎重叠急性戊型肝炎肝细胞免疫损伤过程;IFN-γ、IL-2、IL-10可作为判断重叠感染后肝细胞损伤程度的指标;重叠感染后IFN-γ、IL-2可能影响HBV的复制。     

98例戊型肝炎临床特点分析

目的研究戊型肝炎的流行病学及临床特征,为其防治积累经验。方法回顾性分析2011年1月至2013年12月在本院住院治疗的98例戊型肝炎患者的流行病学及临床特征。结果本组病例年龄为9~79岁,以青壮年(20~50岁)多见(62/98,占63.27%),且男性多于女性(1.88∶1),全年均可发病,多见于无业及退休居民、工人及农民(82/98,占83.67%),部分患者合并基础疾病(24/98,占24.49%)。检查提示氨基转移酶及胆红素明显升高,病原学检查示抗-HEV-Ig M及抗-HEV-Ig G双阳性多见(48/98,48.98%)。经治疗后,治愈71例(71.45%),好转25例(25.51%),死亡2例(2.04%)。有1例老年女性患者迁延不愈,病程已达1年。结论戊型肝炎发病与年龄、性别、职业及有无基础疾病有关,经过早隔离、早治疗后,预后较好,但同时需警惕戊型肝炎的慢性化进程。     

戊型肝炎

戊型肝炎研究新进展(综述)，戊型肝炎病毒细胞培养和动物感染的研究进展(综述)，戊型肝炎及重叠乙型肝炎感染患者丙氨酸转氨酶变化，戊型肝炎病毒Ⅰ、Ⅱ与Ⅲ、Ⅳ基因型B细胞抗原表位的异同……     

380例散发性戊型肝炎临床特征分析

目的回顾性分析散发性戊型肝炎的临床特点。方法对380例散发性戊型肝炎患者的临床资料进行分析,分别按年龄和病因分组,比较各感染人群的临床症状、实验室检查、肝衰竭发生率和治疗转归情况。结果老年患者血清总胆红素高于青壮年组（P〈0.05）,白蛋白水平低于青壮年组（P〈0.05）,住院天数高于青壮年组（P〈0.05）;按病因分组中,乙型/戊型肝炎病毒重叠感染组及戊型肝炎合并酒精性肝病组患者,血清总胆红素高于单纯戊型肝炎组（P〈0.05）,住院天数亦明显高于单纯戊型肝炎组（P〈0.05）。结论戊型肝炎患者以青壮年和男性多见,临床表现以急性黄疸型多见,老年、乙型/戊型肝炎病毒重叠感染组和戊型肝炎合并酒精性肝病患者病情重,但预后均尚好。     

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.     

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。     

Comparison of effects of hepatitis E or A viral superinfection in patients with chronic hepatitis B

Purpose  

To compare the demographics, liver function, and prognosis of Chinese patients infected with chronic hepatitis B (CHB) and superinfected with hepatitis E virus (HEV) or hepatitis A virus (HAV).     

An Unusual Cause for a Hepatic Flare in a Chronic HBV Carrier

Introduction:

Hepatitis E is an emerging disease in developed countries with an increasing incidence. In developed countries, HEV genotype 3 prevails as a zoonotic disease carried by wild boars or pigs, which usually causes asymptomatic infection.

Case Presentation:

An asymptomatic HBsAg carrier was tested regularly at a German university hospital and showed no signs of chronic hepatitis B (CHB) activity. At a routine visit, elevated aminotransferases were detected while HBV DNA remained low and the patient was clinically asymptomatic. The laboratory signs of acute hepatitis resolved spontaneously. When aminotransferases returned to normal limits, the patient showed a flare of HBV-replication, which resolved spontaneously. In follow-up, further investigations revealed a resolved hepatitis E (HEV) superinfection causing an acute hepatitis before the HBV flare. No potential risk factors for HEV infection were identified.

Conclusions:

Elevated aminotransferases in CHB patients are most commonly caused by exacerbation of CHB. Nevertheless, when HBV DNA is not elevated, other reasons should be excluded. Amongst others, superinfection with another hepatotropic virus can be the reason for decompensation of chronic hepatitis B. This case report describes an asymptomatic HEV superinfection followed by a flare in HBV replication in an HBsAg carrier without signs of HBV replication for eight years. In CHB carriers with signs of acute hepatitis, rare causes should be considered as well. HEV should be a part of routine laboratory evaluation for hepatitis flares given the rising number of infections.     

Superimposed acute hepatitis E infection in patients with chronic liver disease.

BACKGROUND: The natural history of infection with hepatitis E virus (HEV) in patients with chronic liver disease (CLD) is not well described. Our study aims to document the presentation, course and outcome of HEV superinfection in patients with CLD. METHODS: Over an 18-month period, ten patients with CLD were diagnosed to have HEV superinfection by detection of anti-HEV IgM antibodies in a setting of acute worsening. These patients were tested for HBsAg, IgM anti-HBc, anti-hepatitis C virus antibodies and IgM anti-hepatitis A virus antibodies, and were followed-up. RESULTS: The etiology of underlying CLD in the 10 patients (9 men; mean [SD] age 42.4 [10.3] years) was alcohol in five patients, hepatitis B in two, hepatitis C in one and cryptogenic in two. Seven patients presented for the first time with recent-onset liver decompensation (median duration 27 days, range 7-45). All 10 had ascites and 7 had hepatic encephalopathy. Four patients developed renal failure during the course of illness. The median (range) bilirubin, ALT and albumin levels at presentation were 18.6 (4.9-32.6) mg/dL, 105 (28-6610) IU/L and 32 (29-41) g/L, respectively. At 8 weeks, only one patient had normalization of serum bilirubin or ALT levels. Three patients (30%) died, including two of renal failure and one of massive upper GI bleed. CONCLUSIONS: Superinfection with HEV in patients with CLD causes severe liver decompensation, which is frequently complicated with hepatic encephalopathy and renal failure. Acute hepatitis E in these patients has a protracted course with high morbidity and mortality.     

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.     

巨噬细胞移动抑制因子与慢性乙型肝炎、乙型肝炎肝硬化的关系

目的 了解慢性乙型肝炎(乙肝)及乙肝肝硬化患者血清细胞因子巨噬细胞移动抑制因子(MIF)表达水平,探讨血清MIF水平与Ⅲ型前胶原肽(PⅢP)、组织金属蛋白酶抑制剂-1(TIMP-1)的相关性.方法 选择44例慢性乙肝患者(肝炎组)、44例乙肝肝硬化患者(肝硬化组)和30名健康者(对照组),取静脉血并应用ELISA方法检测其血清中细胞因子MIF浓度,分析实验组血清MIF水平与PⅢP、TIMP-1相关性.两组间均数比较采用t检验,MIF水平与ALT、AST、TBil、PTA、PⅢP及TIMP-1关系采用直线相关分析.结果 慢性乙肝组及肝硬化组血清MIF、PⅢP及TIMP-1的浓度比健康对照组升高.差异均有统计学意义(t=12.87、5.28、10.98,t=11.22、14.84、11.17)均P<0.05),但该3种细胞因子在慢性乙肝及肝硬化患者之间差异无统计学意义(t=-1.05、1.52、-2.07;均P>0.05);MIF水平与ALT、AST、TBil及PTA均无相关性;HBeAg阳性和高病毒载量(>1×105拷贝/mL)慢性乙肝患者体内MIF水平高于HBeAg阴性和低病毒载量(≤1×105拷贝/mL)患者.MIF水平与PⅢP水平在慢性乙肝组和肝硬化组中均存在正相关(r=0.603,P<0.05;r=0.415,P<0.05);MIF水平与TIMP-1水平在慢性乙肝组中存在正相关(r=0.458,P<0.05),而在肝硬化组无相关性(r=0.210,P>0.05),PⅢ P与TIMP-1在慢性乙肝组及肝硬化组均存在相关性(r=0.649,P<0.05)r=0.424,P<0.05).结论 慢性乙肝及肝硬化患者体内MIF水平明显升高,MIF的早期生成可能与病毒复制有关,与肝功能无关;MIF参与了肝炎,肝纤维化及肝硬化形成过程,可反应肝硬化程度.     

Clinical features of acute hepatitis E super-infections on chronic hepatitis B

AIM To examine the clinical features and risk factors for adverse outcomes in chronic hepatitis B(CHB) superimposed with hepatitis E virus(HEV).METHODS This retrospective cohort study included 228 patients with acute HEV infection(showing clinical acute hepatitis symptomology and positivity for anti-HEV immunoglobulin M) with underlying CHB(confirmed by positivity for hepatitis B surface antigen and/or hepatitis B virus(HBV) DNA over 6 mo) who had been admitted to the Shanghai Public Health Clinical Center, which represents the regional tertiary hospital for infectious diseases in Shanghai city, China. Data for adverse outcomes were collected, and included severe liver diseases(defined as liver failure and/or acute liver decompensation) and liver-related mortality. Logistic regression modeling was performed to determine the risk factors for adverse outcomes.RESULTS The symptoms caused by superimposed acute hepatitis E(AHE) were much more severe in cirrhotic patients(n = 94) than in non-cirrhotic patients(n = 134), as evidenced by significantly higher liver complications(77.7% vs 28.4%, P 0.001) and mortality rate(21.3% vs 7.5%, P = 0.002). Most of the cirrhotic patients(n = 85, 90.4%) had no prior decompensation. Among the non-cirrhotic patients, superimposed AHE caused progressively more severe diseases that corresponded with the CHB disease stages, from immune tolerant to immune reactivation phases. Few risk factors were identified in the cirrhotic patients, but risk factors for non-cirrhotic patients were found to be intermediate HBV DNA levels(OR: 5.1, P = 0.012), alcohol consumption(OR: 6.4, P = 0.020), and underlying diabetes(OR: 7.5, P = 0.003) and kidney diseases(OR: 12.7, P = 0.005). Only 28.7% of the cirrhotic patients and 9.0% of the non-cirrhotic patients had received anti-HBV therapy previously and, in all cases, the efficacy had been suboptimal. CONCLUSION CHB-related cirrhosis and intermediate HBV DNA level were associated with severe disease in superinfected patients, and successful antiviral treatment might counter this outcome.