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。     

48例疑难肝病临床与病理分析

目的：评价肝活组织穿刺检查对疑难肝病的诊断价值。方法对48例临床不能确诊的疑难肝病患者行肝活组织穿刺检查,分析其临床与病理组织学特点。结果48例疑难肝病患者中,肝脏占位性病变24例（其中肝细胞癌7例,转移性肝癌7例,胆管细胞癌2例,肝脓肿3例,慢性肝炎重度1例,肝结核1例,肝海绵状血管瘤1例,未能确诊2例;慢性肝炎与肝硬化鉴别困难者12例（慢性肝炎轻度3例,慢性肝炎中度4例,慢性肝炎重度1例,早期肝纤维化1例,肝硬化3例）;隐源性肝炎5例（急性淤胆型肝炎1例,慢性肝炎中度4例）;隐源性肝硬化3例（结节性肝硬化1例,特发性门静脉高压2例）;慢性肝炎中度伴结节性肝硬化1例;急性淤胆型肝炎1例;自身免疫性肝病1例（原发性胆汁性肝硬化）;肝脏寄生虫病1例。病理组织学确诊46例。结论疑难肝病中以肝脏占位性病变多见,其中以原发性肝癌与转移性肝癌最常见。对疑难肝病行肝活组织穿刺检查可明显提高诊断率。     

浙江省乙型肝炎病毒B、C基因型感染者临床和肝组织病理的比较

目的了解浙江省乙型肝炎病毒B、C基因型慢性HBV感染者的肝组织病理学变化。方法采用荧光PCR方法检测浙江省慢性乙型肝炎患者HBV基因型,并与慢性肝炎的肝功能、凝血酶原时间、乙型肝炎病毒标志、HBV DNA定量、肝组织炎症分级及纤维化分期进行比较。结果1.浙江省HBV基因型B型、C型占94.53%;2.C基因患者HBeAg阳性率及HBV DNA定量略高于B基因患者82.00%vs77.36%;(7.09±1.02)lg vs(6.88±1.26)lg,但差异无统计学意义(P>0.05);3.肝组织学炎症分级和纤维化分期以B、C混合型为重,C型重于B型,B型、C型、B+C型肝组织学炎症分级分别为1.85±1.27vs1.93±1.32vs2.93±0.74;纤维化分期分别为1.86±1.31vs1.84±1.29vs2.95±0.71,三者差异有统计学意义(P<0.01)。结论浙江省HBV基因型以B、C型为主,C型、BC混合型肝组织损害严重。     

不典型淤胆型肝炎30例临床分析

1997年1月~2004年12月,我们收治30例不典型淤胆型肝炎患者,现对其临床资料进行分析。临床资料:本组30例不典型淤胆型肝炎患者,男24例,女6例;年龄(45±5)岁;均符合病毒性肝炎的诊断标准。其中甲型肝炎3例,急性乙型肝炎2例,慢性乙型肝炎12例,戊型肝炎7例,药物型肝炎6例。出现黄疸时间为7~30 d,均有不同程度的消化道症状,全身疲乏,无皮肤瘙痒、大便颜色变浅等情况。均有高胆红素血症,转氨酶(ALT、A ST)不同程度升高,血脂、碱性磷酸酶(AKP)、转肽酶(-γGT)升高不明显。均予硫普罗宁或还原型谷胱甘肽、肝舒宁(葡萄糖醛酸内酯)、维生素C、茵…     

人工肝治疗对重型肝病患者生存期的影响

目的通过前瞻性、多中心、大样本的对照研究,探讨人工肝治疗对重型肝病患者生存期的影响。方法前瞻性地选择首都医科大学附属北京佑安医院等5家医院的重型肝炎和慢性肝炎重度(且凝血酶原活动度<50％)患者518例,将患者分为人工肝治疗组和常规内科治疗对照组,记录其诊断、分期等原始资料并进行随访,采用Kaplain-Maier方法进行生存情况分析。结果急性重型肝炎患者人工肝治疗组的中位生存期为(8．0±0．4)d,内科治疗对照组为(4．0±0．2)d,P=0．004。人工肝治疗2次以上疗效更加明显,它可使慢眭重型肝炎患者生存期由(27．0±1．6)d延长至(39．0±4．0)d,重型肝炎中期患者生存期由(38．0±17．5)d延长至(66．0±18．6)d;晚期患者生存期由(18．0±4．0)d延长至(26．0±2．5)d,差异均有统计学意义。结论人工肝治疗能够延长急性重型肝炎患者、慢性及亚急性重型肝炎中晚期患者的生存时间,多次治疗效果显著优于单次治疗和内科治疗。     

胆维他治疗淤胆型肝炎26例

1 资料与方法 1.1 病例选择 50例患者均为在我院住院的慢性淤胆型肝炎病人,其中乙型肝炎41例,丙型肝炎6例,乙、丙型肝炎病毒混合感染3例,其诊断均符合1995年全国传染病和寄生虫病学术会议制定的淤胆型肝炎诊断标准。随机分成两组,治疗组26例,其中男16例,女10例,平均年龄38.1±10.2岁;对照组24例,男11例,女13例,平均年龄37.6±9.4岁。两组患者在性别、年龄、病程、肝功能异常程度方面均相似,具有可     

戊型病毒性肝炎35例临床分析

目的　了解戊型病毒性肝炎的临床特点。方法　对 3 5例胆汁淤积性戊型病毒性肝炎进行回顾性分析。结果　胆汁淤积性戊型肝炎占同期收治戊型病毒性肝炎的 15 .4%( 3 5 / 2 2 8)。男 2 2例 ,女 13例 ,年龄 5 5 .1± 13 .8岁 ,其中≥ 60岁者为 42 .9%( 15 / 3 5 ) ;乙、戊型肝炎病毒重叠感染者为 2 5 .7%( 9/ 3 5 )。黄疸消退时间为 71.6.± 2 1.82 ( 4 1～ 12 6)天。血清总胆红素为 2 5 5 .5 5± 118.42 μmol/L ,丙氨酸氨基转移酶为 95 7.8± 5 82 .3u/L ,天门冬氨酸氨基转移酶为 612 .4±460 .9u/L ,碱性磷酸酶 (AKP)为 3 16.86± 2 3 7.62u/L ,γ 谷氨酰转移酶 (γ GT)为 2 5 7.74± 199.66u/L ,痊愈 2 2例 ,好转 13例。结论　由戊型病毒性肝炎病毒引起的胆汁淤积性肝炎符合淤胆型肝炎的一般临床特点 ,但肝脏损害较重 ,黄疸程度高 ,持续时间长 ;老年戊型肝炎患者更易发生胆汁淤积     

蛋白吸附再循环系统治疗重型肝炎疗效观察

我科于2004年4月开始应用蛋白吸附再循环系统(PARS)治疗重型肝炎病人,取得了很好的临床效果。材料和方法一、研究对象20例重型肝炎为哈尔滨医科大学附属二院感染性疾病科2004年4月至2005年4月期间的住院病人,随机分为PARS组及对照组。PARS组10例,男8例,女2例,平均年龄(44.3±3.2)岁;对照组10例,男7例,女3例,平均年龄(45.3±3.8)岁。重型肝炎诊断符合2000年第10次全国传染病与寄生虫病学术会议修订标准[1],均为慢性重型肝炎。其中乙型肝炎病毒感染16例,肝炎病毒标志全阴性4例。治疗前并发肝性脑病5例,肝肾综合征3例,自发性腹膜炎4例。二…     

血清γ-谷氨酰转肽酶检测对病毒性肝炎的临床意义

γ 谷氨酰转肽酶 (ＧＧＴ )是肝胆系统疾病常用的生化指标之一。在肝脏炎症、胆汁淤积等情况下往往出现异常。本文对177例病毒性肝炎患者进行分析 ,就ＧＧＴ在不同肝炎临床分型和不同肝功能情况下的临床意义作进一步探讨。资料与方法1999年 8月～ 2 0 0 0年 4月 ,病毒性肝炎患者 177例 ,男15 5例 ,女 2 2例 ,男∶女为 7.0∶1。年龄 18～ 85岁 ,平均 (44±13)岁。按 1995年修订的病毒性肝炎防治方案的诊断标准 ,分为急性肝炎 32例 (18.1% ) ,慢性肝炎轻度 (慢肝轻度 ) 33例(18.6 % ) ,慢性肝炎中度 (慢肝中度 ) 2 4例 (13 .6 % ) ,慢性肝炎重…     

熊去氧胆酸鲁米那联合中药治疗重度淤胆型肝炎39例

1 临床资料 本组病例共71例,均为1998年8月～2000年11月在我院的住院病人,病程最长11年,最短15天,平均1.96年,年龄最大者73岁,最小13岁,平均38岁,诊断符合1995年北京会议修订的病毒性肝炎防治诊断标准。按入院先后随机分为治疗组和对照组。 治疗组39例,男30例,女9例,乙型肝炎33例,其他6例,其中急性淤胆型肝炎11例,慢性淤胆型肝炎28例; 对照组32例,男26例,女6例,乙型肝炎27例,戊型肝炎1例,其他4例,其中急性淤胆型肝炎9例,慢性淤胆型肝     

Hepatic histological findings after transplantation for chronic hepatitis B virus infection, including a unique pattern of fibrosing cholestatic hepatitis

Long-term follow-up of 27 patients with hepatitis B virus-related chronic liver disease treated by transplantation showed that 23 had hepatitis B virus recurrence. In 13 patients late changes in the grafts were similar to those described in other series: minor abnormalities in five cases, chronic active hepatitis in five cases and non-hepatitis B virus-related graft dysfunction in three cases. Three patients had incomplete histological follow-up. Analysis of the histological changes and viral antigen expression in six cases revealed a distinct and novel pattern termed fibrosing cholestatic hepatitis. Development of fibrosing cholestatic hepatitis was associated with rapidly progressive graft dysfunction. It is postulated that this pattern of fibrosing cholestatic hepatitis develops because of a high cytoplasmic expression of viral antigens, including HBsAg. The remaining case had some features of fibrosing cholestatic hepatitis. The main histological features of this unique syndrome include thin, perisinusoidal bands of fibrosis extending from portal tracts to surround plates of ductular-type epithelium; prominent cholestasis; ground-glass transformation; and ballooning of hepatocytes with cell loss and mild mixed inflammatory reaction.     

肝炎患者重度黄疸原因分析

目的观察重度黄疸肝炎病人的原因及转归。方法采用7170A血清生化仪进行检测肝功能,采用SPECTRA酶标仪检测肝炎病毒血清标志物,对281例深度黄疸病人的临床资料进行分析。结果单纯感染肝炎病毒的患者187例,未感染肝炎病毒的患者24例,肝炎病毒重叠感染患者58例,病因未明12例;急性重症肝炎16例,亚急性重症肝炎21例,慢性重症肝炎198例,瘀胆型肝炎43例,其它3例;存活159例,死亡122例。结论嗜肝病毒感染是引发本组病人发病的主要原因,其中感染乙型肝炎病毒者占多数,慢性重症肝炎占70.5%,深度黄疸的患者死亡率高达43.4%。     

Detection of pre-S1 proteins in serum and liver of HBsAg-positive patients: a new marker for hepatitis B virus infection

The presence of pre-S1 proteins in serum and liver of individuals with acute and chronic hepatitis B virus infection was investigated in Western blots using antibodies against a fusion protein, containing amino acids 20-120 of the pre-S region. Pre-S1 proteins were present in 20 of 38 HBsAg-positive sera. All sera positive for pre-S1 proteins were also positive for hepatitis B virus DNA indicating the presence of hepatitis B virions, and 16 of these sera were also positive for HBeAg. In five sera positive for hepatitis B virus DNA, pre-S1 proteins were not found. In an additional study, pre-S1 proteins could be detected in 4 of 6 patients with acute hepatitis B virus infection during the first 2 weeks after admission to the hospital. The presence of pre-S1 proteins showed a good correlation with the detection of hepatitis B virus DNA. After seroconversion from HBeAg to anti-HBe, both hepatitis B virus DNA and pre-S1 proteins were no longer detectable. Pre-S1 proteins were present in three liver tissue specimens from two patients with acute hepatitis B virus infection and from one patient with cirrhosis of the liver. The proteins were not found in the liver of two HBsAg-positive patients with hepatocellular carcinoma (primary liver carcinoma), negative for HBeAg. Pre-S1 proteins can be detected in serum, positive for hepatitis B virus DNA and in liver tissue of hepatitis B virus-infected individuals. The presence of these proteins appears to correspond with the presence of hepatitis B virus DNA, both markers indicating hepatitis B virus replication.     

Liver disease in pregnancy

Liver diseases in pregnancy may be categorized into liver disorders that occur only in the setting of pregnancy and liver diseases that occur coincidentally with pregnancy. Hyperemesis gravidarum, preeclampsia/eclampsia, syndrome of hemolysis, elevated liver tests and low platelets （HELLP）, acute fatty liver of pregnancy, and intrahepatic cholestasis of pregnancy are pregnancy-specific disorders that may cause elevations in liver tests and hepatic dysfunction. Chronic liver diseases, including cholestatic liver disease, autoimmune hepatitis, Wilson disease, and viral hepatitis may also be seen in pregnancy. Management of liver disease in pregnancy requires collaboration between obstetricians and gastroenterologists/hepatologists. Treatment of pregnancy-specific liver disorders usually involves delivery of the fetus and supportive care, whereas management of chronic liver disease in pregnancy is directed toward optimizing control of the liver disorder. Cirrhosis in the setting of pregnancy is less commonly observed but offers unique challenges for patients and practitioners. This article reviews the epidemiology, pathophysiology, diagnosis, and management of liver diseases seen in pregnancy.     

Serodiagnosis of hepatitis C in acute and chronic liver disease in southwestern Saudi Arabia.

The extent of involvement of hepatitis C, as compared to hepatitis A and hepatitis B, virus infection in acute and chronic liver disease in the Asir Region, southwestern Saudi Arabia, was assessed in 898 patients hospitalized during the period from June 1990 to November 1991. Acute icteric hepatitis cases with severe onset were distinguished by their referral to the fever hospital while cases with milder onset and those with chronic hepatitis were followed at two general hospitals. Antibodies to the c-100-3 antigen of hepatitis C virus (anti HCV) were detected in a significant proportion of patients with chronic liver disease (chronic active hepatitis (65%), cirrhosis (44%)). Anti HCV was also detected in patients with acute hepatitis with milder onset at the general hospitals (10.9%) but proportionately much less in patients at the fever referral hospital (< 1%) where hepatitis A (52%) and, to a lesser extent hepatitis B (11%), were mostly diagnosed. These results indicate that HCV is a major identifiable infection in hospitalized patients with chronic liver disease in this region but that anti HCV antibodies (c-100-3) are not detected, at least at onset, in sporadic cases with acute manifestations. Testing for additional viral antigens or RNA and a longer follow-up period would be required before exclusion of a role for HCV in acute disease. Alternatively, other viral and non-viral agents may be sought in this illness.     

Effect of ursodeoxycholic acid in acute viral hepatitis

In previously published studies ursodeoxycholic acid (UDCA) showed beneficial effect on the course of chronic hepatitis. We investigated the effect of UDCA on the course of acute viral hepatitis in a prospective double-blind study. Seventy-eight consecutive patients were randomly assigned either to the UDCA group or to placebo. At 12 months of follow-up 76 patients were available for the final assessment. The analysis of all cases and of the patients with hepatitis B (n = 59) showed a comparable rate of decline of the alanine aminotransferase and other liver function tests in the treatment group and in the placebo group. However, the elevation of alanine aminotransferase persisted more frequently in the placebo group (all cases, p = 0.05; hepatitis B group, p = 0.03). Persistence of the hepatitis B virus infection, measured by the presence of hepatitis B early antigen and hepatitis B virus DNA (polymerase chain reaction and hybridization) at 12 months of follow-up, was observed in I of 33 patients in the UDCA group and in 6 of 25 patients in the placebo group (p = 0.02). Gallstones detected by entry ultrasound dissolved in four of eight cases in the UDCA group and in none of six in the placebo group. We conclude that UDCA has a beneficial effect on the course of the acute viral hepatitis. It may enhance the clearance of the hepatitis B virus and thus prevent the development of chronic hepatitis.     

Post-transfusional vs. sporadic non-A, non-B chronic hepatitis. A clinico-pathological and evolutive study

The clinical, morphological and evolutive features of 60 patients with chronic hepatitis, presumably caused by non-A, non-B virus infection, have been retrospectively analyzed. In all the cases the disease began as an acute episode of viral hepatitis that was followed by persistently abnormal liver function tests. No patient had evidence of current or past hepatitis B virus infection and other known causes of chronic liver disease were excluded. Thirty patients had received blood transfusions in the recent past, five were drug addicts and the source of the infection was not identified in the remaining 25, in whom the disease was considered to be sporadic. Clinical or biochemical differences between patients with post-transfusional and sporadic non-A, non-B chronic hepatitis were not observed, but liver histology showed a higher proportion of patients with chronic persistent hepatitis in the sporadic (72%) than in the transfusional group (53%). On follow-up, sustained normalization of liver function tests was observed in 46% of the cases with sporadic hepatitis but only in 13% of the cases with post-transfusion hepatitis. These observations suggest that non-A, non-B chronic hepatitis is more severe in patients with transfusion-related infection than in sporadic cases.     

Haemagglutinating anti-actin antibodies in acute and chronic liver disease

Anti-actin antibody was measured by the passive haemagglutination test in the serum of 118 patients with various forms of chronic cholestatic and non-cholestatic liver disease, and of 23 patients with acute hepatitis B or non-A, non-B. Tanned sheep erythrocytes and electrophoretically pure actin prepared from rabbit skeletal muscle were employed; absorption tests confirmed the specificity of positive reactions, defined from healthy controls as a titre of greater than 1/80. The presence of anti-actin activity in chronic liver disease corresponded generally to the immunofluorescent demonstration of smooth muscle antibody (P<0.01). However, in acute hepatitis, with one exception (later progressing to subacute disease) raised anti-actin titres were not found. Thus, the weak smooth muscle antibody occasionally demonstrable in this condition may be neither IgM in class, nor directed against actin. Anti-actin antibody was present in significantly high titre in 54% of 37 active chronic hepatitis patients and 79% of 24 ;mixed-form' cholestatic active chronic hepatitis, as compared with only 21% of 29 primary biliary cirrhosis patients, and 11% of alcoholic liver disease. Anti-actin antibody is therefore associated with chronic autoimmune parenchymal liver damage and its appearance may mark the transition from acute hepatitis. No raised anti-actin titres were seen in 10 primary biliary cirrhosis patients positive for mitochondrial antibody by indirect immunofluorescence, but negative by the complement fixation test. This result suggests that the cytoplasmic fluorescence observed is due to low titre mitochondrial antibody rather than cytoplasmic actin and that these patients do not represent a different disease entity. The generation of anti-actin antibody in chronic parenchymal liver disease, perhaps due to unmasking or schlepping of intracellular or SIg/HLA-associated actin, may characterise autoimmune events at hepatocyte level, point to prognosis, and aid in the differential diagnosis of individual patients.     

乙型肝炎病毒核心抗原在慢性乙型肝炎病毒感染者肝细胞内的分布及临床意义

目的 探讨HBcAg在慢性HBV感染者肝细胞内的分布情况及其临床意义.方法 对41例慢性HBV感染者进行肝组织穿刺,用免疫荧光组织化学技术在激光共聚焦显微镜下观察肝细胞内HBcAg的分布情况.计量资料采用Kruskal Wallis检验,计数资料采用卡方检验.结果 41例慢性HBV感染者中,36例肝细胞内HBcAg阳性表达,阳性率为87.8%,其中23例肝功能中度异常,10例肝功能轻度异常,3例肝功能正常.HBcAg有膜、胞质与核三种形式表达.在23例肝功能中度异常者中,6例呈明显膜型表达,无明显胞质型及核型,17例以胞质型与膜型混合表达,未发现核型表达.在10例肝功能轻度异常者中,以单纯胞质型为主,未见膜型与核型表达.在3例肝功能正常者中,以胞质型表达与少许核型表达为主,未见膜型表达.HBcAg表达类型与肝功能之间差异有统计学意义(χ2=10.60,P＜0.01).结论 慢性HBV感染者肝组织损伤与HBcAg的表达有直接联系,提示膜型表达的HBcAg是肝脏免疫损伤过程中的靶抗原.

Abstract：

Objective To explore the distribution and clinical significance of hepatitis B core antigen( HBcAg) in the hepatocytes of chronic hepatitis B virus infected patients. Methods Paraffin sections were made from 41 liver biopsy samples obtained from chronic hepatitis B virus infected patients. The immuno-fluorescence confocal technique was utilized to analyze the expression level and localization of HBcAg in hepatocytes. The data were analyzed by using Kruskal Wallis test and chisquare test. Results HBcAg expression were detected in 36 (87. 8%) patients, among whom 23 cases had moderate abnormal liver function, 10 with mild abnormal liver function and 3 with normal liver function. Among the cases with moderate abnormal liver function, 6 cases showed the simple membrane-type HBcAg expression, 17 cases showed mixed cytosolic-type and membrane-type HBcAg expression without the nuclear-type expression. Twelve cases with mild abnormal liver function only showed simple cytosolic-type HBcAg expression without membrane-type or nuclear-type expression. In the three patients with normal liver function, HBcAg was expressed in cytoplasm and nuclear but not on membrane. The correlation between HBcAg expression pattern and liver function was statistically significant (χ2 =10. 60, P＜0.01). Conclusion HBcAg expression is directly correlated with liver injury in chronic hepatitis B virus infected patients, which indicates that membrane expressed HBcAg is the target antigen during the immuno-attack of liver.