持续性血液灌注治疗暴发性肝衰竭

作者介绍一种治疗暴发性肝衰竭的新方案,即每日同时行血浆交换和持续性血液滤过(CHF),方法简便.现将用此新方法治疗1例暴发性肝衰竭的效果作一报道。患者女性,55岁,1991年7月15日因乏     

对乙酰氨基酚诱发急性肝衰竭动物模型研究现状

在人工肝和肝移植研究的动物实验阶段,大多要用到急性肝衰竭动物模型,对乙酰氨基酚可诱导急性肝衰竭,用其制备模型比手术法简便、经济、符合临床实际,因而引起广大学者的关注。本文就对乙酰氨基酚制备急性肝衰竭动物模型的机制、方法及影响因素进行综述。     

干扰素与甲型肝炎

由甲型肝炎引起的暴发性肝衰竭的预后,通常比由乙型肝炎或非甲非乙型肝炎病毒引起的暴发性肝衰竭预后要好。但是在暴发性肝衰竭发生后,有时还存在着甲型肝炎病毒的持续性复制,严重者需要做肝脏移植手术。     

凝血酶原时间是扑热息痛所致暴发性肝衰竭的预后指标

扑热息痛导致暴发性肝衰竭的病死率较高。哪些因素与预后有关,许多作者已从不同的角度进行了探讨,但单一凝血因子的检查尚未广泛开展。为此,作者对150例由扑热息痛引起的暴发性肝衰竭患者连续测定了凝血酶原时间(PT),以评价PT的变化和峰值时间对扑热息痛引起暴发性肝衰竭的预后价值。 1986年10月～1989年2月收治150例由扑热息痛诱发的暴发性肝衰竭。全部病例符     

急性肝衰竭的分类

“急性”或“暴发性”肝衰竭包括不同病因与病程的状况,而已提出的几种分类法都提示此种综合征先有脑病发生。1986年作者根据出现黄疸至脑病发生的相距时间,将短于2周者称之为“暴发性”肝衰竭,长于2周者称之为“亚暴发性”肝衰竭,其理由     

对乙酰氨基酚诱发急性肝衰竭动物模型研究现状

在人工肝和肝移植研究的动物实验阶段，大多要用到急性肝衰竭动物模型，对乙酰氨基酚可诱导急性肝衰竭，用其制备模型比手术法简便、经济、符合临床实际，因而引起广大学者的关注。本文就对乙酰氨基酚制备急性肝衰竭动物模型的机制、方法及影响因素进行综述。     

肝衰竭的类型与机制

肝衰竭分为慢性和暴发性两类。慢性肝衰竭的病因主要是失代偿性肝硬化和晚期肝癌等;暴发性肝衰竭(FHF)的病理基础则分三型: (一)急性大块肝坏死(坏死型):最主要的病因是暴发性病毒性肝炎,甲型、乙型、非甲非乙型皆可引起。其中乙型最常见,与病毒诱发的免疫反应有关;甲型较少见,与肝细胞过量病毒感染有关。柯萨奇B型病毒和EB病毒等偶可引起暴发性肝     

原位肝移植救治成人暴发性及亚急性肝衰竭

本文对1981年2月至1985年7月的29例各种不同原因的暴发性肝衰竭(FHF)和亚急性肝衰竭(SHF)的患者:进行了分组观察。暴发性肝衰竭即发生严重的肝细胞功能损害兼有肝性脑病(或肝昏迷3～4度)而既往无肝病史者,本组16例。亚急性肝衰竭指起病8～28周内发生严重不可逆性肝衰竭而既往无慢性肝病史者,该组13例。29例     

细胞外组蛋白在急性肝衰竭发病机制中的研究进展

急性肝衰竭是由多种因素引起的短时间内肝脏发生损害的严重临床综合征,死亡率高,且无特效疗法.细胞外组蛋白是一种新发现的炎性介质或危险信号分子,在启动及加重肝损伤中有着重要的作用.本文阐述了细胞外组蛋白结构、生物学特性、来源及导致细胞毒性的机制,从多方面探讨细胞外组蛋白在急性肝衰竭发病中的作用机制.     

在抗结核治疗中联合使用吡嗪酰胺发生暴发性或亚暴发性肝功能衰竭

最近,在发达国家中结核病的发病率增加,导致了抗结核药物的广泛应用。由于大多数药物有抗药性,因此对活动性结核病人常联合使用抗结核药治疗。暴发性肝衰竭(从黄疸到肝性脑病时间少于15天)和亚暴发性肝衰竭(从黄疸到肝性脑病时间为16天～3个月)虽不常见,却是使用异烟肼的并     

Liver transplantation for viral hepatitis

Viral hepatitis is associated with two forms of liver failure that may require liver transplantation: fulminant hepatic failure associated with all forms of acute viral hepatitis and chronic liver failure as a result of chronic hepatitis B and C infection (or both). This review briefly discusses liver transplantation for fulminant hepatitis but focuses on transplantation for hepatitis B- and hepatitis C-associated cirrhosis.     

Fatal liver cell necrosis following administration of glafenine]

The case is described of a patient with fulminant hepatic failure attributed to intake of glafenine 400 mg daily for 15 days. The first symptoms appeared two weeks after discontinuation of glafenine. Other causes of hepatic necrosis could be excluded. Approximately five weeks after the onset of symptoms the patient died of hepatic failure. At autopsy massive hepatic necrosis and massive pancreatic necrosis were demonstrated.     

Wilson's disease presenting as acute fulminant hepatic failure

A fatal case of fulminant hepatic failure in an adolescent is described. Post-mortem examination revealed the cause to be Wilson's Disease. This rare presentation is characterised by apparently atypical changes in copper metabolism. Wilson's Disease should be a differential diagnosis of any adolescent presenting in liver failure.     

Increase of ceramide in the liver and plasma after carbon tetrachloride intoxication in the rat

In fulminant hepatic failure, various toxins causing multi-organ failure increase in plasma. As a novel toxin, levels of ceramide, a well-studied lipid mediator of apoptosis, were determined by LC-MS/MS in the liver and plasma of carbon tetrachloride (CCl4)-intoxicated rats. After 6 h of oral administration of CCl4 (4 mL/kg body weight as a 1:1 mixture of CCl4 and mineral oil) to rats, extensive hepatic failure occurred as evidenced by a severe elevation in plasma AST and ALT. The liver concentration of major ceramide components (C16:0, C24:0, C24:1, C18:0, C22:0, and C24:2 in decreasing order), and the sum of these ceramides increased significantly 2 h after CCl4 intoxication compared to that in the control group given mineral oil. The total ceramide concentration in the plasma was also increased to 4.1 times that in the control 24 h after administration of CCl4. In conclusion, the early increase in liver ceramides may contribute to hepatic cell death and the increase in plasma ceramides during fulminant hepatic failure may cause damage in other organs including the brain and kidney.     

HEV Infection as an Aetiologic Factor for Acute Hepatitis: Experience from a Tertiary Hospital in Bangladesh

Acute hepatitis is seen sporadically round the year in Bangladesh. The incidence of acute viral hepatitis E increases after floods as this allows sewerage contamination of piped and groundwater. The aim of this retrospective study was to assess the burden of hepatitis E virus (HEV infection) in Bangladesh. Patients attending the Hepatology Unit III of the Bangabandhu Sheikh Mujib Medical University, during June 2004–December 2006, were included in the study. All viral markers were tested by enzyme-linked immunosorbent assay. The study population was divided in four groups. Group 1 included 144 patients with acute viral hepatitis. The inclusion criteria were: nausea and/or vomiting, loss of appetite, serum bilirubin >200 μmol/L, raised serum transaminases, and prothrombin time ≥3 seconds prolonged beyond control value. In Group 2, there were 31 pregnant women with acute viral hepatitis. All the patients had prodrome, icterus, raised serum bilirubin and raised serum transaminase levels. Group 3 included 23 patients presenting with fulminant hepatic failure. In Group 4, 69 patients with cirrhosis of liver were included. They presented with features of decompensation for the first time. The inclusion criteria were: patients with established cirrhosis with jaundice and/or ascites and/or hepatic encephalopathy. In Group 1, 58.33% of the 144 patients had acute viral hepatitis E. In Group 2, 45.16% of the pregnant women also had acute viral hepatitis E. HEV was responsible for 56.52% cases of fulminant hepatic failure in Group 3. In 21.7% cases in Group 4, decompensation of cirrhosis was due to HEV. Acute viral hepatitis E in the third trimester of pregnancy and HEV-induced fulminant hepatic failure were associated with 80% of mortality despite the best possible care. In this clinical context, acute viral hepatitis E is the leading cause of wide spectrum of liver disease ranging from severe acute viral hepatitis, fulminant hepatic failure, to decompensation of liver in cirrhotics in Bangladesh. Sewerage contamination of piped water following floods may contribute to the higher incidence of HEV infection.Key words: Hepatitis, Hepatitis E infections, Hepatitis E virus, Retrospective studies, Bangladesh     

Occult malignancy presenting as acute fulminant hepatic failure

Only six cases of hepatic metastatic disease presenting as acute fulminant liver failure have been recorded in the literature. A seventh case is reported here where, after presenting in acute liver failure, it was not possible to establish a tissue diagnosis but evidence of massive liver replacement by tumour was provided by ultrasound imaging and radionuclide scintiscanning.     

Toxic effects of herbal teas

At least 26 herbal teas contain toxic ingredients, many of which have caused serious gastrointestinal, hematologic, cardiac, and nervous system disease. The severity of illness following herbal tea use has ranged from contact dermatitis to fulminant hepatic failure and death. Most of these teas are available in health food stores and there is no requirement that their toxic potential be labeled for consumer protection. Patients on anticoagulant drugs should avoid herbal teas containing coumarin.     

Genetic analysis of precore/core and partial pol genes in an unprecedented outbreak of fulminant hepatitis B in India

SUMMARY We investigated an unprecedented outbreak of fulminant hepatitis B virus (HBV) that occurred in Modasa, Gujarat (India) in 2009. Genomic analysis of all fulminant hepatic failure cases confirmed exclusive predominance of subgenotype D1. A1762T, G1764A basal core promoter (BCP) mutations, insertion of isoleucine after nt 1843, stop codon mutation G1896A, G1862T transversion plus seven other mutations in the core gene caused inhibition of HBeAg expression implicating them as circulating precore/BCP mutant virus. Two rare mutations at amino acids 89 (Ile→Ala) and 119 (Leu→Ser) in addition to other mutations in the polymerase (pol) gene may have caused some alteration in either of four pol gene domains to affect encapsidation of pregenomic RNA to enhance pathogenicity. Sequence similarity among patients' sequences suggested an involvement of a single hepatitis B mutant strain/source to corroborate the finding of gross and continued usage of HBV mutant-contaminated syringes/needles by a physician which resulted in this unprecedented outbreak of fulminant hepatitis B. The fulminant exacerbation of the disease might be attributed to mutations in the BCP/precore/core and pol genes that may have occurred due to selection pressure during rapid spread/mutation of the virus.     

TT virus. A review of the literature

In 1997, a new DNA virus was cloned by a Japanese team and designated TT virus (TTV). This virus seemed to be associated with non-A, non-G post-transfusion hepatitis. It was isolated by polymerase chain reaction (PCR) and was presumed to be human Circoviridae. The virus is heterogenous; 16 different genotypes are currently registered, and it can be classified as a "swarm" of at least 5 different viruses. Depending on the PCR technique used, the prevalence of infection ranges from 1.9 to 36% among blood donors, from 11.5 to 71% in hemodialysis patients, from 47 to 82% among patients with non-A, non-B or non-C fulminant hepatic failure, and the most elevated percentage is found in hemophiliacs. Epidemiological studies have established that the routes of TTV infection might be parenteral, oral-fecal, and possibly salivary. Mother-to-infant transmission is controversial. TTV may play a role in the pathogenesis of non-A, non-B or non-C fulminant hepatic failure. Patients co-infected with hepatitis C virus (HCV) and TTV have a significantly higher histological grade score than patients with isolated HCV infection. Treatment with interferon seems to decrease TT viremia, according to results obtained outside the context of clinical trials. TTV seems to be a light pathogenic virus. Its widespread presence in the blood of infected subjects contrasts with the apparent absence of pathological symptoms. PCR standardization is needed to clearly establish its real prevalence worldwide.     

Serious adverse events attributed to nevirapine regimens for postexposure prophylaxis after HIV exposures--worldwide, 1997-2000

In September 2000, two instances of life-threatening hepatotoxicity were reported in health-care workers taking nevirapine (NVP) for postexposure prophylaxis (PEP) after occupational human immunodeficiency virus (HIV) exposure. In one case, a 43-year-old female health-care worker required liver transplantation after developing fulminant hepatitis and end-stage hepatic failure while taking NVP, zidovudine, and lamivudine as PEP following a needlestick injury (1). In the second case, a 38-year-old male physician was hospitalized with life-threatening fulminant hepatitis while taking NVP, zidovudine, and lamivudine as PEP following a mucous membrane exposure. To characterize NVP-associated PEP toxicity, CDC and the Food and Drug Administration (FDA) reviewed MedWatch reports of serious adverse events in persons taking NVP for PEP received by FDA (Figure 1). This report summarizes the results of that analysis and indicates that healthy persons taking abbreviated 4-week NVP regimens for PEP are at risk for serious adverse events. Clinicians should use recommended PEP guidelines and dosing instructions to reduce the risk for serious adverse events.