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慢性乙型肝炎患者的个体化免疫调节治疗
慢性乙型肝炎(简称"慢性乙肝")需要长期抗病毒治疗的概念已经形成共识.按照循证医学的原则和根据新的研究成果,美国肝脏病研究协会( American Association for the Study of Liver Diseases,AASLD)和欧洲肝脏病协会(European Association for the Study of the Liver,EASL)分别发布了乙型肝炎实践指南[1-2],我国在2010年12月发布了修改的<慢性乙型肝炎防治指南>[3],这使得慢性乙肝的抗病毒治疗更加规范、科学、合理.
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熊去氧胆酸治疗胆汁淤积性疾病应用进展
胆汁淤积是指由于肝胆酸流受阻而导致的血清胆汁酸浓度升高.胆道上皮病变导致胆汁酸转运障碍,增加了血清胆汁酸浓度,普遍特征是胆汁酸在肝脏和血液中蓄积伴胆汁流减少,慢性胆汁淤积肝损伤主要由肝内淤积的高浓度肝细胞毒性疏水胆汁酸(如石胆酸及其前体鹅去氧胆酸)介导,它们溶解胞膜脂质,致胞膜损坏、细胞完整性破坏及胞内成分漏出,并能引发免疫激活介导的肝损伤,以进展性肝内胆酸潴留导致肝损伤、肝硬化和死亡为特征.
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小儿肝病诊治研究进展与存在问题
小儿肝病系常见多发病,许多成年期的慢性肝病源自儿童期感染或发生于儿童.我国乙型肝炎(乙肝)病毒携带者和慢性乙肝患者中90%以上为生命早期感染所致.儿童期的肝病在儿童期的不同年龄段特征也各不相同,仅靠临床症状或凭经验治疗,会使许多患儿因误诊、漏诊或得不到正确及时的治疗,而延误病情,至成年时发展至终末期肝病.
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重视重症肝病患者深部真菌感染的诊断与治疗
近10余年来,临床深部真菌感染呈持续增多趋势,其原因有:①由于医药科技的高速发展带来的负面作用,如高效广谱抗生素、皮质类固醇激素广泛应用,抗肿瘤细胞毒药物治疗、器官移植免疫抑制剂深入开展,外科静脉营养、其他导管介入性治疗等治疗手段不断实施;
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自身免疫重叠综合征
自身免疫性肝病(autoimmune liver diseases)是指由于机体的自身免疫反应攻击肝组织而非病毒感染所致肝病,主要包括自身免疫性肝炎(autoimmune hepatitis,AIH)、原发性胆汁性肝硬化(primary biliary cirrhosis,PBC)及原发性硬化性胆管炎(primary sclerosing cholangitis,PSC),前者主要表现为肝细胞炎症坏死、后二者主要表现为肝内胆汁淤积.自身免疫性肝病的表现有时不典型或相互重叠,给临床诊断和治疗带来困难,称为自身免疫重叠综合征(autoimmuneoverlap syndromes),是指AIH、PBC、PSC相互重叠.自身免疫重叠综合征诊断应包括对临床、血清学、影像学及组织学等的综合分析.目前对自身免疫重叠综合征的解释:(1)当综合标准提示三种自身免疫性肝病,单项指标缺乏特异性时,提示重叠综合征;(2)自身免疫性胆管炎(autoimmune cholangitis,AIC)为AIH加胆汁淤积,他不是一个独立疾病,应考虑为抗线粒体抗体(AMA)阴性的PBC,宜按PBC治疗;(3)部分重叠综合征仅系疾病早期表现,以后可呈现某一种自身免疫性肝病;(4)伴有界面性肝炎的PBC或PSC可用免疫抑制剂加熊去氧胆酸治疗,前者无效则应撤除,以免产生骨骼脱钙.
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非酒精性脂肪肝病中环氧合酶-2和基质金属蛋白酶的作用
由于人们饮食结构的改变以及预防保健措施的相对滞后,非酒精性脂肪肝病(nonalcoholic fatty liver disease,NAFLD)的发病率逐年上升.NAFLD的发病过程及其相关因素的研究越来越受到重视.研究表明NAFLD的发生、发展伴随着物质代谢紊乱及肝细胞坏死、炎变和纤维化的形成.大量实验证实环氧合酶-2(COX-2)和基质金属蛋白酶(MMPs)参与了这一过程.
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非酒精性脂肪性肝炎的发病机制及治疗的研究进展
非酒精性脂肪性肝炎(nonalcoholic steatohepatitis,NASH)作为非酒精性脂肪性肝病(non-alcoholic fatty liver diseases,NAFLD)关键性的中间阶段,其发病机制的探讨可为临床治疗提供重要依据.大量研究认为胰岛素抵抗、氧应激、细胞因子是发病环节中的重要因素,目前有前景的治疗方案多数围绕NASH的关键性致病因子及发生环节展开.
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TT病毒在肝病患者的感染状况及致病性
目的:研究TTV在肝病人群中的感染率及致病性情况.方法:研究对象:(1)非甲-非戊型肝炎组83例,男58例,女25例;(2)慢性肝病组75例,男53例,女22例;(3)查体人群组105例,男55例,女50例.采用非翻译区(UTR)及ORFl区二套引物进行PCR检测TTV-DNA,用RFLP方法对ORFl引物PCR产物进行酶切分型,并对部分PCR产物测序.结果:rrV在非甲-非戊型肝炎组,慢性肝病组及查体人群组中阳性率分别为95.2%,93.3%及87.6%,三组间无显著性差异(P>0.05).经RFLP分型,三组中G1型TTV检出率分别为32.5%,38.7%及19.0%,前二组Gl型TTV阳性率均显著高于查体人群组阳性率(P<0.05,P<0.01).乙型肝炎后肝硬化及肝癌患者中G1型Trv阳性率(25.0%)与慢性乙型肝炎,HBsAg携带者中阳性率(37.1%)无显著性差异(P>0.05);丙型肝炎后肝硬化及肝癌患者中Gl型TTV阳性率(40%)与慢性丙型肝炎患者阳性率(100%)也无显著性差异(P>0.05).查体人群中TTV感染率与性别无相关性,21-30岁年龄段TTV感染率(72.2%)显著低于31-40岁年龄段感染率(96.2%,P<0.01)及41-50岁年龄段感染率(93.1%,P<0.05).结论:TTV在普通人群及肝病患者中有很高的感染率,30岁以下普通人群中感染率较低.GI型TTV与肝脏相关,但对慢性乙型肝炎,慢性丙型肝炎的病程及预后无影响,提示GI型TTV的致病性较弱.
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AIM To understand the relationship between levels of endotoxin and cytokines in serum and to clarify thecause of cytokines change in liver diseases.METHODS Serum endotoxin level was determined by quantitative limulus amebocyte lysate chromogenicassay in 89 cases of acute and chronic liver diseases. Cytokines (TNF-a, IL-2, IL-6, IL-8, G-CSF) wereassayed by ELISA. Patients were divided into two groups based on oral administration of lactulose or not.Mean concentration of endotoxin and cytokines was compared before and 20 days after lactulose treatment.RESULTS The highest serum level of endotoxin was found in patients with cirrhosis (69.3±23.6pg/mL)and the lowest in patients with chronic hepatitis (28.4±7.9pg/mL), the moderate in patients with acutehepatitis (44.6±14.3pg/mL) (P<0.01). Serum levels of TNF-a, IL-2, IL-6, IL-8, G-CSF were higher inpatients with acute hepatitis than those with chronic hepatitis (P<0.05). No difference was noted betweenchronic hepatitis and cirrhosis (P >0.05). In all cases, serum levels of endotoxin were positively correlatedwith the concentration of TNF-a (r=0.555, P<0.05), IL-6 (r=0.531, P<0.01), IL-8 (r=0.440,P<0.05) and G-CSF (r =0.440, P<0.05), but not with IL-2 (r =0.10l, P<0.05). The decrease of serumlevels of endotoxin was greater in patients taking lactulose than controls (25.6±14.4pg/mL, n = 49 cases vs.10.9±9.Spg/mL, n = 40 cases, P < 0.01), the recovery from endotoxemia was higher in group withlactulose treatment than in controls (94.7%, n = 19 vs 36.4%, n = 22, P < 0.01 ). The decrease ofendotoxin resulted in decreases of TNF-a, IL-6, IL-8, G-CSF, ALT, AST and TB.CONCLUSION Endotoxemia is common in liver diseases, which could induce production and release ofcytokine from monocytes and macrophages and has harmful effects on hepatocytes. Treatment with lactulosecould decrease serum levels of endotoxin and cytokines, suggesting that lactulose could protect liver cells frominjury by reducing the absorption of endotoxin in intestine.
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Advances in molecular biology made possible the discovery of the virus that causes hepatitis C. However,little is known about the fundamental aspects of hepatitis C virus (HCV) replication, primarily because arobust cell culture has not been established. As a result, the currently available drugs for the treatment ofhepatitis C are not specifically directed against HCV. Based on what is known about the molecular biology ofHCV, however, drugs can now be developed against specific viral and cellular targets. The next generationof drugs for the treatment of hepatitis C will likely be directed against non-structural HCV proteins withknown enzymatic activities, such as the proteases, RNA helicase and RNA polymerase. Others agentstargeted against the viral RNA, core protein that assembles into the virion capsid and putative cellular“receptors” that bind HCV envelope proteins are also being developed. These drugs should have fewer sideeffects than those currently available and be much more effective for the treatment of chronic hepatitis C.
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AIM To study the nosocomial infection in the patients with liver diseases and its risk factors.METHODS A prospective survey of nosocomial infection in 848 patients with various liver diseases wascarried out in our hospital for a 24-month period.RESULTS Incidence of nosocomial infection in patients with liver diseases was 9.20%, nosocomialinfection rate in severe hepatitis was significantly higherthan in mild and moderate liver diseases. Infectionof respiratory tract accounted for 44.33%. Infection rate in abdominal cavity, intestinal tract, gallbladderand bile ducts, oral region, and other regions was 15.46%, 12.37%, 8.25%, 7.22% and 12.37%,respectively.CONCLUSION The factors related to nosocomial infection were the severity of liver diseases, cellularimmunological condition, Co-infection of hepatitis virus, severe accompanying diseases, improper medicalmanipulations and use of broad-spectrum antibiotics. Nosocomial infection obviously affects the prognosis ofliver diseases.
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INTRODUCTIONA newly discovered DNA virus,transfusion transmitted virus (TTV), was reported as a cause of post-transfusion hepatitis of unknown etiology in Japan[1]. In order to investigate TTV prevalence in southern China, a study was carried out among blood donors, patients with liver diseases and hemodialysis to determine the epidemiological charateristics.
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解读2011年美国肝脏病学会关于基因1型慢性丙型肝炎治疗指南的更新
慢性丙型肝炎病毒(HCV)感染的标准抗病毒治疗方案是聚乙二醇化干扰素-α(Peg-IFN-α)2a或Peg-IFN-α 2b联合利巴韦林(RBV)治疗.基因1型慢性丙型肝炎初治患者48周持续病毒学应答(sustained virologic response,SVR)为40%~54%,复发率大约为15%~25%[1].随着直接作用(direct-acting antiviral,DAA)抗病毒药物的研发,两种针对HCV的蛋白酶抑制剂--telaprevir(TVR)和boceprevir(BOC)相继在欧美被批准用于慢性丙型肝炎的抗病毒治疗.随之2011年美国肝脏病学会(American association forthe study of liver diseases,AASLD)更新了关于基因1型慢性丙型肝炎的抗病毒治疗指南[2].本文就指南的要点作一解读.
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2007年香港肝病研究学会关于慢性乙型肝炎处理的陈述
1 评估1.1 肝纤维化和肝硬化肝活检为金标准,需要评估至少6个门管区,Ishak评分≥ 4~6提示严重的肝纤维化或肝硬化.
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贴报-P2临床毒理学、药理学和疗效研究
5-Flourouracil(5-FU) is one of well known anti-cancer drugs, but its toxicity in normal lymphocytes remains a major problem in chemotherapy. The eastern traditional drug, Bupleuri radix(BR), has been used for the treatment of liver diseases and contains series of triterpene saponins.
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2012年英国基因1型慢性丙型肝炎蛋白酶抑制治疗共识指南解读
直接抗丙型肝炎病毒(HCV)药物中的蛋白酶抑制剂telaprevir (TVR)和boceprevir (BOC)相继在欧洲、美国获得批准上市.随之,美国肝病研究学会(American Association for the Study of Liver Diseases,AASLD)更新了基因1型慢性丙型肝炎治疗的指南,还有一些专家自发组成的小组发表应用的指南.
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2011年美国肝病学会基因l型慢性丙型肝炎病毒感染治疗指南更新解读
美国肝病学会(American Association for the Study of Liver Diseases,AASLD)于2011年8月对《慢性丙型肝炎诊断、处理和治疗临床实践指南》进行了部分更新,并于10月正式发表.按照AASLD的惯例,一旦有新的诊断和治疗进展,就对指南进行更新.由于自2009年发表上一版指南以来,主要的进展集中在针对基因1型的直接抗病毒药物(direct acting antiviral agents,DAA)取得突破性进展,其中telaprevir (TVR)和boceprevir ( BOC)在欧美相继获得批准上市.
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2011年英国胃肠病学会自身免疫性肝炎指南解读
1 背景介绍自身免疫性肝炎(autoimmune hepatitis,AIH)是一种慢性炎症性肝病,若不采取治疗常进展至肝硬化、肝衰竭甚至死亡[1].2011年英国胃肠病学会(British Society of Gastroenterology,BSG)在美国肝病学会(American Association forthe Study of Liver Diseases,AASLD)2002年发表及2010年更新的AIH诊断和治疗指南[2,3]基础上,尝试对其进一步优化[4].
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冬虫夏草挥发油成分分析
1 IntroductionCordyceps sinensis (Berk.) Sacc. is a parasitic fungus on the larvae of Leidoptera. The fruiting bodies of C. sinensis have been used as food and tonic herbal medicine for a variety of dieases for centuries, named Dong-Chong-Xia-Cao in mandarin. C. sinensis extract has been used for the treatment of hyperglycemia, hyperlipidemia, respiratory and liver diseases, renal dysfunction, renal failure[1], and its antioxidant properties have also been widely used. The extract of C. sinensis has been shown to increase the level of high-energy phosphates in mouse liver[2] and steroidogenesis[3] ,superoxide dismutase activity in red blood cell (RBC), and to decrease plasma malonedialdehyde and oxygen free radicals in older patients.
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肝脏疾病影像学诊断与鉴别诊断(Ⅲ)肝脏病变的影像学诊断与鉴别诊断(上)
肝脏疾病中存在着许多相似的病理改变,可呈现一些类似的影像学表现,给影像学诊断和鉴别诊断带来困难.本节中介绍的内容包括肝脏富血管性病变、肝脏囊性病变、肝脏弥漫性病变、伴中央疤痕的肝脏病变、伴钙化的肝脏病变、伴出血的肝脏病变、伴有脂肪的肝脏病变、伴肝包膜回缩的肝脏病变、肝脏结节样病变及肝内肿块(瘤)性病变等十方面病变的诊断与鉴别.