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1.
慢性乙型肝炎是我国常见的慢性传染病之一,乙型肝炎肝硬化是慢性乙型肝炎发展的结果,严重危害人民健康。乙型肝炎肝硬化分为代偿期肝炎肝硬化与失代偿期肝炎肝硬化,抗病毒治疗是阻断代偿期进人失代偿期的关键。现回顾2004年5月至2005年5月代偿期肝炎肝硬化患者60例,其中拉米夫定治疗组30例,干扰素治疗组30例,治疗1年,检测HBV DNA,HBeAg下降幅度及肝功能改善程度以观察抗病毒疗效,在1年短期抗病毒疗效中拉米夫定明显优与干扰素。  相似文献   

2.
拉米夫定治疗失代偿期活动性乙型肝炎肝硬化   总被引:3,自引:0,他引:3  
选择肝功能不稳定、HBV复制活跃的失代偿期肝硬化患者18例,在综合治疗的基础上加服拉米夫定100mg/d,观察48周后患者临床征状、体征、肝功能、肝形态学及HBV-DNA的变化,并于同期经综合治疗的对照组18例进行对比,观察米拉夫定治疗失代偿期活动性乙型肝炎肝硬化患者的临床疗效。结果:治疗后患者临床肝生化指标、Child-pugh平分、HBV-DNA定量与对照组相比有明显差异。提示拉米夫定治疗可有效抑制失代偿期活动性乙型肝炎硬化患者体内HBV的复制,稳定肝功能.进一步获得临床和生化的改善。  相似文献   

3.
目的:观察应用恩替卡韦(ETV)治疗失代偿期肝硬化的疗效。方法:选择HBV—DNA阳性的肝硬化失代偿期患者16例,在保肝等基础治疗上应用恩替卡韦抗病毒治疗,0.5mg/d,治疗24周。结果:恩替卡韦治疗后,患者症状、肝功能明显改善,HBV—DNA迅速转阴。结论:恩替卡韦能够抑制乙肝病毒复制,显著改善肝功能。  相似文献   

4.
目的:观察阿德福韦酯联合拉米夫定治疗乙型肝炎肝硬化失代偿期患者的近期疗效。方法:将20例HBV—DNA阳性肝硬化失代偿期患者随机分为二组:拉米夫定治疗组,阿德福韦酯、拉米夫定联合治疗组。治疗前后分别进行生化指标及HBV—DNA定量检测。结果:阿德福韦酯联合拉米夫定治疗组在肝脏生化指标改善及存活率方面均优于对照组,差异有显著性(P〈0.05)。结论:阿德福韦酯、拉米夫定联用可发挥优势互补作用,对乙肝肝硬化失代偿期患者的近期疗效更满意。  相似文献   

5.
目的:探讨失代偿期肝硬化治疗中肠内营养支持+谷氨酰胺联合治疗对改善患者营养状况、肝功能以及肠屏障功能效果。方法:选择60例失代偿期肝硬化患者作为研究对象,通过数字奇偶法分为对照组与观察组,各30例。对照组对失代偿期肝硬化行常规疗法治疗;观察组对失代偿期肝硬化通过肠内营养支持+谷氨酰胺联合疗法治疗。最终对治疗效果进行对比。结果:与对照组失代偿期肝硬化患者人体参数相比,观察组失代偿期肝硬化患者改善程度显著,差异有统计学意义(P<0.05);与对照组失代偿期肝硬化患者凝血酶原(PT)水平、总胆红素(TBIL)水平以及Child Paugh评分结果比较,观察组失代偿期肝硬化患者改善程度显著(P<0.05)。结论:临床在开展失代偿期肝硬化治疗工作期间,合理选择肠内营养支持+谷氨酰胺加以联合施治,对于患者营养状况的改善、肝功能改善以及肠道屏障功能改善均可以做出保证,从而优化失代偿期肝硬化患者的预后能力。  相似文献   

6.
目的研究拉米夫定治疗失代偿期肝硬化对病情改善、预后和安全性的影响。方法将活动期肝硬化和静止期肝硬化患者分别分成两组。两组均给予常规治疗,治疗组在此基础上给予拉米夫定100mg/d,疗程12个月。观察患者治疗前后肝功能、HBV DNA、Child-Pugh评分、HBeAg阴转和病毒变异等。结果治疗组患者经治疗后肝功能明显改善,Child-Pugh评分缩短(P<0.05),HBV DNA定量下降(P<0.05),HBgAg阳性率明显减少(P<0.05),但病毒变异宰差异无显著性(P>0.05)。结论失代偿期肝硬化患者应用拉米夫定治疗可改善肝功能、阻止病情进一步发展;一年期病毒变异率较低,未见严重后果发生。  相似文献   

7.
目的:观察拉米夫定治疗乙型肝炎失代偿期肝硬化的疗效.方法:40例乙型肝炎失代偿期肝硬化患者随机分为治疗组和对照组,治疗组给予口服拉米夫定100 mg/d,52 W,对照组不用抗病毒药物.在治疗前、后分别检测肝功能、HBV血清标志物、HBV-DNA、内毒素(ET)、IL-6以及TNF-α水平.结果:拉米夫定可以抑制活动性肝硬化患者病毒复制,改善肝功能,降低ET、IL-6和TNF-α水平,缓解病情.结论:拉米夫定可用于治疗失代偿期乙型肝炎肝硬化.  相似文献   

8.
目的:观察抗病毒治疗乙型肝炎肝硬化肝功能失代偿腹水患者的临床疗效。方法:选取乙型肝炎肝硬化肝功能失代偿腹水患者64例作为研究对象,随机分为对照组和治疗组,治疗组34例,对照组30例,所有患者均对症治疗。治疗组同时给予拉米夫定抗病毒治疗1年,观察两组患者治疗前后血清标志物转阴情况及腹水再发情况。结果:经过1年治疗后,治疗组34例患者均产生病毒学应答,应答率100%,4例再次出现腹水。对照组30例患者1例HBV-DNA转阴,余均仍为阳性,15例再次出现腹水。结论:抗病毒治疗可有效抑制HBV病毒的复制,减轻HBV病毒对肝脏的持续损伤程度,改善肝组织健康状态,可有效控制腹水的再发,是临床治疗乙型肝炎肝硬化肝功能失代偿期腹水患者的重要治疗措施。  相似文献   

9.
目的:观察恩替卡韦治疗失代偿期乙型肝炎肝硬化的效果和安全性。方法:42例失代偿期肝硬化患者,给予恩替卡韦(0.5 mg/d)治疗48周,观察患者治疗前后临床症状、生化指标、病毒学指标、纤维化指标及Child-pugh计分等情况。结果:2例死亡,40例存活患者肝功能各项指标明显改善,乙型肝炎病毒HBV DNA转阴,肝纤维化指标明显下降,Child-pugh分级明显上升。结论:恩替卡韦能迅速有效地改善大多数乙型肝炎肝硬化失代偿期患者的病情,提高其生活质量。  相似文献   

10.
目的:观察恩替卡韦治疗失代偿期乙型肝炎肝硬化的效果和安全性。方法:42例失代偿期肝硬化患者,给予恩替卡韦(0.5 mg/d)治疗48周,观察患者治疗前后临床症状、生化指标、病毒学指标、纤维化指标及Child-pugh计分等情况。结果:2例死亡,40例存活患者肝功能各项指标明显改善,乙型肝炎病毒HBV DNA转阴,肝纤维化指标明显下降,Child-pugh分级明显上升。结论:恩替卡韦能迅速有效地改善大多数乙型肝炎肝硬化失代偿期患者的病情,提高其生活质量。  相似文献   

11.
Dioscin is a natural steroid saponin derived from several plants, showing potent anti-cancer effect against a variety of tumor cell lines. In the present study, we investigated the anti-cancer activity of dioscin against human LNCaP cells, and evaluated the possible mechanism involved in its antineoplastic action. It was found that dioscin(1, 2 and 4 μmol/L) could significantly inhibit the viability of LNCaP cells in a time- and concentration-dependent manner. Flow cytometry revealed that the apoptosis rate was increased after treatment of LNCaP cells with dioscin for 24 h, indicating that apoptosis was an important mechanism by which dioscin inhibited cancer. Western blotting was employed to detect the expression of caspase-3, Bcl-2 and Bax in LNCaP cells. The expression of cleaved caspase-3 was significantly increased, and meanwhile procaspase-3 was markedly decreased. The expression of anti-apoptotic protein Bcl-2 was down-regulated, whereas the pro-apoptotic protein Bax was up-regulated. Moreover, the Bcl-2/Bax ratio was drastically decreased. These results suggested that dioscin possessed potential anti-tumor activity in human LNCaP cells through the apoptosis pathway, which might be associated with caspase-3 and Bcl-2 protein family.  相似文献   

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13.
Although infectious diseases are still common in Chinese children, great changes have taken place in the spectrum of the diseases. Two severe contagious diseases, smallpox and poliomyelitis, were eliminated many years ago, and other infectious diseases under effective control are measles, diphtheria, whooping cough, neonatal tetanus, epidemic cerebrospinal meningitis, epidemic encephalitis type B, typhoid, scarlet fever, dysentery, malaria, viral hepatitis, tuberculosis, syphilis,  相似文献   

14.
乙型肝炎(乙肝)是一种常见的严重肝脏疾病。据世界卫生组织(WHO)2008年报告,全球约有20亿人曾感染过乙肝病毒(HBV),其中3.5亿人为慢性HBV感染者。戊型肝炎(戊肝)是由戊型肝炎病毒(HEV)引起的一种自限性疾病,它主要在发展中国家流行,但在发达国家也有散发病例[1]。  相似文献   

15.
Objective To investigate the role of TNF receptor-associated factor 2 (TRAF-2) and TRAF6 in CD40-induced nuclear factor-κB (NF-κB) signaling pathway and whether CD40 signaling requires TRAF2. Methods Human B cell lines were transfected with plasmids expressing wild type TRAF2 or dominant negative TRAF2,TRAF2-shRNA,or TRAF6-shRNA. The activation of NF-κB was detected by Western blot,kinase assay,transfactor enzyme-linked immunosorbent assay (ELISA),and fluorescence resonance energy transfer (FRET). Analysis of the role of TRAF-2 and TRAF-6 in CD40-mediated NF-κB activity was examined following stimulation with recombinant CD154. Results TRAF2 induced activity of IκB-kinases (IKKα,IKKi/ε),phosphorylation of IκBα,as well as nuclear translocation and phosphorylation of p65/RelA. In contrast,TRAF6 strongly induced NF-κB activation and nuclear translocation of p65 as well as p50 and c-Rel. Engagement of CD154-induced nuclear translocation of p65 was inhibited by a TRAF6-shRNA,but conversely was enhanced by a TRAF2-shRNA. Examination of direct interactions between CD40 and TRAFs by FRET documented that both TRAF2 and TRAF6 directly interacted with CD40. However,the two TRAFs competed for CD40 binding. Conclusions These results indicate that TRAF2 can signal in human B cells,but it is not essential for CD40-mediated NF-κB activation. Moreover,TRAF2 can compete with TRAF6 for CD40 binding,and thereby limit the capacity of CD40 engagement to induce NF-κB activation.  相似文献   

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BACKGROUND: Rheumatoid arthritis (RA), as a common systemic inflammatory autoimmune disease, affects approximately 1 in 100 individuals. Effective treatment for RA is not yet available because current research does not have a clear understanding of the etiology and pathogenesis of RA. Xinfeng Capsule, a patent Chinese herbal medicine, has been used in the treatment of RA in recent years. Despite its reported clinical efficacy, there are no large-sample, multicenter, randomized trials that support the use of Xinfeng Capsule for RA. Therefore, we designed a randomized, double-blind, multicenter, placebo-controlled trial to assess the efficacy and safety of Xinfeng Capsule in the treatment of RA. METHODS AND DESIGN: This is a 12-week, randomized, placebo-controlled, double-blind, multicenter trial on the treatment of RA. The participants will be randomly assigned to the experimental group and the control group at a ratio of 1:1. Participants in the experimental group will receive Xinfeng Capsule and a pharmaceutical placebo (imitation leflunomide). The control group will receive leflunomide and an herbal placebo (imitation Xinfeng Capsule). The American College of Rheumatology (ACR) Criteria for RA will be used to measure the efficacy of the Xinfeng Capsule. The primary outcome measure will be the percentage of study participants who achieve an ACR 20% response rate (ACR20), which will be measured every 4 weeks after randomization. Secondary outcomes will include the ACR50 and ACR70 responses, the side effects of the medications, the Disease Activity Score 28, RA biomarkers, quality of life, and X-rays of the hands and wrists. The first four of the secondary outcomes will be measured every 4 weeks and the others will be measured at baseline and after 12 weeks of treatment. DISCUSSION: The result of this trial will help to evaluate whether Xinfeng Capsule is effective and safe in the treatment of RA. TRIAL REGISTRATION: This trial has been registered in ClinicalTrials.gov. The identifier is N CT01774877.  相似文献   

18.
Multifocal motor neuropathy (MMN) is a rare,.focal,inflammatory,demyelinating disease of the peripheral nerves with pure motor involvementJ MMN is clinically characterized by slowly progressive,asymmetric,distal,upper limb predominant weakness,in the absence of sensory disturbances) Weakness is usually multifocal and connected to a distinct motor nerve,such as the musculocutaneous nerve resulting in biceps weakness,the posterior interosseus nerve resulting in finger drop,the median,ulnar,or radial nerve resulting in dexterity problems or grip weakness,or the peroneal nerve resulting in a foot drop.Onset of clinical manifestations is between 20 and 50 years of age.The prevalence of MMN is reported as 1-2 per 100 000.2 MMN is three times more frequent in men as compared to women.  相似文献   

19.
Low back pain is a common public health problem in western industrialized societies and the world as well.Studies indicate that the prevalence rate ranges to 35%, with around 10% of patients from 12% becoming chronically disabled. It also places an enormous economic burden on society. Although the exact cause of low back pain has yet to be defined, intervertebral disc degeneration is considered a major source of it. Since patients with degenerative discs are often asymptomatic, the mechanisms of it are still unclear.  相似文献   

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