安体维康治疗慢性丙型肝炎疗效分析

本文依据《中华医学会丙型肝炎防治指南》诊断标准Ⅲ，选用目前对丙型肝炎的最新检测指标HCV—RNA、CD4、CD8、T细胞数量等，评价安体维康对丙型肝炎的确切疗效，总结如下。 1对象和方法 1．1对象 选择18～60岁，HCVRNA阳性患者共29例，分为治疗组和对照组。均未经其他抗病毒治疗。治疗组16例，男12例，女4例，年龄26～52岁，病程6～36个月，平均病程1．2a；对照组13例，男9例，女4例，年龄32～57岁，病程6～48个月，平均病程1～3a。     

56例丙型肝炎肝硬化抗病毒治疗临床观察

目的采用从小剂量开始逐渐加量（LADR）方案治疗代偿期丙型肝炎肝硬化及失代偿期丙型肝炎肝硬化患者,并观察临床疗效。方法代偿期丙型肝炎肝硬化患者给予peg-IFNα-2a（派罗欣,上海罗氏制药有限公司）67.5μg/周＋利巴韦林600mg/d,失代偿期肝硬化患者给予IFNα（赛若金,深圳科兴生物工程有限公司）100万U,隔日一次肌内注射,加利巴韦林600mg/d,逐渐增加剂量。若化验及患者症状允许,peg-IFNα-2a及IFNα每2～4周增加一次剂量,peg-IFNα-2a由90μg/周增加至135μg/周,IFNα增加至300万U。利巴韦林每2周增加200mg/d至有效剂量。结果 44例代偿期肝硬化患者有38例完成了疗程,治疗后12周ALT、AST、TBIL、HCV RNA水平与治疗前相比无明显差异。治疗后24周ALT、AST、TBIL、HCV RNA水平与治疗前相比明显下降,差异有统计学意义。肝纤维化指标在治疗后24周HA、LN、PC-Ⅲ、C-Ⅳ水平与治疗前相比下降,差异有统计学意义。12例失代偿肝硬化患者有8例完成了IFNα＋利巴韦林疗程,治疗后12周ALT、AST、TBIL、胆碱酯酶（CHE）、HCV RNA水平与治疗前相比差异无统计学意义。治疗后24周ALT、AST、CHE、HCV RNA水平与治疗前相比明显下降,差异有统计学意义。TBIL与治疗前相比无明显差异。肝纤维化指标在治疗后12周血清透明质酸（HA）、层黏蛋白（LN）、Ⅲ型前胶原（PC-Ⅲ）、Ⅳ型胶原（C-Ⅳ）水平与治疗前相比无明显差异。治疗后24周HA、LN、PC-Ⅲ、C-Ⅳ水平与治疗前相比差异有统计学意义。结论丙型肝炎肝硬化患者采用LADR方案抗病毒治疗,可以改善肝硬化患者的肝功能,降低肝纤维化程度,抑制病毒复制,且效果安全可靠。     

慢性乙型肝炎患者初始抗病毒治疗时机选择

过去的10余年,对于慢性乙型肝炎（CHB）的抗病毒治疗已取得了长足的进步。现阶段,对于临床医生来说,问题不再是哪些患者是抗病毒治疗的对象,而是初始抗病毒时机选择,即何时开始抗病毒治疗。     

慢性丙型肝炎患者治疗依从性及影响因素的研究

目的了解慢性丙型肝炎患者接受干扰素联合利巴韦林治疗的依从性及影响因素。方法分析2010年1月至2012年12月的306例住院治疗的慢性丙型肝炎患者的相关资料,包括一般资料、病史资料以及慢性丙型肝炎知识问卷。结果 306例患者中完成规范抗病毒治疗的104例,因干扰素不良反应不建议继续治疗的34例,未经医生同意不完成规范抗病毒治疗的168例。Logistic回归分析显示男性(OR=3.845,P=0.004)、费用子女承担(OR=4.264,P=0.002)、对不良反应耐受程度高(OR=3.436,P=0.013)以及丙型肝炎知识知晓程度好(OR=19.537,P<0.001)是慢性丙型肝炎患者接受干扰素联合利巴韦林治疗依从性的影响因素。结论慢性丙型肝炎患者接受干扰素治疗依从性较差,建议加强健康教育,积极针对药物不良反应进行干预,以期提高慢性丙型肝炎患者接受干扰素联合利巴韦林治疗的依从性。     

肝脂肪变性促进慢性丙型肝炎病程进展的研究

目的 研究脂肪变性在慢性丙型肝炎疾病进程中的作用.方法 收集治疗前行肝穿刺病理检查的慢性丙型肝炎患者159例,按照感染HCV基因亚型分为基因1b型组、基因2a型组和其他基因型组,荧光定量PCR法检测所有病例血清HCV载量,组织学评估各组穿刺肝组织炎症坏死、纤维化和肝细胞脂肪变性程度.结果 HCV基因1b型和2a型感染患者占总病例的65.41%,63.52%(101/159)的慢性丙型肝炎患者发生肝细胞脂肪变性,不同基因型组间脂肪变性程度无统计学差异.不同基因型组HCV慢性感染者间炎症活动度、纤维化程度和脂肪变性程度无统计学差异(P均>0.05).肝脂肪变性与肝纤维化和炎症活动度均密切相关(r值分别为0.34和0.29,P均<0.01),但HCV感染病毒量与脂肪变性、肝纤维化和炎症活动度间无明显相关性.结论 脂肪变性促进慢性丙型肝炎病程进展.     

慢性丙型肝炎治疗进展

慢性丙型肝炎(CHC)是由丙型肝炎病毒(HCV)引起的一种隐匿性发病、持续性进展的慢性、传染性疾病,通过有效的药物及时进行抗病毒治疗后,可以达到清除病毒、改善肝组织炎     

干扰素治疗慢性丙型肝炎患者合并甲状腺功能异常

目的观察应用干扰素联合利巴韦林治疗慢性丙型肝炎对甲状腺功能的影响。方法慢性丙型肝炎患者共计213例,在应用干扰素联合利巴韦林抗病毒治疗前以及治疗后每3个月检测甲状腺功能及甲状腺抗体水平,观察甲状腺功能异常情况。结果 213例患者累计甲状腺功能异常60例,占28.17%;其中治疗前甲状腺功能异常19例,占8.92%,治疗后甲状腺功能异常41例,占19.25%,治疗前后甲状腺功能异常率比较差异有统计学意义(P<0.05),经综合治疗后均完成抗病毒疗程。结论干扰素联合利巴韦林治疗慢性丙型肝炎患者可引起甲状腺功能异常,其中以亚临床甲状腺功能减退症常见,经治疗后不影响继续抗病毒治疗。     

白细胞介素-18和白细胞介素-10在慢性丙型肝炎抗病毒治疗中的动态变化

目的:观察血清细胞因子白细胞介素-18(IL-18)和白细胞介素-10(IL-10)在慢性丙型肝炎患者干扰素联合利巴韦林抗病毒治疗过程中的动态变化,探讨它们在慢性丙型肝炎发病中的作用及抗病毒治疗对它们水平的影响.方法:采用酶联免疫吸附法(EuSA)检测30例正常人、82例慢性丙型肝炎患者抗病毒治疗前、治疗4、8、12、24周血清中IL-18和IL-10的水平,同时检测肝功能和HCV RNA(定量PCR法).结果:慢性丙型肝炎患者治疗前血清IL-18和IL-10的水平显著高于正常人(P<0.01),其值与丙氨酸氨基转移酶(ALT)活性呈显著正相关.抗病毒有效者,在治疗4个时间点血清IL-18和IL-10的水平均较治疗前显著下降(P<0.05);完全应答组较无应答组细胞因子水平治疗前后改变更显著.结论:细胞因子IL-18和IL-10与慢性丙型肝炎肝脏炎症活动和肝脏损害密切相关.干扰素能够调节机体的免疫状态而发挥抗病毒作用.     

慢性丙型肝炎与糖尿病关系的研究进展

慢性丙型肝炎与2型糖尿病共存这一现象是近年大家关注和研究的热点，糖尿病的出现是因为丙型肝炎病毒（HCV）感染导致糖尿病发病率升高，还是糖尿病患者易于感染HCV，糖代谢紊乱是肝损害所继发还是HCV直接干扰所致，慢性丙型肝炎合并2型糖尿病后是否增加肝纤维化和肝癌的发生率，是否影响长效干扰素的治疗应答率，是否改变女性丙型肝炎患者的生存期，两者共存的2型糖尿病与普通糖尿病在临床特征、治疗以及预后上有何区别，还有诸多临床医师感到困惑的问题。现将近期国外流行病学调查、临床病例分析、动物实验研究的新进展做一综述。     

2015中国慢性乙型肝炎指南更新要点解析

随着国内外研究进展,在中华医学会第十七次全国病毒性肝炎及肝病学术会议上发布了2015版《中国慢性乙型肝炎防治指南》,概念明确、内容细化,总结了流行病学、发病机制、肝纤维化非侵袭性诊断等方面的新进展,突出抗病毒治疗的重要性,包括特殊人群抗病毒均给出详实推荐意见,同时指出未来乙型肝炎防治的方向。总之,新版指南的颁布必将有助于进一步规范与提高我国乙型肝炎防治水平。     

Managing chronic hepatitis. Recent advances in diagnosis and treatment

A variety of effective therapies are now available for chronic hepatitis of various causes. Most patients with autoimmune chronic active hepatitis respond to immunosuppressive therapy, and those with Wilson's disease respond to copper-chelating therapy. Patients with drug-induced chronic hepatitis improve with cessation of the medication. About 30% to 40% of patients with chronic hepatitis B infection respond to interferon alfa, as do about 50% of those with chronic hepatitis C infection.     

Future treatment of chronic hepatitis C

The current standard therapy for chronic hepatitis C is peginterferon plus ribavirin and yields a sustained virological response rate of approximately 50% overall. Over the past 2-3 years, many new therapeutic agents directed at a number of different viral targets have entered into development for the treatment of patients with chronic hepatitis C. Many of these agents exhibit high levels of potency against the hepatitis C virus and have a rapid onset of activity. Some agents have been abandoned because of lack of efficacy or toxicity, but many others have shown promise and are undergoing further testing. Although debated, new therapies in the immediate future will most likely be used in combination with peginterferon, either alone or with ribavirin. This concise review is focused on new drugs undergoing development for the treatment of patients with chronic hepatitis C, and on drugs that have shown efficacy in preliminary investigations and progressed to Phase II or III trials. This information should allow physicians involved in the care of patients with chronic hepatitis C to provide realistic expectations of what types of drugs are progressing in clinical development, the likelihood that new treatment will include peginterferon with or without ribavirin, and when these novel therapies might become available.     

Recent advances of basic research and clinical application of lactoferrin as an antiviral reagent against chronic hepatitis C

Hepatitis C virus(HCV), discovered in 1989, is the major causative agent of chronic viral hepatitis. Most patients progress to liver cirrhosis and hepatocellular carcinoma. In the therapy of hepatitis C, only interferon has been used effectively as an anti-HCV reagent in Japan, but its effectiveness is limited to about 30% of cases. Using human hepatocyte cell line which could support efficient HCV replication, we previously found that lactoferrin inhibited HCV infection, and demonstrated that this inhibiting activity was due to the interaction of lactoferrin with HCV. Further analysis found that the carboxyl region of lactoferrin, which partially shows amino acid sequence homology to human CD81, specifically bound to the HCV E2 envelope protein, and identified a 33 amino acids as a critical binding domain of lactoferrin. On the other hand, it has been shown that bovine lactoferrin was effective in some patients with chronic hepatitis received an 8-week course of lactoferrin treatment. Further clinical trials showed that lactoferrin is a promising candidate for adjuvant therapy with interferon in patients with chronic hepatitis C.     

Recent progress and prospective view of chronic hepatitis C research

Hepatitis C is a major public health problem because of the high incidence of its related hepatocellular carcinoma. With the progress in molecular biology, the mechanisms of persistent infection, chronic inflammation, and hepatocarcinogenesis have been described in terms of virus, host, and virus-cell interactions. On the other hand, clinically, some recent studies using a large number of subjects with long-term observation after interferon therapy showed that improving hepatic inflammation might be associated with regression or retardation of fibrosis. However, current therapy for hepatitis C, although effective in some patients, is problematic even though the efficacy of combination therapy, interferon plus ribavirin, or PEG-interferon has been reported. Here we review the progress and discuss the prospective view of hepatitis C virus research from a point of view of both basic and clinical aspects.