中医治疗重型肝炎进展

重型肝炎是病毒性肝炎中最严重的一种类型。根据起病的缓急及有无慢性肝病基础，可分为急性、亚急性和慢性重型肝炎。急性、亚急性重型肝炎是指既往无慢性肝炎病史，以急剧发病，黄疽迅速加深，内毒素血症，不同程度的精神、神经症状，凝血酶原时间明显延长、凝血酶原活动度低于40％为特点，病情进展快，短期出现肝功能、肾功能衰竭。急性和亚急性重型肝炎出现肝衰竭的期限不同，     

重型肝炎的治疗进展

重型肝炎是病毒性肝炎中最严重的一型,治疗难度大,是病毒性肝炎领域中亟待解决的难题. 1重型肝炎的治疗原则 ①早期诊断,早期治疗.     

重型肝炎

单纯血浆置换治疗慢性重型肝炎32例临床观察——陈伟奇等(江苏泰州市人民医院225300)；《中华现代中西医杂志》，2003，1(11)：980—981[目的：观察单纯血浆置换治疗慢性重型肝炎的疗效、安全性。方法：将慢性重型肝炎60例随机分成治疗组和对照组。治疗组在综     

36例重型肝炎临床救治与预后因素分析

目的探讨影响重型肝炎预后的临床及治疗因素。方法通过分析36例患者的临床资料,了解影响预后的因素。结果凝血酶原活动度≤15%的36例重型肝炎病人,治愈或好转者12例(33.3%),死亡24例(66.7%)。该型肝炎预后与凝血酶原活动度、甲胎蛋白、总胆红素、年龄、并发症、病人心理压力、以及日达仙和抗生素的使用情况等8种因素密切相关。结论重型肝炎预后凶险,需多方防治才能挽救部分病人的生命。     

重型肝炎的临床诊治和研究进展——第六讲 重型肝炎并发上消化道出血的诊治进展

肝脏是合成凝血因子、抗凝血物质、纤溶及抗纤溶物质的主要场所，在清除活化凝血因子和纤溶激活酶过程中起重要作用。当重型肝炎发生和发展过程中患者的凝血-抗凝血系统及纤溶。抗纤溶系统各个环节均发生了障碍，导致凝血功能异常，临床上常发生出血，包括上消化道出血、颅内出血、皮肤瘀斑等。     

重型肝炎的临床诊治和研究进展——第七讲 重型肝炎并发肝肾综合征的诊治进展

肝肾综合征(HRS)是重症肝病患者在无肾脏原发病变的情况下发生的一种进行性功能性肾衰竭，常并发于重型肝炎和肝硬化晚期。其特征为：(1)肾脏无器质性病变，肾小管回吸收功能良好；(2)肝移植后肾功能可完全恢复，而将肾脏移植于非肝病肾衰竭患者，移植肾的功能良好。HRS的发病机制历来存在两种学说，一是“肝肾反射学说”，二是“肾外动脉扩张学说”，两种学说的交汇点，就是肾血流量或灌注压不足、肾小球滤过率下     

血浆置换治疗重型肝炎的临床观察

重型肝炎病死率高 ,目前尚无特效治疗方法。为探讨血浆置换在重型肝炎治疗中的疗效 ,提高成活率 ,我们对 16例重型肝炎病人在内科综合治疗的基础上加用血浆置换治疗 ,取得了一定的疗效 ,现报告如下。材料与方法一、病例为 1998～ 2 0 0 0年我院住院的 33例重型肝炎病人 ,16例为治疗组 ,男 15例 ,女 1例 ,年龄 19～ 5 0岁 ,亚急性重型肝炎 6例 ,慢性重型肝炎 10例 ;17例为对照组 ,男 15例 ,女 2例 ,年龄19～ 6 0岁 ,亚急性重型肝炎 7例 ,慢性重型肝炎 10例。两组病人各型肝炎血清学检查结果见表 1;肝功能情况见表 2。表 1　甲～戊各型肝炎病…     

重型肝炎综合治疗进展的临床教学实践及体会

对于临床肝病工作者而言,慢性病毒性肝炎的抗病毒疗法、重型肝炎的综合治疗以及抗肝纤维化的有效措施仍为今日和未来研究的三大热点。重型肝炎其病理基础为肝功能衰竭及多脏器衰竭引起的一系列临床重症,属危重病急救医学领域之一。也是传染病科、消化内科、普通外科、急诊科和I     

10例亚急性重型肝炎救治体会

从1995年1月～1995年12月我们共收治10例亚急性重型肝炎患者,取得较好治疗效果,现报道如下。 1 一般资料 10例病人中男8例,女2例。年龄最小者23岁,最大者67岁,平均39岁。病原学分型:乙型肝炎病毒感染者7例(早期内毒素血症3例),乙、戊型肝炎病毒重叠感染者1例,戊型肝炎病毒感染者1例,病原未明者1例。血清胆红素定量171～375.8μmol/,凝血酶原活动度<40％者7例、41％～50％者3例。有其他并发症者4例,其中乙、戊型肝炎病毒感染的1例病人合并糖尿病及自发性腹膜炎,乙型肝炎病毒感染的病人中,1例合并自发性腹膜炎,2例合并肝性脑病。10例患者的诊断均符合1995年北京第5次全国传染病寄生虫病学术会议修订的病毒性肝炎诊断标准。     

Natural history of hepatic fibrosis progression in chronic hepatitis C virus infection in India

Background and Aim:  The rate of fibrosis progression per year can predict the time for the development of cirrhosis in chronic hepatitis C (CHC). We assessed the rate of fibrosis progression and the predictors of disease severity in Indian CHC patients.
Methods:  Of the 355 treatment-naïve, histologically-proven CHC patients, the precise duration of infection (from the time of exposure to HCV until liver biopsy) could be determined in 213 patients (age = 41.6 ± 14.7 years, male : female = 139 : 74, genotype 3 = 75%). The rate of fibrosis progression per year was calculated. The correlation of the advanced degree of fibrosis and age, duration of infection, age at the onset of infection, sex, mode of infection, hepatitis C virus (HCV) genotype, histological activity index (HAI), and the presence of diabetes mellitus were studied.
Results:  The median rate of fibrosis progression per year was 0.25 (0.0–1.5) fibrosis units. The fibrosis progression rate was higher in patients who acquired infection at > 30 years of age, those < 30 years (0.33 vs 0.15; P  < 0.001), and those who acquired HCV infection with a history of blood transfusion than with other modes of transmission (0.25 vs 0.19; P  = 0.04). The median time to progress to cirrhosis was 16 years. The multivariate analysis found that the HAI score (odds ratio [OR]= 14.03; P  < 0.001) and the duration of infection > 10 years (OR = 4.83; P  < 0.001) correlated with severe liver disease (fibrosis ≥ 3).
Conclusion:  The median rate of fibrosis progression per year in Indian CHC patients is 0.25 fibrosis units. A higher HAI and longer duration of infection are associated with a significant risk of advanced liver disease, and merit early therapeutic interventions.     

Disease progression and the risk factor analysis for chronic hepatitis C

Background/Aims: The present study aimed to assess the incidence of advanced cirrhotic complications and to identify the risk factors associated with such complications in chronic hepatitis C. Methods: The data of 1137 chronic hepatitis C patients were retrospectively reviewed. We analysed the incidence rate and risk factors for ‘disease progression’, as defined by the occurrence of an increase of at least 2 points in the Child–Pugh score, oesophageal/gastric variceal bleeding, spontaneous bacterial peritonitis, hepatic encephalopathy, death related to liver disease or development of hepatocellular carcinoma (HCC). Results: Of the 1137 patients enrolled for analysis, 490 patients received antiviral treatment. The overall annual incidence rate of disease progression was 0.8 and 3.7% for patients with and without antihepatitis C virus (anti‐HCV) therapy respectively. The development of HCC was the most common cause of disease progression. In patients with anti‐HCV therapy, treatment response, platelet level and aspartate aminotranferase:platelet ratio index (APRI) were independent factors associated with disease progression. For those without anti‐HCV therapy, older age, male sex, diabetes, platelet level and APRI were independent factors for disease progression. APRI was strongest predictor for disease progression. Conclusions: The present study demonstrated that the development of HCC was the most common cause of disease progression, and we also identified the risk factors associated with disease progression. Thus, patients at such risks need close monitoring for disease progression, and especially for detecting HCC. Moreover, the active application of antiviral therapy and efforts to improve the antiviral response are required.     

Studying the association of microRNA‐210 level with chronic hepatitis B progression

We studied the relationship between hypoxia and microRNA‐210 (miR‐210) levels, the miR‐210 levels in patients with hepatitis B and the roles of miR‐210 in liver inflammation. We used the concanavalin A (Con A) murine hepatitis model and inflammation, hypoxia and miR‐210 levels were examined. In these patients, we studied serum miR‐210 levels and clinical indexes related to hepatitis in 90 patients with different stages of chronic hepatitis B and 30 controls. Two functional assays of miR‐210 in vitro under hypoxic condition were conducted. The animal experiments indicated that the liver and serum miR‐210 levels significantly increased with liver hypoxia and inflammation. In humans, serum miR‐210 levels enhanced with hepatitis severity and were related to serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TB) and prothrombin activity (PTA) levels. The miR‐210 functional assays showed that miR‐210 elevation might be related to the decreases in HepG2.2.15 cell dehydrogenase activity and HBV replication under hypoxic conditions. Because the liver inflammation causes liver hypoxia which also results in liver and serum miR‐210 level elevation, the serum miR‐210 level may serve as a molecular biomarker for the severity of hepatitis and increases in liver miR‐210 that we see may be a response of hepatocytes to hypoxia during hepatitis progression.     

Monitoring SCCA-IgM complexes in serum predicts liver disease progression in patients with chronic hepatitis

Summary.  About 30% of the patients with chronic hepatitis develop a progressive liver disease and one of the most intriguing issues is the detection of noninvasive markers for fibrosis stage and disease progression. High levels of squamous cell carcinoma antigen (SCCA)-immunoglobulin M (IgM) are detectable in hepatocellular carcinoma and their increase in cirrhotic patients can predict tumour development. As SCCA-IgM can also be detectable at low percentages in patients with chronic hepatitis, the aim of this study was to assess SCCA-IgM complexes in relation to disease outcome in this group of patients. An ELISA assay was used to determine the presence of SCCA-IgM in 188 patients with chronic hepatitis and in 100 controls. An additional serum sample was available after a median period of 6 years in 57 untreated patients: these patients were subdivided in group A, including eight patients with a fibrosis score increase ≥2 in a second liver biopsy and group B, including 49 patients without fibrosis progression during a similar follow up. SCCA-IgM complexes were detectable in 63 of 188 (33%) patients but in none of the controls. A significant increase of SCCA-IgM levels over time was observed in patients with fibrosis progression (mean ± SD: 117 ± 200 U/mL/year), but not in those without histologic deterioration (mean ± SD: –8.8 ± 31 U/mL/year, P  <   0.0001). In conclusion, monitoring SCCA-IgM levels over time appears a useful approach to identify patients with chronic hepatitis at higher risk for cirrhosis development.     

The treatment of chronic hepatitis C in HIV-infected patients: a meta-analysis

OBJECTIVE: Hepatitis C virus (HCV) disease progression appears to be accelerated in patients coinfected with HIV. The impact of HCV on coinfected patients is being realized as patients are now living longer. The objective of our study was to further elucidate incremental improvement and safety concerns with combinations of pegylated interferon (peginterferon), interferon and ribavirin based on data obtained from prospective randomized controlled trials. METHODS: A search of MEDLINE and the Cochrane database for material published between 1966 and 29 August 2005 and a hand search of abstracts from national meetings held between 2001 and August 2005 were performed. Trials comparing the use of peginterferon plus ribavirin vs peginterferon or interferon plus ribavirin were assessed. RESULTS: In six randomized controlled trials, 1756 patients were randomized. Sustained virological response was greater for patients treated with peginterferon plus ribavirin compared with patients treated with interferon plus ribavirin [odds ratio (OR) 3.00; 95% confidence interval (CI) 2.27-3.96]. This increased sustained virological response with peginterferon and ribavirin was found for patients with HCV genotype 1 or 4 (OR 4.40; 95% CI 2.75-7.03) and genotype 2 or 3 (OR 2.56; 95% CI 1.71-3.85). Sustained virological responses were also higher with peginterferon and ribavirin as compared with peginterferon monotherapy (OR 2.60; 95% CI 1.84-3.67). Severe adverse effects (OR 1.09; 95% CI 0.74-1.4) and withdrawal rates (OR 0.97; 95% CI 0.75-1.25) were similar between patients treated with peginterferon plus ribavirin and patients treated with interferon plus ribavirin. CONCLUSIONS: Patients with chronic HCV/HIV coinfection have a greater likelihood of achieving a sustained virological response with peginterferon plus ribavirin. The likelihoods of serious adverse effects and study withdrawal were similar.     

Development of transient autoimmune hepatitis during interferon treatment of chronic hepatitis B

Summary A 42-year-old man was treated with interferon- for chronic hepatitis B; during the fourth week of treatment he developed an exacerbation of liver disease, and nuclear and smooth muscle autoantibodies, which were previously negative, were detected in very high titers. After discontinuation of interferon therapy, ALT values subsided promptly and autoantibodies disappeared within a few months. This sequence of events strongly suggests a direct relationship between IFN treatment and a self-limited hepatitis with autoimmune markers in this case.     

Fibrosis progression rates between chronic hepatitis B and C patients with elevated alanine aminotransferase levels

BACKGROUND: We evaluated the annual rate of fibrosis progression in chronic hepatitis B and C patients with elevated alanine aminotransferase (ALT) levels. METHODS: Forty-nine chronic hepatitis B patients and 21 chronic hepatitis C patients, each of whom had undergone two or more liver biopsies at an interval of more than 1 year, were enrolled in this retrospective clinical research protocol. The annual rate of fibrosis progression was calculated by dividing the change in fibrosis stage between the first and second liver biopsies by the interval in years between them. RESULTS: The median interval in chronic hepatitis B and C was 3.4 (first and third quartiles, 1.8-4.7) and 3.2 (2.1-6.5) years, respectively. Overall, the mean fibrosis progression rate was 0.21 +/- 0.31 (mean +/- SD) fibrosis units (FU) per year in 49 patients with chronic hepatitis B, and 0.13 +/- 0.18 FU/year in 21 patients with chronic hepatitis C. The ALT level was an independent variable correlating with fibrosis progression. In patients whose median ALT level was 70 IU/l or more, the mean fibrosis progression rate was 0.28 +/- 0.32 FU/year in 36 patients with chronic hepatitis B, and 0.22 +/- 0.23 FU/year in eight patients with chronic hepatitis C. CONCLUSION: This paired-biopsy study of untreated chronic hepatitis B or C demonstrated that fibrosis progression occurred largely in patients with continuously elevated ALT levels even over a relatively short period, and that liver fibrosis might progress by one stage within an average of 4-5 years of follow-up in patients with elevated ALT of 70 IU/l or more.     

Relationship of genotypes of hepatitis B virus to mutations, disease progression and response to antiviral therapy

SUMMARY: Phylogenetic analysis has led to the classification of hepatitis B virus into eight genotypes, designated A to H. The genotypes have differences in biological properties and show heterogeneity in their global distribution. These attributes of the genotypes may account not only for differences in the prevalence of hepatitis B virus mutants in various geographic regions, but also be responsible for differences in the clinical outcome and response to antiviral treatment in different population groups.     

Host immunity influences disease progression and antiviral efficacy in humans infected with hepatitis B virus

Hepatitis B virus (HBV) infection can lead to several severe liver diseases, including hepatitis, cirrhosis and hepatocellular carcinoma, although the underlying mechanisms responsible for the clinical outcome have not been well characterized. In this review, we retrospectively examine the history of immunological responses to HBV infection and summarize the current understanding of innate and adaptive immunity in the context of HBV-associated liver disease. Recent data indicate that the interaction between HBV and the host immune response not only substantially drives disease progression, but also significantly influences antiviral efficacy in HBV-infected individuals. Advances in the field have provided insight into the immunopathology of HBV infection. Based on the characteristics of host immune responses in patients with HBV infection, a ‘climbing slope hypothesis’ is proposed to suggest that therapeutic strategies aimed at modulating the immune activity of the host may represent a complementary approach to antiviral drug treatment for the management of chronically HBV-infected patients.     

丙型肝炎防治指南(2015年更新版)

为规范丙型肝炎的预防、诊断和抗病毒治疗,中华医学会肝病学分会和感染病学分会根据丙型肝炎病毒(HCV)感染的特点、国内外最新的循证医学证据和药物的可及性,于 2015 年组织国内有关专家修订了《丙型肝炎防治指南》.完善的病毒学检测是慢性 HCV 感染筛查、监测、诊断和治疗的基础.根据我国社会和经济发展情况,还需要积极发展适宜于资源有限地区HCV RNA 定量和 HCV 基因分型的检测试剂.政府、社会组织、学术团体、制药企业共同努力,以达到新型抗病毒治疗的可及和可负担.