《美国肝病研究学会-感染疾病研究学会关于成人感染HCV筛查、管理和治疗指南(2015)》简介

美国肝病研究学会(American Association for the Study of Liver Diseases,AASLD)和美国感染疾病研究学会(Infectious Diseases Society of America,IDSA)联合制定的《美国肝病研究学会-感染疾病研究学会关于成人感染HCV筛查、管理和治疗指南(2015)》已于2015年6月在线发表于《Hepatology》,对丙型肝炎最新筛查、管理、治疗办法进行了具体介绍。本文对该指南推荐意见进行高度概括并予以介绍。     

2014年与2015年欧洲肝病学会抗HCV治疗指南比较

<正>鉴于抗HCV药物研制进展非常迅速,针对抗HCV治疗的指南更新也非常及时。2014年美国感染病学会(Infectious Diseases Society of America,IDSA)及美国肝病学会(American Association for the Study of Liver Diseases,AASLD)联合发布了一部丙型肝炎诊治指南[1],同年世界卫生组织(WHO)发布了关于丙型肝炎管理及治疗的指南[2]。欧洲肝病学会(European Association for the Study of the Liver,EASL)在2014年发布了关     

美国肝病学会儿科肝移植患者长期医学管理实践指南推荐意见

<正>美国肝病学会(AASLD)与美国移植学会近期发布了关于儿科肝移植(liver transplantation,LT)患者的长期医学管理指南,同时北美儿科胃肠病学会也批准了这项指南。在此对指南的推荐意见进行翻译,以供临床参考。建议分级参考表1。     

《2015年美国肝病学会指南更新版:慢性乙型肝炎的治疗》摘译

该指南是美国肝病学会(American Association for the Studyof Liver Diseases,AASLD)对于成人及儿童慢性HBV感染治疗方案的官方推荐.与以往的AASLD指南不同,该指南是遵守医学标准学会可信赖实践指南的准则以及使用“推荐分级的评价、制订与评估”方法制订的.指南编写小组对相关文献进行了全面系统的评价分析以支持指南的推荐意见.读者可通过阅读系统评价分析中的相关内容,以加深对指南的理解.该指南重点关注慢性HBV感染的抗病毒治疗方案,与疾病筛查、预防、监控等相关的内容未详细阐述.关于疾病诊断、监控、预防及特殊人群的治疗(例如:肝移植接受者)也未在该指南中阐述.2009年AASLD指南以及最近发布的世界卫生组织(WHO)指南都是非常好的参考材料.     

高催乳素血症的诊治——介绍美国内分泌学会临床应用指南

美国内分泌学会的临床指南小组遵循国际GRADE组织(Grading of Recommendations,Assessment,Development,and Evaluation goup)的分级推荐标准,结合近期相关领域的研究成果,编写了该指南(以符号(+)○○○、(+)(+)○ ○、(+)(+)(+)○和(+)(+)(+)(+)分别表示从低到高的证据质量).指南建议的内容又分为“推荐”和“建议”,分别用“1”和“2”表示,根据推荐施行,通常对患者利多于弊,而如按建议执行时则需要更多考虑患者的个体化情况.     

从防控危险因素角度看2017美国心脏病学会/美国心脏协会高血压指南

<正>2017年美国心脏协会(American Heart Association,AHA)学术年会上,公布了新版美国心脏病学会(American College of Cardiology,ACC)/AHA高血压指南(新指南)~([1]),此次指南的发布可谓是万众瞩目。指南包含106项推荐,值得我们结合我国国情,深入思考。总体上来说,新指南体现了初始预防(针对危险因素的预防)及一级预防理念在美国整个慢性病防控战略中的全面渗透。     

2013美国心脏病学会/美国心脏学会血脂指南重点推荐

<正>美国心脏病学会(ACC)、美国心脏学会(AHA)与美国心肺血液研究所(NHLBI)联合制定的《2013 ACC/AHA降低成人动脉粥样硬化性心血管疾病(ASCVD)风险之血胆固醇治疗指南》(以下简称新指南)于近期公布,指南英文全文在线发表于11月12日的《循环》(Circulation)杂志和《美国心脏病学学会杂志》(JACC)。新指南确定了适合他汀类药物治疗的四组一级和二级预防患者,四组患者及治疗推荐包括:(1)伴有临床动脉粥样硬化性心血管疾病     

英国2014年《心律植人装置感染的诊断、预防和处理指南》的解读

<正>2014年,英国5个医学学会在JAC(Journal of Antimicrobial Chemotherap)杂志联合发表了《心律植入装置感染的诊断、预防和处理指南》~([1]),该指南是继美国心律学会(HRS)于2009年和美国心脏学会(AHA)于2010年修定发表"心律植入装置感染指南"后,时隔5年发表的同一专题的指南。与以往指南不同,本次指南由英国抗感染治疗学会、英国心律学会、英国心血管病学会、英国心脏瓣膜学会、英国心脏超声学会5个学术组织联手制     

2010年美国肝病学会肝细胞癌诊疗指南介绍

美国杂志于2010年7月在线发布了由Bruix和Sherman共同执笔的美国肝病学会肝细胞癌(HCC)诊断与治疗的临床实践指南,经历若干小修改后正式刊出.现摘译指南中推荐的建议及部分重要的图表.     

《2016年欧洲肝病学会、欧洲糖尿病学会和欧洲肥胖学会临床实践指南:非酒精性脂肪性肝病》摘译

本指南是由欧洲肝病学会(European Association for the Study of the Liver,EASL)、欧洲糖尿病学会(European Association for the Study of Diabetes,EASD)和欧洲肥胖学会(European Association for the Study of Obesity,EASO)共同推出的关于非酒精性脂肪性肝病(NAFLD)的诊断、治疗和随访的临床实践指南.推荐意见依据证据水平(A:高质量;B:中等质量;C:低或极低质量)和推荐强度(1:强烈推荐;2:较弱推荐)分级.     

Autoimmune hepatitis versus viral hepatitis C

Abstract: Numerous viruses are capable of inducing the syndrome of chronic hepatitis. Among them are the hepatitis B, C and D viruses. Out of the most common agents of chronic hepatitis, the hepatitis C virus has been found to be strikingly associated with autoimmune diseases and serological markers of autoimmunity. Conversely, the syndrome of genuine autoimmune hepatitis lacks evidence of previous or ongoing virus infection and is diagnosed by additionally excluding metabolic, toxic, and genetic causes of chronic hepatitis, and by the response to immunosuppressive treatment. This review article summarizes the current knowledge of hepatotropic virus-induced autoimmunity. It focuses on the present molecular and immunological definitions, the clinical and molecular distinction between autoimmune hepatitis and chronic viral hepatitis and the implications for the safe and efficacious therapy of these disease entities.     

Acute hepatitis C

Symptomatic acute hepatitis C occurs in only about 15% of patients who are infected with hepatitis C virus (HCV). Acute hepatitis C is most often diagnosed in the setting of post-exposure surveillance, or seroconversion in high-risk individuals (eg, health-care professionals or injecting drug users) previously known to be seronegative. Although transmission via transfusion and injecting drug use has declined in developed countries, unsafe blood products and medical practices continue to increase transmission of HCV in many developing countries. Clinically, acute hepatitis C can increase concentrations of alanine aminotransferase to ten times the upper limit of normal but almost never causes fulminant hepatic failure. Diagnosis of HCV infection in the acute phase is difficult since production of antibodies against HCV can be delayed by up to 12 weeks, and about a third of infected individuals might not have detectable antibody at the onset of symptoms. Therefore, testing for HCV RNA by PCR is the only reliable test for the diagnosis of acute infection. Symptomatic patients with jaundice have a higher likelihood of spontaneous viral clearance than do asymptomatic patients, and thus should be monitored for at least 12 weeks before initiating antiviral therapy. By contrast, asymptomatic patients have a much lower chance of spontaneous clearance, and might benefit from early antiviral therapy. Antiviral therapy for 12 weeks is generally effective in treating patients who are HCV RNA negative after 4 weeks of treatment; lengthier courses could be needed for those who relapse or fail to show early virological clearance.     

Chronic hepatitis C

The goal of antiviral therapy for patients with chronic hepatitis C virus (HCV) infection is to attain a sustained virologic response (SVR), which is defined as undetectable serum HCV-RNA levels at 6 months after the cessation of treatment. Major improvements in antiviral therapy for chronic hepatitis C have occurred in the past decade. The addition of ribavirin to interferon-alfa therapy and the introduction of pegylated interferon (PEG-IFN) have substantially improved SVR rates in patients with chronic hepatitis C. The optimization of HCV therapy with PEG-IFN and ribavirin continues to evolve. Studies are ongoing that use viral kinetics to tailor therapy to an individual's antiviral response and determine the ideal length of treatment to maximize the chance of SVR. Improved SVR can be achieved with new specific inhibitors that target the HCV NS3/4A protease and the NS5B polymerase. Several long-term follow-up studies have shown that SVR, when achieved, is associated with a very low risk of virologic relapse. Furthermore, antiviral therapy can reduce the morbidity and mortality rates associated with chronic hepatitis C by reducing fibrosis progression, the incidence of cirrhosis, and hepatocellular carcinoma.     

Viral hepatitis C

More than 170 million people worldwide are chronically infected with the hepatitis C virus (HCV), which is responsible for more than 100000 cases of liver cancer per year, with similar numbers of digestive haemorrhage and ascites episodes. Major breakthroughs have been made in diagnosis and treatment, and advances in molecular biology mean that the replicative state of the virus can now be assessed. Genotype and serum viral load are useful predictors of response to treatment. The combination of pegylated interferon and ribavirin can eradicate the virus in more than 50% of patients. These antiviral treatments reduce liver fibrosis progression and can reverse cirrhosis. Unfortunately, even in developed countries, death due to hepatitis C is increasing because of inadequate detection and treatment.     

Chronic hepatitis C

Opinion statement Infection with hepatitis C virus (HCV) accounts for 40% of cases of chronic liver disease in the United States and is now the most common indication for liver transplantation. Estimates suggest that 4 million people (1.8%) of the American population are or have been infected with HCV. Currently, the treatment of choice for patients with chronic HCV infection is recombinant interferon alfa with ribavirin. Pegylated interferons are a promising new development, and in combination with ribavirin, they will rapidly become the standard of care. The goals of therapy are to slow disease progression, improve hepatic histology, reduce infectivity, and reduce the risk of hepatocellular carcinoma. Sustained virologic response, which generally implies the absence of viremia for 6 months or more following completion of therapy, is increasingly being regarded as a cure, with evidence of slowing or even regression of fibrosis on follow-up liver biopsy. A number of factors have been shown to be predictive of a sustained response, including viral genotype other than 1, low serum HCV RNA levels, absence of cirrhosis, younger age, female gender, and shorter duration of infection. Disease severity as assessed by liver biopsy, comorbidities, and possible contraindications to therapy should be weighed in the decision to begin treatment. Counseling patients regarding transmission, natural history, and drug and alcohol abstinence also should be included in management. Close monitoring should be done during treatment for side effects of interferon, including depression and bone marrow suppression. Hemolytic anemia is the major side effect of ribavirin.     

Acute hepatitis C

To understand spontaneous and treatment-related recovery, continuing efforts should be directed toward the study of host-virus interactions during acute hepatitis C. A multidisciplinary approach will be required to generate suitable technical methods, increase clinician and lay awareness, and identify patients promptly following infection. In the confrontation between HCV and the human immune system, such an approach might tip the balance in our favor.