NIH Consensus Statement on Management of Hepatitis C: 2002.
NIH Consensus Statement on Management of Hepatitis C: 2002.
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2002
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目标 为卫生保健提供者、患者和公众提供有关丙型肝炎管理和治疗的当前可用数据的负责任的评估。 参与者 一个由 12 名成员组成的非联邦、非倡导性小组，代表传染病、胃肠病学、肿瘤内科、分子遗传学、老年病学、内科和公众领域。此外，这些相同领域的专家向专家小组和大约 300 名会议观众介绍了数据。 证据 专家的演示；对医疗保健研究和质量机构提供的医学文献进行系统回顾；以及由国家医学图书馆编写的大量丙型肝炎研究论文参考书目。科学证据优先于临床轶事经验。会议流程 专家组在回答预先确定的问题后，根据公开论坛中提出的科学证据和科学文献起草了一份声明。声明草案在会议最后一天进行了全文宣读，并分发给专家和观众征求意见。该小组随后召开执行会议，审议这些意见，并在会议结束时发布了修订后的声明。会议结束后，该声明立即发布在万维网上：http://consensus.nih.gov。本声明是该小组的独立报告，并非 NIH 或联邦政府的政策声明。结论 在美国，新感染丙型肝炎的发病率有所下降。这种下降主要是由于注射吸毒者病例减少（原因尚不清楚），以及在较小程度上由于对献血者进行丙肝病毒检测所致。该病毒通过血液传播，目前这种传播主要通过注射吸毒、与受感染的伴侣或多个伴侣发生性行为以及职业接触等方式进行。大多数感染都会变成慢性，因此 HCV 感染的患病率很高，目前估计约有 300 万美国人患有慢性感染。 HCV 是肝硬化的主要原因，是 HCC 的常见原因，也是美国肝移植的主要原因。与HCV感染相关的疾病谱差异很大。各种研究表明，3% 至 20% 的慢性感染患者将在 20 年内发展为肝硬化，而这些患者有患 HCC 的风险。感染时年龄较大的人、持续接触酒精的患者以及同时感染 HIV 或 HBV 的患者会加速进展为更晚期的肝病。相反，年轻时感染的个体在几十年内很少或没有疾病进展。慢性丙型肝炎感染的诊断通常通过 ALT 水平异常来提示，并通过 EIA 和 HCV RNA 的确认测定来确定。一些敏感和特异性测定现在已部分自动化，用于检测 HCV RNA 和量化病毒水平。尽管病毒水平和疾病表现之间几乎没有相关性，但这些检测已被证明有助于识别那些更有可能从治疗中受益的患者，特别是证明对 SVR 定义的治疗的成功反应。肝活检有助于确定肝病的基线异常，并使患者和医疗保健提供者能够就抗病毒治疗做出决定。无创测试目前无法提供可通过肝活检获得的信息。有关病毒基因型的信息对于指导治疗决策非常重要。基因型 1 在美国最常见，它比基因型 2 或 3 更难治疗。因此，抗病毒治疗的临床试验需要基因分型信息来对受试者进行适当的分层。最近在确定的选定人群中进行的治疗试验清楚地表明，干扰素和利巴韦林的组合比单一疗法更有效。此外，使用聚乙二醇化干扰素的试验已提高了 SVR 率，同时具有相似的毒性特征。然而，结果继续表明，SVR 率在基因 1 感染、HCV RNA 水平较高或纤维化较晚期的患者中不太常见。基因型 1 感染需要治疗 48 周，而基因型 2 和 3 感染则可以接受较短的治疗。在基因型 1 中，缺乏早期病毒学应答（HCV RNA 减少 < 2 个对数）与未能实现 SVR 相关。晚期肝病患者的 SVR 低于无肝硬化患者。正在进行的试验正在探索联合疗法在不同人群中的有效性。在注射吸毒者、艾滋病毒合并感染者、儿童和其他特殊群体中的初步经验表明，在这些人群中可以实现类似的反应。急性丙型肝炎患者可以接受治疗，但抗病毒治疗的具体建议必须等待进一步评估病毒自发清除率并确定开始治疗的最佳时间。血库实践之外的预防措施包括及时识别感染者、认识到围产期传播的可能性、实施安全注射实践、将吸毒者与戒毒治疗计划联系起来，以及实施以社区为基础的教育和支持计划以改变危险行为。其中一些措施已成功用于控制艾滋病毒感染，并且理所当然地，它们对于减少丙型肝炎病毒传播具有重要意义。丙型肝炎诊断和管理的未来进展需要对这种感染的传播保持警惕，将治疗范围扩大到以前未在治疗试验中评估的人群，并引入更有效的疗法。
OBJECTIVE To provide health care providers, patients, and the general public with a responsible assessment of currently available data regarding the management and treatment of hepatitis C. PARTICIPANTS A non-Federal, nonadvocate, 12-member panel representing the fields of infectious diseases, gastroenterology, medical oncology, molecular genetics, geriatrics, internal medicine, and the public. In addition, experts in these same fields presented data to the panel and to a conference audience of approximately 300. EVIDENCE Presentations by experts; a systematic review of the medical literature provided by the Agency for Healthcare Research and Quality; and an extensive bibliography of hepatitis C research papers, prepared by the National Library of Medicine. Scientific evidence was given precedence over clinical anecdotal experience. CONFERENCE PROCESS Answering predefined questions, the panel drafted a statement based on the scientific evidence presented in open forum and the scientific literature. The draft statement was read in its entirety on the final day of the conference and circulated to the experts and the audience for comment. The panel then met in executive session to consider these comments and released a revised statement at the end of the conference. The statement was made available on the World Wide Web at http://consensus.nih.gov immediately after the conference. This statement is an independent report of the panel and is not a policy statement of the NIH or the Federal Government. CONCLUSIONS The incidence of newly acquired hepatitis C infection has diminished in the United States. This decline is largely due to a decrease in cases among IDUs for reasons that are unclear and, to a lesser extent, to testing of blood donors for HCV. The virus is transmitted by blood and such transmission now occurs primarily through injection drug use, sex with an infected partner or multiple partners, and occupational exposure. The majority of infections become chronic, and therefore the prevalence of HCV infections is high, with about 3 million Americans now estimated to be chronically infected. HCV is a leading cause of cirrhosis, a common cause of HCC and the leading cause of liver transplantation in the United States. The disease spectrum associated with HCV infection varies greatly. Various studies have suggested that 3 to 20 percent of chronically infected patients will develop cirrhosis over a 20-year period, and these patients are at risk for HCC. Persons who are older at the time of infection, patients with continuous exposure to alcohol, and those co-infected with HIV or HBV demonstrate accelerated progression to more advanced liver disease. Conversely, individuals infected at a younger age have little or no disease progression over several decades. The diagnosis of chronic hepatitis C infection is often suggested by abnormalities in ALT levels and is established by EIA followed by confirmatory determination of HCV RNA. Several sensitive and specific assays are now partly automated for the purposes of detecting HCV RNA and quantifying the viral level. Although there is little correlation between viral level and disease manifestations, these assays have proven useful in identifying those patients who are more likely to benefit from treatment and, particularly, in demonstrating successful response to treatment as defined by an SVR. Liver biopsy is useful in defining baseline abnormalities of liver disease and in enabling patients and healthcare providers to reach a decision regarding antiviral therapy. Noninvasive tests do not currently provide the information that can be obtained through liver biopsy. Information on the genotype of the virus is important to guide treatment decisions. Genotype 1, most commonly found in the United States, is less amenable to treatment than genotypes 2 or 3. Therefore, clinical trials of antiviral therapies require genotyping information for appropriate stratification of subjects. Recent therapeutic trials in defined, selected populations have clearly shown that combinations of interferons and ribavirin are more effective than monotherapy. Moreover, trials using pegylated interferons have yielded improved SVR rates with similar toxicity profiles. However, results continue to show that the SVR rate is less common in patients with genotype 1 infections, higher HCV RNA levels, or more advanced stages of fibrosis. Genotype 1 infections require therapy for 48 weeks, whereas shorter treatment is feasible in genotype 2 and 3 infections. In genotype 1, the lack of an early virologic response (< 2 log decrease in HCV RNA) is associated with failure to achieve an SVR. The SVR is lower in patients with advanced liver disease than in patients without cirrhosis. Ongoing trials are exploring the usefulness of combination therapy in various populations. Preliminary experience in IDUs, individuals co-infected with HIV, children, and other special groups suggests similar responses are achievable in these populations. Patients with acute hepatitis C may be treated, but specific recommendations for antiviral treatment must await further evaluation of the rate of spontaneous clearance of the virus and determination of the optimal time to initiate treatment. Preventive measures beyond blood-banking practices include prompt identification of infected individuals, awareness of the potential for perinatal transmission, implementation of safe-injection practices, linkage of drug users to drug treatment programs, and implementation of community-based education and support programs to modify risk behavior. Some of these measures have been successfully implemented in the control of HIV infections, and it stands to reason that they would be valuable for reducing HCV transmission. Future advances in the diagnosis and management of hepatitis C require continued vigilance concerning the transmission of this infection, extending treatment to populations not previously evaluated in treatment trials, and the introduction of more effective therapies.