American Gastroenterological Association Technical Review on the Management of Hepatitis C
2006; Elsevier BV; Volume: 130; Issue: 1 Linguagem: Inglês
10.1053/j.gastro.2005.11.010
ISSN1528-0012
AutoresJules L. Dienstag, John G. McHutchison,
Tópico(s)Hepatitis B Virus Studies
ResumoIn the United States, hepatitis C virus (HCV) infection accounts for approximately 40% of all chronic liver disease, results in an estimated 8000–10,000 deaths annually, and is the most frequent indication for liver transplantation.1Lauer G.M. Walker B.D. Hepatitis C virus infection.N Engl J Med. 2001; 345: 41-52Google Scholar, 2Alter M.J. Mast E.E. The epidemiology of viral hepatitis in the United States.Gastroenterol Clin North Am. 1994; 23: 437-455Google Scholar, 3World Health OrganizationGlobal surveillance and control of hepatitis C. Report of a WHO consultation organized in collaboration with the Viral Hepatitis Prevention Board, Antwerp, Belgium.J Viral Hepat. 1999; 6: 35-47Google Scholar, 4Bellentani S. Tiribelli C. Saccoccio G. Sodde M. Fratti N. De Martin C. Cristianini G. Dionysos Study GroupPrevalence of chronic liver disease in the general population of northern Italy the Dionysos study.Hepatology. 1994; 20: 1442-1449Google Scholar, 5Kim W.R. Gross Jr, J.B. Poterucha J.J. Locke III, G.R. Dickson E.R. Outcome of hospital care of liver disease associated with hepatitis C in the United States.Hepatology. 2001; 33: 201-206Google Scholar, 6Detre K.M. Belle S.H. Lombardero M. Liver transplantation for chronic viral hepatitis.Viral Hepat Rev. 1997; 2: 219-228Google Scholar, 7Féray C. Gigou M. Sameul D. Paradis V. Wilber J. David M.F. Urdea M. Reynes M. Brechot C. Bismuth H. The course of hepatitis C virus infection after liver transplantation.Hepatology. 1994; 20: 1137-1143Google Scholar The Third National Health and Nutrition Examination Survey, conducted between 1988 and 1994 among 21,000 adults, revealed antibodies to HCV (anti-HCV) in 1.8%, three fourths of whom had detectable serum HCV RNA levels.8Alter M.J. Kruszon-Moran D. Nainan O.V. McQuillan G.M. Gao F. Moyer L.A. Kaslow R.A. Margolis H.S. The prevalence of hepatitis C virus infection in the United States, 1988 through 1994.N Engl J Med. 1999; 341: 556-562Google Scholar Generalized to the population of the United States, these findings suggest that approximately 4 million persons have been infected and that 3 million have chronic HCV infection. Among those aged 40–59 years and among black subjects, the prevalence of anti-HCV was even higher. Moreover, the results of such serologic surveys may actually provide conservatively low estimates, failing to include representative proportions of high-risk populations such as injection drug users, incarcerated persons, and homeless persons. Projections based on the current prevalence of infection and anticipated rates of progression raise concerns over the potential impact of HCV during the next 2 decades. A computer cohort simulation of the US population for 2010–2019 suggests that the morbidity and mortality associated with chronic hepatitis C will increase dramatically, resulting in 165,900 deaths from chronic liver disease, 27,200 deaths from hepatocellular carcinoma (HCC), and $10.7 billion in direct medical expenditures related to HCV.5Kim W.R. Gross Jr, J.B. Poterucha J.J. Locke III, G.R. Dickson E.R. Outcome of hospital care of liver disease associated with hepatitis C in the United States.Hepatology. 2001; 33: 201-206Google Scholar, 9Wong J.B. McQuillan G.M. McHutchison J.G. Poynard T. Estimating future hepatitis C morbidity, mortality, and costs in the United States.Am J Public Health. 2000; 90: 1562-1569Google Scholar, 10Kim W.R. The burden of hepatitis C in the United States.Hepatology. 2002; 36: S30-S34Google Scholar, 11Kim W.R. Brown Jr, R.S. Terrault N.A. El-Serag H. Burden of liver disease in the United States summary of a workshop.Hepatology. 2002; 36: 227-242Google Scholar, 12Davis G.L. Albright J.E. Cook S.E. Rosenberg D. Projecting future complications of chronic hepatitis C in the United States.Liver Transpl. 2003; 9: 331-338Google Scholar On a global scale, based on current estimates that as many as 175 million persons are infected with HCV, the morbidity, mortality, and current and projected health care costs associated with HCV infection are staggering. These alarming statistics and projections focus attention on the critical need to prevent and control HCV infection. Although effective vaccines to prevent HCV infection are not likely to be practical, virtual elimination of HCV from the blood supply by donor screening and changes in behavior to prevent HCV infection associated with injection drug use have reduced dramatically the frequency of new infections.13Alter H.J. Purcell R.H. Shih J.W. Melpolder J.C. Houghton M. Choo Q.-L. Kuo G. Detection of antibody to hepatitis C virus in prospectively followed transfusion recipients with acute and chronic non-A, non-B hepatitis.N Engl J Med. 1989; 321: 1494-1500Google Scholar, 14Donahue J.G. Munoz A. Ness P.M. Brown D.E.J. Yawn D.H. McAllister H.A.J. Reitz B.A. Nelson K.E. The declining risk of post-transfusion hepatitis C virus infection.N Engl J Med. 1992; 327: 369-373Google Scholar, 15Schreiber G.B. Busch M.P. Kleinman S.H. Korelitz J.J. The risk of transfusion-transmitted viral infection.N Engl J Med. 1996; 334: 1685-1690Google Scholar, 16Aach R.D. Stevens C.E. Hollinger F.B. Mosley J.W. Peterson D.A. Taylor P.E. Johnson R.G. Barbosa L.H. Nemo G.J. Hepatitis C virus infection in post-transfusion hepatitis an analysis with first- and second-generation assays.N Engl J Med. 1991; 325: 1325-1329Google Scholar, 17Williams I. Epidemiology of hepatitis C in the United States.Am J Med. 1999; 107: 2S-9SGoogle Scholar, 18Orland J.R. Wright T.L. Cooper S. Acute hepatitis C.Hepatology. 2001; 33: 321-327Google Scholar, 19Stramer S.L. Glynn S.A. Kleinman S.H. Strong M. Caglioti S. Wright D.J. Dodd R.Y. Busch M.P. National Heart Lung and Blood Institute Nucleic Acid Test Study GroupDetection of HIV-1 and HCV infections among antibody-negative blood donors by nucleic acid-amplification testing.N Engl J Med. 2004; 351: 760-768Google Scholar Still, because of the residua of several decades of high-incidence acute hepatitis C in at-risk populations, a large reservoir of chronic HCV infection persists.20Armstrong G.L. Alter M.J. McQuillan G.M. Margolis H.S. The past incidence of hepatitis C virus infection implications for the future burden of chronic liver disease in the United States.Hepatology. 2000; 31: 777-782Google Scholar Fortunately, substantial progress in antiviral therapy has taken place; this chronic viral disease can be cured in a substantial proportion of patients, and the ultimate impact of hepatitis C is likely to be minimized by these and future advances in management.21Buti M. San Miguel R. Brosa M. Cabasés J.M. Medina M. Casado M.A. Fosbrook L. Esteban R. Estimating the impact of hepatitis C virus therapy on future liver-related morbidity, mortality and costs related to chronic hepatitis C.J Hepatol. 2005; 42: 639-645Google Scholar To support this technical review,22American Gastroenterological AssociationPosition and policy statement policy statement on the use of medical practice guidelines by managed care organizations and insurance carriers.Gastroenterology. 1995; 108: 925-926Google Scholar a comprehensive search of electronic databases (including MEDLINE, the Cochrane Database of Systematic Reviews Database of Abstracts of Reviews of Effectiveness, American College of Physicians Journal Club, British Medical Journal Clinical Evidence, EMB Reviews, CINAHL, EMBASE, and HealthSTAR) was performed by a professional evidence-based medicine company to identify relevant articles from 1990 to 2003. The search was restricted to articles involving human studies that were available in English. Additional relevant articles published after the search was completed that were identified by the authors were also included. In the United States, of the anticipated 3–4 million persons with hepatitis C, only approximately half a million have been treated, and the majority have not been identified. Most diagnoses of chronic hepatitis C are made by medical serendipity, when persons with asymptomatic hepatitis C attempt to donate blood or when they have blood drawn as part of routine medical evaluations or during insurance physical examinations. Because the frequency of hepatitis C in the general population is low (<2%) and because screening tests for anti-HCV, like any other diagnostic test, have a fixed frequency of nonspecificity, routine screening of all asymptomatic adults (who have a low prior probability of HCV infection) is not recommended. For example, among asymptomatic blood donors with an anti-HCV prevalence of 1%–2%, a screening test that is 98%–99% specific is likely to identify as many persons with false-positive as true-positive reactivity. In contrast, among high-risk groups with a high prior probability of true infection (eg, persons who underwent transfusion before 1992 [when donor screening for anti-HCV was introduced], those with a past or recent history of injection drug use, those with hemophilia who received clotting factors before 1987 [when processing to inactivate viruses was introduced], those with frequent percutaneous exposures, those with clinical or biochemical evidence for chronic liver disease, or immigrants from countries with a high prevalence of HCV infection),23Centers for Disease Control and PreventionRecommendations for prevention and control of hepatitis C virus (HCV) infection and HCV-related chronic disease.MMWR Morb Mortal Wkly Rep. 1998; 47: 1-39Google Scholar true-positive results outweigh false-negative results so substantially that a positive test result is highly predictive of the presence of infection. In such populations, even among asymptomatic persons, diagnostic testing for HCV infection has been recommended by the US Public Health Service, expert panels, and professional medical specialty societies.23Centers for Disease Control and PreventionRecommendations for prevention and control of hepatitis C virus (HCV) infection and HCV-related chronic disease.MMWR Morb Mortal Wkly Rep. 1998; 47: 1-39Google Scholar, 24National Institutes of Health Consensus Development ConferenceManagement of hepatitis C.Hepatology. 1997; 26: 1S-156SGoogle Scholar, 25Consensus statement. EASL International Consensus Conference on Hepatitis C.J Hepatol. 1999; 30: 956-961Google Scholar, 26National Institutes of Health Consensus Development Conference statementmanagement of hepatitis C 2002—June 10–12, 2002.Hepatology. 2002; 36: S3-S20Google Scholar Recently, the US Preventive Services Task Force concluded, based on a literature-based analysis, that even among high-risk groups and even though antiviral therapy is effective in treating hepatitis C, insufficient data exist to demonstrate that screening in this setting improves long-term outcomes.27U.S. Preventive Services Task ForceScreening for hepatitis C virus infection in adults recommendation statement.Ann Intern Med. 2004; 140: 462-464Google Scholar, 28Chou R. Clark E.C. Helfand M. Screening for hepatitis C virus infection a review of the evidence for the U.S. Preventive Services Task Force.Ann Intern Med. 2004; 140: 465-479Google Scholar Although such long-term outcome data have yet to be developed, other professional societies and the American Gastroenterological Association take issue with the conclusion of the US Preventive Services Task Force that data do not warrant a recommendation for screening of high-risk persons for hepatitis C. Based on many factors (the documented progression, albeit slow in most cases, of chronic hepatitis C to cirrhosis, hepatic decompensation, HCC, liver transplantation, and/or death7Féray C. Gigou M. Sameul D. Paradis V. Wilber J. David M.F. Urdea M. Reynes M. Brechot C. Bismuth H. The course of hepatitis C virus infection after liver transplantation.Hepatology. 1994; 20: 1137-1143Google Scholar, 29Freeman A.J. Dore G.J. Law M.G. Thorpe M. Von Overbeck J. Lloyd A.R. Marinos G. Kaldor J.M. Estimating progression to cirrhosis in chronic hepatitis C virus infection.Hepatology. 2001; 34: 809-816Google Scholar, 30Tong M.J. El-Farra N.S. Reikes A.R. Co R.L. Clinical outcomes after transfusion-associated hepatitis C.N Engl J Med. 1995; 332: 1463-1466Google Scholar, 31Niederau C. Lange S. Heintges T. Erhardt A. Buschkamp M. Hurter D. Nawrocki M. Kruska L. Hensel F. Petry W. Haussinger D. Prognosis of chronic hepatitis C results of a large, prospective cohort study.Hepatology. 1998; 28: 1687-1695Google Scholar, 32Yano M. Kumada H. Kage M. Ikeda K. Shimamatsu K. Inoue O. Hashimoto E. Lefkowitch J.H. Ludwig J. Okuda K. The long-term pathological evolution of chronic hepatitis C.Hepatology. 1996; 23: 1334-1340Google Scholar, 33Matsumara H. Moriyama K. Goto I. Okubo J. Arakawa T. Natural course of progression of fibrosis in Japanese patients with chronic liver disease type C—a study of 527 patients at one establishment.J Viral Hepat. 2000; 7: 268-275Google Scholar, 34Takahashi M. Yamada G. Miyamoto R. Doi T. Endo H. Tsuji T. Natural course of chronic hepatitis C.Am J Gastroenterol. 1993; 88: 240-243Google Scholar, 35Fattovich G. Giustina G. Degos F. Tremolada F. Diodati G. Almasio P. Nevens F. Solinas A. Mura D. Brouwer J.T. Thomas H. Njapoum C. Casarin C. Bonetti P. Fuschi P. Basho J. Tocco A. Bhalla A. Galassini R. Noventa F. Schalm S.W. Realdi G. Morbidity and mortality in compensated cirrhosis type C a retrospective follow-up study of 384 patients.Gastroenterology. 1997; 112: 463-472Abstract Full Text Full Text PDF Scopus (1262) Google Scholar, 36Di Bisceglie A.M. Hepatitis C and hepatocellular carcinoma.Hepatology. 1997; 26: 34S-38SGoogle Scholar, 37El-Serag H.B. Hepatocellular carcinoma and hepatitis C in the United States.Hepatology. 2002; 36: S74-S83Google Scholar, 38Kiyosawa K. Sodeyama T. Tanaka E. Gibo Y. Yoshizawa K. Nakano Y. Furuta S. Akahane Y. Nishioka K. Purcell R.H. et al.Interrelationship of blood transfusion, non-A, non-B hepatitis and hepatocellular carcinoma analysis by detection of antibody to hepatitis C virus.Hepatology. 1990; 12: 671-675Google Scholar, 39Ikeda K. Saitoh S. Suzuki Y. Kobayashi M. Tsubota A. Koida I. Arase Y. Fukuda M. Chayama K. Murashima N. Kumada H. Disease progression and hepatocellular carcinogenesis in patients with chronic viral hepatitis a prospective observation of 2215 patients.J Hepatol. 1998; 28: 930-938Google Scholar; the documented benefits of antiviral therapy in curing this viral disease in half of treated persons [side effects notwithstanding]40Manns M.P. McHutchison J.G. Gordon S.C. Rustgi V.K. Shiffman M. Reindollar R. Goodman Z.D. Koury K. Ling M. Albrecht J.K. Peginterferon alfa-2b plus ribavirin compared with interferon alfa-2b plus ribavirin for initial treatment of chronic hepatitis C a randomised trial.Lancet. 2001; 358: 958-965Abstract Full Text Full Text PDF Scopus (5923) Google Scholar, 41Fried M.W. Shiffman M.L. Reddy K.R. Smith C. Marinos G. Goncales Jr, F.L. Haussinger D. Diago M. Carosi G. Dhumeaux D. Craxi A. Lin A. Hoffman J. Yu J. Peginterferon alfa-2a plus ribavirin for chronic hepatitis C virus infection.N Engl J Med. 2002; 347: 975-982Google Scholar, 42Hadziyannis S.J. Sette H.J. Morgan T.R. Balan V. Diago M. Marcellin P. Ramadori G. Bodenheimer H.J. Bernstein D. Rizzetto M. Zeuzem S. Pockros P.J. Lin A. Ackrill A.M. PEGASYS International Study GroupPeginterferon-alpha2a and ribavirin combination therapy in chronic hepatitis C a randomized study of treatment duration and ribavirin dose.Ann Intern Med. 2004; 140: 346-355Google Scholar; the slowing among treated persons in progression of fibrosis and even the reversal of fibrosis and cirrhosis among treated patients43Shindo M. Di Bisceglie A.M. Hoofnagle J.H. Long-term follow-up of patients with chronic hepatitis C treated with alpha-interferon.Hepatology. 1992; 15: 1013-1016Google Scholar, 44Poynard T. McHutchison J. Davis G.L. Esteban-Mur R. Goodman Z. Bedossa P. Albrecht J. Impact of interferon alfa-2b and ribavirin on progression of liver fibrosis in patients with chronic hepatitis C.Hepatology. 2000; 32: 1131-1137Google Scholar, 45Shiratori Y. Imazeki F. Moriyama M. Yano M. Arakawa Y. Yokosuka O. Kuroki T. Nishiguchi S. Sata M. Yamada G. Fujiyama S. Yoshida H. Omata M. 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Yokosuka O. Kinoyama S. Yamada G. Omata M. IHIT Study GroupInterferon therapy reduces the risk for hepatocellular carcinoma national surveillance program of cirrhotic and noncirrhotic patients with chronic hepatitis C in Japan.Ann Intern Med. 1999; 131: 174-181Google Scholar, 49Nishiguchi S. Kuroki T. Nakatani S. Morimoto H. Takeda T. Nakajima S. Shiomi S. Seki S. Kobayashi K. Otani S. Randomised trial of effects of interferon-α on incidence of hepatocellular carcinoma in chronic active hepatitis C with cirrhosis.Lancet. 1995; 346: 1051-1055Abstract Full Text PDF Scopus (902) Google Scholar; and the impact of antiviral therapy on prolonging survival50Yoshida H. Arakawa Y. Sata M. Nishiguchi S. Yano M. Fujiyama S. Yamada G. Yokosuka O. Shiratori Y. Omata M. Interferon therapy prolonged life expectancy among chronic hepatitis C patients.Gastroenterology. 2002; 123: 483-491Abstract Full Text Full Text PDF Scopus (217) Google Scholar), the American Gastroenterological Association advocates strongly the position that members of such high-risk groups, even those who are asymptomatic, should be screened for evidence of hepatitis C infection. Patients in these high-risk groups, and especially those with an established diagnosis of hepatitis C, should be counseled about the natural history of hepatitis C; availability, effectiveness, and side effects of therapy; avoidance of alcohol; risk of sexual transmission; and US Public Health Service recommendations for hepatitis A and B vaccination.23Centers for Disease Control and PreventionRecommendations for prevention and control of hepatitis C virus (HCV) infection and HCV-related chronic disease.MMWR Morb Mortal Wkly Rep. 1998; 47: 1-39Google Scholar Recommendation category: III22American Gastroenterological AssociationPosition and policy statement policy statement on the use of medical practice guidelines by managed care organizations and insurance carriers.Gastroenterology. 1995; 108: 925-926Google Scholar, 51NHS Center for Reviews and DisseminationUndertaking systematic reviews of research on effectiveness. University of York, York1996Google Scholar (Table 1)Table 1Coding System for Hierarchy of Evidence Adopted by the American Gastroenterological AssociationLevel of evidenceIWell-designed RCTsII-1aWell-designed controlled trials with pseudo-randomizationII-1bWell-designed controlled trials with no randomizationII-2aWell-designed cohort (prospective) study with concurrent controlsII-2bWell-designed cohort (prospective) study with historical controlsII-2cWell-designed cohort (retrospective) study with concurrent controlsII-3Well-designed case-control (retrospective) studyIIILarge differences from comparisons between times and/or places with and without intervention (in some circumstances these may be equivalent to level II or I)IVOpinions of respected authorities based on clinical experience; descriptive studies; reports of expert committeesNOTE. In an attempt to standardize recommendations, the American Gastroenterological Association Practices Guidelines Committee has developed categories of evidence based on the quality of the data supporting specific recommendations,22American Gastroenterological AssociationPosition and policy statement policy statement on the use of medical practice guidelines by managed care organizations and insurance carriers.Gastroenterology. 1995; 108: 925-926Google Scholar as adapted from CRD report #4.51NHS Center for Reviews and DisseminationUndertaking systematic reviews of research on effectiveness. University of York, York1996Google Scholar These are noted at the end of each guideline. When studies of different hierarchical levels support a recommendation, the highest level is cited. Open table in a new tab NOTE. In an attempt to standardize recommendations, the American Gastroenterological Association Practices Guidelines Committee has developed categories of evidence based on the quality of the data supporting specific recommendations,22American Gastroenterological AssociationPosition and policy statement policy statement on the use of medical practice guidelines by managed care organizations and insurance carriers.Gastroenterology. 1995; 108: 925-926Google Scholar as adapted from CRD report #4.51NHS Center for Reviews and DisseminationUndertaking systematic reviews of research on effectiveness. University of York, York1996Google Scholar These are noted at the end of each guideline. When studies of different hierarchical levels support a recommendation, the highest level is cited. After acute HCV infection, most of which is asymptomatic or only mildly symptomatic,52Alter H.J. Seeff L.B. Recovery, persistence, and sequelae in hepatitis C virus infection a perspective on long-term outcome.Semin Liver Dis. 2000; 20: 17-35Google Scholar, 53Hoofnagle J. Hepatitis C the clinical spectrum of disease.Hepatology. 1997; 26: 15S-20SGoogle Scholar recovery is the exception; persistent infection occurs in approximately 85% of cases. Among those with chronic hepatitis C, however, the rate of disease progression is variable, and, to some extent, assessments of the natural history of chronic hepatitis C are colored by selection and referral biases; hepatitis C appears to be a more progressive disease in liver specialty clinics and tertiary care centers30Tong M.J. El-Farra N.S. Reikes A.R. Co R.L. Clinical outcomes after transfusion-associated hepatitis C.N Engl J Med. 1995; 332: 1463-1466Google Scholar but much less so in community practices.29Freeman A.J. Dore G.J. Law M.G. Thorpe M. Von Overbeck J. Lloyd A.R. Marinos G. Kaldor J.M. Estimating progression to cirrhosis in chronic hepatitis C virus infection.Hepatology. 2001; 34: 809-816Google Scholar Retrospective and prospective studies have suggested that progression to cirrhosis during the first 20 years of infection occurs in approximately 20% of patients with transfusion-associated hepatitis and of patients seen in liver clinics30Tong M.J. El-Farra N.S. Reikes A.R. Co R.L. Clinical outcomes after transfusion-associated hepatitis C.N Engl J Med. 1995; 332: 1463-1466Google Scholar, 54Seeff L.B. Natural history of chronic hepatitis C.Hepatology. 2002; 36: S35-S46Google Scholar but in only 7% of patients with community-acquired hepatitis C, only 4% of blood donors with HCV infection, and 2%–4% of young children with transfusion-associated chronic hepatitis C.29Freeman A.J. Dore G.J. Law M.G. Thorpe M. Von Overbeck J. Lloyd A.R. Marinos G. Kaldor J.M. Estimating progression to cirrhosis in chronic hepatitis C virus infection.Hepatology. 2001; 34: 809-816Google Scholar, 55Vogt M. Lang T. Frosner G. Klinger C. Sendl A.F. Zeller A. Wiebecke B. Langer B. Meisner H. Hess J. Prevalence and clinical outcome of hepatitis C infection in children who underwent cardiac surgery before the implementation of blood-donor screening.N Engl J Med. 1999; 341: 866-870Google Scholar A dramatic dichotomy in progression rates, not explained by demonstrable differences in HCV genotype or other viral factors, is reflected by the 0–2% progression to cirrhosis among young women followed up for 17–20 years after acquiring HCV infection from contaminated anti-D Rh globulin56Kenny-Walsh E. Irish Hepatology Research GroupClinical outcomes after hepatitis C infection from contaminated anti-D immune globulin.N Engl J Med. 1999; 340: 1228-1233Google Scholar, 57Wiese M. Berr F. Lafrenz M. Porast H. Oesen U. East German Hepatitis C Study GroupLow frequency of cirrhosis in a hepatitis C (genotype 1b) single-source outbreak in Germany a 20-year multicenter study.Hepatology. 2000; 32: 91-96Google Scholar versus the 30% progression rate in less than 11 years among patients with agammaglobulinemia who received HCV-contaminated intravenous immunoglobulin.58Bjøro K. Frøland S.S. Yun Z. Samdal H.H. Haaland T. Hepatitis C infection in patients with primary hypogammaglobulinemia after treatment with contaminated immune globulin.N Engl J Med. 1994; 331: 1607-1611Google Scholar Estimates based on serial histologic assessments over time or single histologic assessments coupled with assumptions about the duration of HCV infection have suggested that the rate of fibrosis in hepatitis C can be slow, moderate, or rapid32Yano M. Kumada H. Kage M. Ikeda K. Shimamatsu K. Inoue O. Hashimoto E. Lefkowitch J.H. Ludwig J. Okuda K. The long-term pathological evolution of chronic hepatitis C.Hepatology. 1996; 23: 1334-1340Google Scholar, 59Poynard T. Bedossa P. Opolon P. OBSVIRC, METAVIR, CLINIVIR, DOSVIRC GroupsNatural history of liver fibrosis progression in patients with chronic hepatitis C.Lancet. 1997; 349: 825-832Google Scholar, 60Marcellin P. Asselah T. Boyer N. Fibrosis and disease progression in hepatitis C.Hepatology. 2002; 36: S47-S56Google Scholar, 61Ghany M.G. Kleiner D.E. Alter H. Doo E. Khokar F. Promrat K. Herion D. Park Y. Liang T.J. Hoofnagle J.H. Progression of fibrosis in chronic hepatitis C.Gastroenterology. 2003; 124: 97-104Google Scholar; however, progression of fibrosis may not be linear,60Marcellin P. Asselah T. Boyer N. Fibrosis and disease progression in hepatitis C.Hepatology. 2002; 36: S47-S56Google Scholar, 61Ghany M.G. Kleiner D.E. Alter H. Doo E. Khokar F. Promrat K. Herion D. Park Y. Liang T.J. Hoofnagle J.H. 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