The natural course of hepatitis C virus infection 18 years after an epidemic outbreak of non-A, non-B hepatitis in a plasmapheresis centre

Datz, Christian; Cramp, M.; Haas, Thorsten; Dietze, Otto; Nitschko, Hans; Froesner, G; Muss, N; Sandhofer, F; Vogel, Wolfgang

doi:10.1136/gut.44.4.563

Cited by 60 publications

(14 citation statements)

References 34 publications

(29 reference statements)

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“…Kenny‐Walsh's data suggest that progression is slower at the beginning and faster later on. This result is consistent with the findings reported by Datz et al [14] and Matsumura et al [15]. However, Poynard et al 's data show another pattern, with progression being more rapid initially, slowing down and then increasing again.…”

Section: Discussionsupporting

confidence: 92%

“…While this assumption is convenient, it may not reflect the true nature of disease progression. For example, Datz et al [14] studied 20 HCV‐infected individuals, and found that the rates of progression are not constant. In one case, fibrosis remained almost static for 11 years before progressing rapidly to advanced cirrhosis within 5 years.…”

Section: Introductionmentioning

confidence: 99%

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Improving the accuracy of long‐term prognostic estimates in hepatitis C virus infection

Wang

Krahn

2004

Journal of Viral Hepatitis

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Obtaining unbiased estimates of HCV prognosis is difficult because of potential biases associated with study design and calculation methods. We propose a new method for estimating fibrosis progression rates. A Markov model with fibrosis health states (F0-F4) was created. The maximum likelihood method was used to estimate stage-specific progression rates. We compared the standard method to the new method using two well-known cohort studies. The known stage distribution at the end of follow-up was compared with stage predicted by the Markov model using both methods of calculating transition rates. We also compared rates obtained using both methods to known fibrosis rates in a series of Monte Carlo simulations. For Kenny-Walsh's study (1999), transition rates between F0-F1, F1-F2, F2-F3, and F3-F4 were 0.042, 0.045, 0.097 and 0.070 fibrosis units/year (new method) and 0.045 units/year (standard method). The new method predicted fibrosis stage and known transition rates in Monte Carlo simulations more accurately. The standard method underestimates 30-year cirrhosis rates by up to 40%. The new (Markov maximum likelihood or MML) method allows accurate estimation of stage-specific transition probabilities from the many studies in which only a single biopsy is available. Application of the method supports the hypothesis that rates of fibrosis vary between stages.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Improving the accuracy of long‐term prognostic estimates in hepatitis C virus infection

Wang

Krahn

2004

Journal of Viral Hepatitis

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“…In a 17‐year follow‐up study of young women infected with HCV from contaminated anti‐D immunoglobulin, most were found to have histological liver inflammation but only 2% (7 of 363) had probable or definite cirrhosis 1 . In contrast, a similar study reported an 18‐year follow up of 20 of 30 patients who developed acute non‐A, non‐B (later documented as HCV) hepatitis in a plasmapheresis center 2 . Progressive hepatic fibrosis occurred in 50%, and 20% of patients developed cirrhosis.…”

Section: Natural Historymentioning

confidence: 99%

Management issues in chronic viral hepatitis: Hepatitis C

Sievert

2002

J of Gastro and Hepatol

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The natural history of chronic hepatitis C virus (HCV) infection and intervention with antiviral therapy are closely linked issues that cause the greatest controversy and concern for the person infected with HCV, as well as for the clinician involved in the assessment and treatment of people with chronic HCV infection. The outstanding challenge of natural history is to identify the person who is likely to develop serious liver disease, and to make that determination early in the course of chronic HCV infection when treatment is likely to be of the greatest benefit. Significant advances in the therapy of chronic HCV infection have occurred over the past decade. A sustained virological response (SVR), defined as undetectable HCV-RNA in blood 6 months after completing antiviral treatment, is the best indicator of a beneficial treatment effect. Relapse, breakthrough or non-response should all be regarded as unsuccessful outcomes of therapy. Interferons are still the mainstay of antiviral therapy for chronic HCV infection. The combination of interferon and ribavirin has improved SVR by decreasing the relapse rate. Treatment responses vary according to host factors such as age and gender, fibrotic severity and to viral factors like genotype and viral load. Patients with genotype 1 HCV and a high viral load require 12 months of treatment to achieve a SVR in approximately 30%, compared to those with genotypes 2 or 3 who achieve a SVR in approximately 65% after 6 months. Patients who relapse after an end-oftreatment response to interferon monotherapy have a good chance of responding to combination interferon and ribavirin given for 6 months, but a longer treatment course should be considered in less optimal cases. At present, the treatment of those with non-response is less clear, but there is interest in more intense forms of interferon therapy, such as induction dosing or pegylated interferon in combination with ribavirin. Clinicians need to be aware of the common side-effects of interferon and ribavirin so that appropriate counseling and testing can be instituted before and during therapy. The combination of pegylated interferon and ribavirin will be the new standard of therapy for hepatitis C and pegylated interferon monotherapy provides quite acceptable efficacy for those patients intolerant of ribavirin. Current data strongly support the concept that SVR in HCV infection (or treatment-induced latency) provides a cure in terms of its beneficial effects on quality of life and sustained amelioration of liver injury.

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“…In contrast, other patients can rapidly progress to cirrhosis and hepatocellular carcinoma within 10–15 years. Approximately 20% of individuals with chronic HCV infection develop cirrhosis within 20 years [26, 27]. In the average patient with chronic HCV, 15 years transpire before diagnosis, 20 years before evidence of cirrhosis, and over 25–30 years before clinical presentation of hepatocellular carcinoma [26, 28, 29].…”

Section: Natural Historymentioning

confidence: 99%