Estimation of stage-specific fibrosis progression rates in chronic hepatitis C virus infection: A meta-analysis and meta-regression

Thein, Hla-Hla; Yi, Qilong; Dore, Gregory J.; Krahn, Murray

doi:10.1002/hep.22375

Cited by 742 publications

(649 citation statements)

References 74 publications

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“…In a meta-analysis of the stage-specific fibrosis progression rate in different populations of HCV-patients, the mean progression rate among the IDUs were: F0-F1 0.116, F1-F2 0.085, F2-F3 0.085 and F3-F4 0.130 [20]. This corresponds well to the overall mean progression rate of 0.097 in our study.…”

Section: Discussionsupporting

confidence: 88%

“…The median fibrosis progression rate of 0.07 per year observed in this cohort was similar to or lower than reported in other studies of patients with chronic HCV-infection [16][17][18][19][20], but the progression rate was higher than in studies of young females who contracted an HCVinfection accidentally as a result of infected anti-D immunoglobulin in Ireland and Germany [5,21]. In a meta-analysis of the stage-specific fibrosis progression rate in different populations of HCV-patients, the mean progression rate among the IDUs were: F0-F1 0.116, F1-F2 0.085, F2-F3 0.085 and F3-F4 0.130 [20].…”

Section: Discussionsupporting

confidence: 86%

See 1 more Smart Citation

Liver fibrosis progression at autopsy in injecting drug users infected by hepatitis C: A longitudinal long-term cohort study

Kielland

Delaveris

Rogde

et al. 2014

Journal of Hepatology

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Section: Discussionsupporting

confidence: 88%

Section: Discussionsupporting

confidence: 86%

Liver fibrosis progression at autopsy in injecting drug users infected by hepatitis C: A longitudinal long-term cohort study

Kielland

Delaveris

Rogde

et al. 2014

Journal of Hepatology

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“…However, the overall liver cirrhosis rate in this group was well below the predicted natural cirrhosis progression rate of 45% at 30 years after infection. 7 Decreased rates of advanced liver fibrosis and cirrhosis were also detected in patients who achieved SVR after antiviral treatment over the last few decades. Analysis of the overall survival probability confirmed enhanced survival in the Fig.…”

Section: Discussionmentioning

confidence: 99%

“…[4][5][6] The predicted cumulative probability of cirrhosis approximates 20% at 20 years after HCV infection and increases to 45% at 30 years after infection. 7 However, recent estimates on the natural fibrosis progression rates of hepatitis C largely depend on study design, study setting, and the selected study population. In theory, prospective multicenter, community-based long-term follow-up studies in large representative patient cohorts with a defined onset of HCV infection from a single identified source constitute the optimal setting for the evaluation of the natural course of chronic HCV infection.…”

mentioning

confidence: 99%

Evaluation of liver disease progression in the German hepatitis C virus (1b)-contaminated anti-D cohort at 35 years after infection

Wiese¹,

Fischer

Löbermann

et al. 2013

Hepatology

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The natural course of HCV infection remains controversial. The German HCV (1b)-contaminated anti-D cohort provides an ideal population to investigate the natural course of HCV infection in a large, homogenous cohort of young women from the date of HCV inoculation. Our previous follow-up studies at 20 and 25 years after infection suggested slow fibrosis progression rates in this unique cohort. The aim of our prospective, community-based, multicenter study was to reevaluate the liver disease progression in 718 patients of the original anti-D cohort at 35 years after infection. Patients with self-limited HCV infection (n 5 189) were compared to those who failed to eliminate the virus spontaneously (n 5 529), comprising patients who were treatment na€ ıve (n 5 197) or achieved a sustained virological response (SVR; n 5 149), respectively, failed to clear the virus (non-SVR; n 5 183) after antiviral therapy. In the overall cohort, 9.3% of patients showed clinical signs of liver cirrhosis at 35 years after infection. Liver disease progression largely depended on HCV infection status. The highest proportion of patients with clinical signs of end-stage liver disease was observed in the non-SVR group (15.3%), whereas decreased cirrhosis rates were detected in the SVR group (6%) and in patients with self-limited HCV infection (1.1%; P 5 6.2 3 10 26 ). Overall survival was significantly enhanced after SVR, compared to treatment-na€ ıve patients or non-SVR (P 5 0.027). Conclusion: The present study provides further evidence for a mild, but significant, disease progression at 35 years after infection in the German HCV (1b)-contaminated anti-D cohort. Patients with self-limited HCV infection or SVR after antiviral treatment were protected from progressive liver disease and showed the best clinical long-term outcome. (HEPATOLOGY 2014;59:49-57) H epatitis C virus (HCV) infection is the leading cause of end-stage liver disease (ESLD) in the world and represents a major burden for national health systems. 1 The World Health Organisation (WHO) and international consensus conferences refer to the high chronification rate of HCV infection, the risk of subsequent HCV-related complications, including end-stage liver cirrhosis and hepatocellular carcinoma (HCC) and the high costs for antiviral therapy, respectively, liver transplantation (LT). 2,3 It is estimated that HCV-related morbidity and mortality will increase in the next decade. [4][5][6] The predicted cumulative probability of cirrhosis approximates 20% at 20 years after HCV infection and

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“…Furthermore, these markers are only used for a dichotomous differentiation of patients into two crude (no/mild vs. moderate/severe) fibrosis categories, whereas fibrosis progression is nonlinear. 82,83 Furthermore, even when using the dichotomous classification there is a high indeterminate rate with an inability to stage fibrosis in 30%-70% of patients with intermediate fibrosis stages. To complicate matters, the amount of hepatic fibrous tissue increases exponentially with every fibrosis stage, 72 whereas these surrogates are continuous variables.…”

Section: Noninvasive Means To Assess Liver Fibrosis and Fibrogenesismentioning

confidence: 99%

Targeting liver fibrosis: Strategies for development and validation of antifibrotic therapies

2009

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We have made striking progress in our understanding of the biochemistry and cell biology that underlies liver fibrosis and cirrhosis, including the development of strategies and agents to prevent and reverse fibrosis. However, translation of this knowledge into clinical practice has been hampered by (1) the limitation of many in vitro and in vivo models to confirm mechanisms and to test antifibrotic agents, and (2) the lack of sensitive methodologies to quantify the degree of liver fibrosis and the dynamics of fibrosis progression or reversal in patients. Furthermore, whereas cirrhosis and subsequent decompensation are accepted hard clinical endpoints, fibrosis and fibrosis progression alone are merely plausible surrogates for future clinical deterioration. In this review we focus on an optimized strategy for preclinical antifibrotic drug development and highlight the current and future techniques that permit noninvasive assessment and quantification of liver fibrosis and fibrogenesis. The availability of such noninvasive methodologies will serve as the pacemaker for the clinical development and validation of potent antifibrotic agents. (HEPATOLOGY 2009;50:1294-1306

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Estimation of stage-specific fibrosis progression rates in chronic hepatitis C virus infection: A meta-analysis and meta-regression

Abstract: Our large systematic review provides increased precision in estimating fibrosis progression in chronic HCV infection and supports nonlinear disease progression. Estimates of progression to cirrhosis from studies conducted in clinical settings were lower than previous estimates.

Cited by 742 publications

References 74 publications

Liver fibrosis progression at autopsy in injecting drug users infected by hepatitis C: A longitudinal long-term cohort study

Liver fibrosis progression at autopsy in injecting drug users infected by hepatitis C: A longitudinal long-term cohort study

Evaluation of liver disease progression in the German hepatitis C virus (1b)-contaminated anti-D cohort at 35 years after infection

Targeting liver fibrosis: Strategies for development and validation of antifibrotic therapies

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