Impact of common risk factors of fibrosis progression in chronic hepatitis C

S Rüeger ¹, P-Y Bochud ², J-F Dufour ³

¹Department of Medical Genetics, University of Lausanne, Lausanne, Switzerland Institute of Social and Preventive Medicine, University Hospital and University of Lausanne, Lausanne, Switzerland Swiss Institute of Bioinformatics, Lausanne, Switzerland.
²Infectious Diseases Service, University Hospital and University of Lausanne, Lausanne, Switzerland.
³Department of Hepatology, University of Berne, Berne, Switzerland.
⁴Department of Gastroenterology and Hepatology, University Hospital of Zurich, Zurich, Switzerland.
⁵Department of Gastroenterology, Canton Hospital St Gallen, St Gallen, Switzerland.
⁶Department of Gastroenterology and Hepatology, University Hospital of Basel, Basel, Switzerland.
⁷Department of Gastroenterology and Hepatology, University Hospital and University of Lausanne, Lausanne, Switzerland.
⁸Epatologia, Clinica Moncucco, Lugano, Switzerland.
⁹Pourtalès Hospital, Neuchatel, Switzerland.
¹⁰Institute for Immunology and Allergy Research, Westmead Millennium Institute, University of Sydney, Sydney, Australia.
¹¹Institute for Immunology and Allergy Research, Westmead Millennium Institute, University of Sydney, Sydney, Australia Storr Liver Unit, Westmead Millennium Institute and Westmead Hospital, University of Sydney and University of Sydney Medical Foundation, Sydney, Australia.
¹²Storr Liver Unit, Westmead Millennium Institute and Westmead Hospital, University of Sydney and University of Sydney Medical Foundation, Sydney, Australia.
¹³Laboratoire d'Immunologie et de Génétique des Maladies Parasitaires, INSERM-UMR 906/Université de la Méditerranée, Marseilles, France.
¹⁴Laboratoire Alphabio, Hôpital Ambroise Paré, Marseilles, France.
¹⁵Service d'Hépato-gastroentérologie, Hôpital Saint-Joseph, Marseilles, France.
¹⁶Division of Gastroenterology and Hepatology, Weill Cornell Medical College, New York, USA.
¹⁷Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM, U980, Imagine Institute, Paris, France University Paris Descartes, Paris, France.
¹⁸University Paris Descartes, Paris, France Département d'Hépatologie, INSERM Unité 1016, Groupe Hospitalier Cochin-Hôtel Dieu-Broca, Paris, France.
¹⁹Université Pierre et Marie Curie, Service d'Hépato-gastroentérologie, Hôpital Pitié-Salpêtrière (AP-HP), Paris, France.
²⁰Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM, U980, Imagine Institute, Paris, France University Paris Descartes, Paris, France St Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, New York, USA.
²¹Institute of Social and Preventive Medicine, University Hospital and University of Lausanne, Lausanne, Switzerland Swiss Institute of Bioinformatics, Lausanne, Switzerland.
²²Clinical Pathology, University Hospitals of Geneva, Geneva, Switzerland Department of Gastroenterology and Hepatology, University Hospitals of Geneva, Geneva, Switzerland.

⁰Department of Medical Genetics, University of Lausanne, Lausanne, Switzerland Institute of Social and Preventive Medicine, University Hospital and University of Lausanne, Lausanne, Switzerland Swiss Institute of Bioinformatics, Lausanne, Switzerland.

Most factors accelerating liver fibrosis progression in chronic hepatitis C are unmodifiable. Key contributors include age at infection, sex, route of infection, and hepatitis C virus (HCV) genotype, alongside specific genetic variants.

Area Of Science

Hepatology and Viral Gastroenterology
Clinical Research
Genetics and Genomics

Background

Chronic hepatitis C (HCV) progression to advanced liver disease varies significantly among patients.
Accurate patient profiling is crucial for predicting fibrosis progression and managing liver disease risk.
Understanding the multifactorial drivers of liver fibrosis is essential for targeted interventions.

Purpose Of The Study

To determine the relative contributions of various factors to liver fibrosis progression in chronic hepatitis C.
To identify key risk factors for accelerated fibrosis progression rate (FPR) in a large patient cohort.
To validate findings across multiple independent cohorts and through meta-analysis.

Main Methods

Analysis of 1461 chronic hepatitis C patients with estimated infection dates and liver biopsies.
Logistic regression used to identify risk factors for accelerated FPR (≥ 0.13 Metavir units/year).
Assessment of factors including demographics, lifestyle, coinfections, and genetic polymorphisms (SNPs).

Main Results

Age at infection (28.7%), route of infection (16.5%), sex (8.2%), and HCV genotype (7.9%) were significant contributors to accelerated FPR.
Specific genetic variants (rs738409, rs4374383, rs910049) also significantly increased the risk of accelerated FPR.
Significant alcohol consumption, BMI, HIV coinfection, and diabetes did not show a significant association with accelerated FPR.

Conclusions

The primary drivers of accelerated liver fibrosis progression in chronic hepatitis C are largely unmodifiable factors.
Age, sex, route of infection, HCV genotype, and specific genetic variations are key determinants of fibrosis progression.
These findings underscore the importance of considering demographic and genetic factors in managing chronic hepatitis C.

Keywords:

CIRRHOSIS FIBROSIS HEPATITIS C

Impact of common risk factors of fibrosis progression in chronic hepatitis C

Summary

Area Of Science

Background

Purpose Of The Study

Main Methods

Main Results

Conclusions

Keywords:

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Impact of common risk factors of fibrosis progression in chronic hepatitis C

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Summary

Area Of Science

Background

Purpose Of The Study

Main Methods

Main Results

Conclusions

Keywords:

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