Zusammenfassung
Die nichtalkoholische Fettlebererkrankung (NAFLD) mit Ausbildung einer Steatohepatitis (NASH) und die chronische Hepatitis-C-Virus-(HCV-)Infektion sind die häufigsten Ursachen für Leberzirrhose und hepatozelluläres Karzinom (HCC). Die Entstehung der NAFLD/NASH ist mit Insulinresistenz, Diabetes mellitus Typ 2, Dyslipidämie und Adipositas assoziiert. In der Normalbevölkerung liegt die Prävalenz der NAFLD bei 20–30%, bei Patienten mit chronischer Hepatitis C bei 40–80%. Die Steatosis hepatis bei Patienten mit chronischer Hepatitis C steht in Zusammenhang mit viralen Faktoren wie Genotyp-3-Infektion und metabolischen Faktoren wie Diabetes mellitus und einem erhöhten Body-Mass-Index. HCV kann durch direkte und indirekte Interaktion mit zellulären Signalwegen eine Steatosis hepatis auslösen. Die klinische Bedeutung liegt in einem erhöhten Leberzirrhose- und HCC-Risiko und einem schlechteren Ansprechen auf eine antivirale Therapie bei nicht mit Genotyp 3 infizierten Patienten. Die Therapie der Steatosis hepatis bei Patienten mit chronischer Hepatitis C besteht in einer viralen Eradikation und in der Behandlung der Adipositas und der Insulinresistenz.
Abstract
Non-alcoholic fatty liver disease (NAFLD) with development of steatohepatitis (NASH) and chronic hepatitis C virus (HCV) infection are the most frequent causes of chronic liver disease and its sequelae. NAFLD has a prevalence of 20–30% in the general population, whereas liver steatosis is observed in 40–80% of patients with chronic hepatitis C. Steatohepatitis in patients with chronic hepatitis C is associated with viral factors, such as genotype 3 infection and with diabetes mellitus and obesity as host factors. HCV has been shown to cause liver steatosis by direct and indirect interference with cellular signal transduction pathways. Liver steatosis in patients with chronic hepatitis C is clinically relevant because of its association with an increased risk for liver cirrhosis, hepatocellular carcinoma and failure to respond to interferon-based antiviral therapy in genotype non-3 infected patients. Treatment of liver steatosis in patients with chronic hepatitis C should aim at viral eradication and treatment of obesity, insulin resistance and diabetes mellitus.
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Interessenkonflikt
Die Autoren weisen auf folgende Beziehungen hin:
PD Dr. Bernd Kronenberger: Vortragshonorare von Bristol-Myers Squibb, Essex, Falk, Gilead, Novartis, Roche.
Prof. Dr. Stefan Zeuzem: Vortragshonorare von Bristol-Myers Squibb, Bayer, Essex, Falk, Gilead, Novartis, Roche.
PD Dr. Jörg Bojunga: Vortragshonorare von Bristol-Myers Squibb, Essex, Novartis, MSD.
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Kronenberger, B., Zeuzem, S. & Bojunga, J. NASH und Hepatitis C. Gastroenterologe 5, 116–122 (2010). https://doi.org/10.1007/s11377-009-0371-6
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DOI: https://doi.org/10.1007/s11377-009-0371-6
Schlüsselwörter
- Nicht alkoholische Steatohepatitis (NASH)
- Chronische Hepatitis C
- Hepatozelluläres Karzinom
- Leberzirrhose
- Insulinresistenz