These authors shared senior authorship.
Evaluation of liver disease progression in the German hepatitis C virus (1b)-contaminated anti-D cohort at 35 years after infection
Article first published online: 18 NOV 2013
© 2013 by the American Association for the Study of Liver Diseases
Volume 59, Issue 1, pages 49–57, January 2014
How to Cite
Wiese, M., Fischer, J., Löbermann, M., Göbel, U., Grüngreiff, K., Güthoff, W., Kullig, U., Richter, F., Schiefke, I., Tenckhoff, H., Zipprich, A., Berg, T., Müller, T. and for the East German HCV Study Group (2014), Evaluation of liver disease progression in the German hepatitis C virus (1b)-contaminated anti-D cohort at 35 years after infection. Hepatology, 59: 49–57. doi: 10.1002/hep.26644
Potential conflict of interest: Dr. Schiefke advises Baxter and received grants from Gilead and MSD. Dr. Löbermann is on the speakers' bureau and owns stock in Janssen-Cilag and Gilead. She received grants and owns stock in Roche.
This work was supported by the German Competence Network for Viral Hepatitis (Hep-Net), funded by the German Ministry of Education and Research (BMBF; grant no.: 01 KI 0437; project no.: 10.1.3; core project no.: 10.1; Genetic host factors in viral hepatitis and Genetic Epidemiology Group in viral hepatitis), by the EU-Vigilance network of excellence combating viral resistance (VIRGIL; project no.: LSHM-CT-2004-503359), and by the BMBF Project: Host and viral determinants for susceptibility and resistance to hepatitis C virus infection (grant no.: 01KI0787)
- Issue published online: 20 DEC 2013
- Article first published online: 18 NOV 2013
- Accepted manuscript online: 8 AUG 2013 07:53AM EST
- Manuscript Accepted: 16 JUL 2013
- Manuscript Received: 6 MAR 2013
Vol. 61, Issue 4, 1446–1447, Article first published online: 13 FEB 2015
Additional Supporting Information may be found in the online version of this article.
|hep26644-sup-0001-suppfig1.tif||1603K||Supporting Information Figure 1: Comparison of clinical outcomes at 20 years, 25 years and 35 years after infection.|
|hep26644-sup-0002-suppfig2.tif||1679K||Supporting Information Figure 2: Evaluation of liver fibrosis at 35 years after infection by transient elastography. Transient elastography (FibroScan®, Echosens, Paris) was used for non-invasive fibrosis assessment. The measurements were performed according to the manufacturer's instructions (10 valid results required). Fibrosis stages were defined as METAVIR F2 with measurements >8.7 kPa, F3 (advanced fibrosis) >9.6 kPa and F4 (cirrhosis) >14.5 kPa.|
|hep26644-sup-0003-suppfig3.tif||1595K||Supporting Information Figure 3: Evaluation of liver fibrosis at 35 years after infection by liver biopsy. Liver biopsies were recommended to all viremic women to assess the individual inflammatory activity and fibrosis stage. Biopsies were scored for inflammation (grading 0-18) and fibrosis (staging 0-6) according to the Ishak score by the pathologists assigned to the respective centers.|
|hep26644-sup-0004-suppfig4.tif||1878K||Supporting Information Figure 4: Comparison of histological fibrosis stages at 20 years, 25 years and 35 years after infection. Biopsies were scored for inflammation (grading 0-18) and fibrosis (staging 0-6) according to the Ishak score by the pathologists assigned to the respective centers.|
|hep26644-sup-0005-suppfig5.tif||1564K||Supporting Information Figure 5: Interleukin 28B (IL28B) polymorphism in relation to the natural and treatment-induced course of HCV infection. The IL28B gene polymorphism rs12979860 was determined by real-time polymerase chain reaction and melting curve analysis.|
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