Circulating fibronectin isoforms predict the degree of fibrosis in chronic hepatitis C

• Verfasst von: Hackl, Norman J. [VerfasserIn]
• Verfasst von: Bersch, Claus [VerfasserIn]
• Verfasst von: Feick, Peter [VerfasserIn]
• Verfasst von: Antoni, Christoph Helmer [VerfasserIn]
• Verfasst von: Franke, Andreas [VerfasserIn]
• Verfasst von: Singer, Manfred V. [VerfasserIn]
• Verfasst von: Nakchbandi, Inaam [VerfasserIn]
• Titel: Circulating fibronectin isoforms predict the degree of fibrosis in chronic hepatitis C
• Verf.angabe: Norman J. Hackl, Claus Bersch, Peter Feick, Christoph Antoni, Andreas Franke, Manfred V. Singer & Inaam A. Nakchbandi
• Jahr: 2010
• Umfang: 8 S.
• Fussnoten: Gesehen am 28.06.2021
• Titel Quelle: Enthalten in: Scandinavian journal of gastroenterology
• Ort Quelle: Abingdon : Taylor & Francis Group, 1966
• Jahr Quelle: 2010
• Band/Heft Quelle: 45(2010), 3, Seite 349-356
• ISSN Quelle: 1502-7708
• DOI: doi:10.3109/00365520903490606
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: Adult
• Sach-SW: Biomarkers
• Sach-SW: Biopsy, Needle
• Sach-SW: Case-Control Studies
• Sach-SW: Cross-Sectional Studies
• Sach-SW: Female
• Sach-SW: Fibronectins
• Sach-SW: Hepatic Stellate Cells
• Sach-SW: Hepatitis C, Chronic
• Sach-SW: Humans
• Sach-SW: Liver Cirrhosis
• Sach-SW: Male
• Sach-SW: Middle Aged
• Sach-SW: Predictive Value of Tests
• Sach-SW: Protein Isoforms
• K10plus-PPN: 1761391011

Abstract

OBJECTIVE: Hepatic stellate cells only produce fibronectin isoforms in disease states. The isoform-defining domains can be detected in the blood circulation. This study examines whether circulating levels of fibronectin isoforms show a relationship with liver fibrosis on histology in patients with chronic hepatitis C. MATERIAL AND METHODS: In a prospective study, 50 patients with chronic hepatitis C who underwent a liver biopsy were compared to 50 matched controls and 35 patients with other liver conditions. RESULTS: Circulating levels of the fibronectin isoforms were significantly higher in patients with chronic hepatitis C compared to healthy controls [oncofetal fibronectin (oFN) 2.45 +/- 0.17 versus 1.76 +/- 0.16 mg/l, P < 0.005; extra domain-A (EDA) 1.05 +/- 0.06 versus 0.86 +/- 0.06 mg/l, P < 0.05; and extra domain-B (EDB) 14.55 +/- 0.74 versus 9.31 +/- 0.58 mg/l, P < 0.001], even though total fibronectin was lower (198.9 +/- 3.5 versus 343.6 +/- 14.5 mg/l, P < 0.001). A correlation with the fibrosis score was found for both oFN (r = 0.46, P < 0.005) and EDA (r = 0.51, P < 0.001). The combination of an elevation in both markers (oFN and EDA) in the upper quartile was associated with a specificity of > 99% for predicting significant fibrosis (stages 2-4) and 95% for predicting advanced fibrosis (stages 3-4). A combination of decreased values in the lowest tertile for both markers had a specificity of 94% for excluding significant fibrosis. Based on these findings, 30% of the patients scheduled for a liver biopsy could be correctly classified as having or not having significant fibrosis. The remainder would have to proceed with a biopsy. CONCLUSION: Circulating fibronectin isoforms produced by activated stellate cells represent a viable marker for the presence of significant fibrosis or a lack thereof.