Xamila Salcedo and Jesús Medina contributed equally to this work.
The potential of angiogenesis soluble markers in chronic hepatitis C†
Article first published online: 15 AUG 2005
Copyright © 2005 American Association for the Study of Liver Diseases
Volume 42, Issue 3, pages 696–701, September 2005
How to Cite
Salcedo, X., Medina, J., Sanz-Cameno, P., García-Buey, L., Martín-Vilchez, S., Borque, M. J., López-Cabrera, M. and Moreno-Otero, R. (2005), The potential of angiogenesis soluble markers in chronic hepatitis C. Hepatology, 42: 696–701. doi: 10.1002/hep.20828
Conflict of interest: Nothing to report.
- Issue published online: 22 AUG 2005
- Article first published online: 15 AUG 2005
- Manuscript Accepted: 20 JUN 2005
- Manuscript Received: 14 FEB 2005
- BBVA –Carolina Foundation
- Instituto de Salud Carlos III. Grant Number: CO3/02
- Ministerio de Ciencia y Tecnología, Spain. Grant Number: SAF 2004-07885
Angiogenesis, the formation of new vessels, has been reported to play a significant pathogenic role in liver damage–associated hepatitis C virus infection. Most of our current knowledge derives from immunohistochemical studies of hepatic biopsy samples obtained from chronic hepatitis C (CHC) patients. We evaluated whether CHC is associated with elevated serum levels of angiogenesis markers and whether these are modulated by therapy. Vascular endothelial growth factor (VEGF), angiopoietin-2 (Ang-2), and soluble Tie-2 (sTie-2) were determined in the serum of 36 CHC patients, before and after receiving antiviral combination therapy with pegylated interferon alpha-2b plus ribavirin, and in 15 healthy controls. CHC patients showed elevated baseline VEGF and Ang-2 levels. After treatment, both factors were decreased, whereas antiangiogenic sTie-2 was increased, indicating a shift toward an “anti-angiogenic” profile of serum markers in CHC patients. In conclusion, this suggests that serum VEGF, Ang-2, and sTie-2 levels could be useful as noninvasive, mechanistically based markers of response to therapy and disease progression in CHC. (HEPATOLOGY 2005.)