Fibrosis in chronic liver diseases: diagnosis and management Massimo Pinzani, Krista Rombouts, Stefano Colagrande  Journal of Hepatology  Volume 42, Issue 1, Pages S22-S36 (April 2005) DOI: 10.1016/j.jhep.2004.12.008 Copyright © 2004 European Association for the Study of the Liver Terms and Conditions

Fig. 1 Fibrosis vs. fibrogenesis. Immunohistochemistry for (A) collagen type I and (B) platelet-derived growth factor (PDGF) beta receptor, on a liver biopsy cryostat section obtained from a patient with chronic hepatitis C (METAVIR: F2). Staining for collagen type I defines the existing fibrillar ECM deposition and is the net result of deposition/degradation (fibrosis). Staining for PDGF beta receptor identifies populations of activated ECM-producing cells (hepatic stellate cells, myofibroblasts) surrounding the area of fibrotic expansion of the portal tract. It is conceivable that hyperplasia of these cell types will lead to further active deposition of fibrillar ECM (fibrogenesis). Journal of Hepatology 2005 42, S22-S36DOI: (10.1016/j.jhep.2004.12.008) Copyright © 2004 European Association for the Study of the Liver Terms and Conditions

Fig. 2 Arterial perfusion phase helical CT scans at liver hilum level, performed after administration of iodinated contrast media. Scans show enhancement of peripheral hepatic parenchyma (white arrows) with relative hypodensity of central area in cirrhotic liver, without portal thrombosis. This pattern is due to the relative portal hypoperfusion of cirrhotic distal parenchyma with arterial compensation, in the attempt to maintain a steady flow condition. Journal of Hepatology 2005 42, S22-S36DOI: (10.1016/j.jhep.2004.12.008) Copyright © 2004 European Association for the Study of the Liver Terms and Conditions