1. Controversies in the management of hepatitis C patients with advanced fibrosis and cirrhosis 
Robert J Fontana, Gregory T Everson, Sony Tuteja, Hugo E Vargas, Mitchell L Shiffman 
Clinical Gastroenterology and Hepatology 
Volume 2, Issue 3, Pages (March 2004)
DOI: /S (04)

2. Figure 1
Spectrum of clinical outcomes in hepatitis C. Adapted and reprinted from Hoofnagle4 by permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.
Clinical Gastroenterology and Hepatology 2004 2, DOI: ( /S (04) )

3. Figure 2
Molecular pathogenesis of hepatic fibrosis in chronic hepatitis C (CHC). (A) Early CHC is characterized by periportal lymphoid follicles and mild lobular hepatitis. HCV infection leads to release of fibrinolytic enzymes termed matrix metalloproteinases from stellate cells that break down the low density matrix in the subendothelial space. In addition, recruitment, activation, and proliferation of hepatic stellate cells and Kupffer cells in the subendothelial space lead to production of an extracellular matrix (ECM) with increasing amounts of types 1 and 3 collagen.37 (B) CHC with advanced fibrosis. Advanced fibrosis in CHC is characterized by the presence of portal-central and portal-portal bands of collagen. Over time the density of these bands and the extent of cross-linking increase, leading to reduced nutrient exchange to surrounding hepatocytes, architectural distortion, and increased resistance to blood flow. Activated hepatic stellate cells and Kupffer cells are believed to be the primary mediators of hepatic fibrogenesis through the release of profibrogenic cytokines and paracrine molecules including transforming growth factor-B.37
Clinical Gastroenterology and Hepatology 2004 2, DOI: ( /S (04) )