Viral Hepatitis in Liver Transplantation Gonzalo Crespo, Zoe Mariño, Miquel Navasa, Xavier Forns  Gastroenterology  Volume 142, Issue 6, Pages 1373-1383.e1 (May 2012) DOI: 10.1053/j.gastro.2012.02.011 Copyright © 2012 AGA Institute Terms and Conditions

Figure 1 Model of pathogenesis of accelerated fibrogenesis in patients with recurrent hepatitis C after LT. Recurrent hepatitis C is characterized by hepatocellular damage, infiltration of the liver with inflammatory cells, and tissue remodeling that ultimately results in progressive fibrosis and cirrhosis. Infiltrating inflammatory cells at the sites of liver injury secrete chemokines that stimulate hepatic stellate cells, which proliferate and produce extracellular matrix proteins. Indeed, stellate cells are key players in recurrent hepatitis C and these cells can be activated by a number of stimuli in the liver transplant setting: production of ROS (I/R injury, old donor), secretion of cytokines by immune cells (acute rejection, CMV infection), hyperglycemia, and chronic cholestasis (biliary complications). The combination of a variety of factors explains the accelerated progression of fibrosis in HCV-infected liver transplant recipients. Gastroenterology 2012 142, 1373-1383.e1DOI: (10.1053/j.gastro.2012.02.011) Copyright © 2012 AGA Institute Terms and Conditions

Figure 2 Proposed algorithm for follow-up and management of hepatitis C recurrence following LT. DM, diabetes mellitus. Gastroenterology 2012 142, 1373-1383.e1DOI: (10.1053/j.gastro.2012.02.011) Copyright © 2012 AGA Institute Terms and Conditions

Figure 3 Mechanisms and potential consequences of interactions between protease inhibitors and immunosuppressant drugs. Because both protease inhibitors (PI) and calcineurin inhibitors are metabolized by the CYP3A4 system, initiation of boceprevir or telaprevir therapy will increase CsA or TAC levels with the potential occurrence of severe adverse events: renal failure, hypertension, diabetes, or neurologic damage. On the contrary, interruption of boceprevir or telaprevir after treatment completion (or due to adverse effects) will precipitate a rapid decrease in CsA or TAC levels, which might lead to rejection episodes. TAC, tacrolimus; BOC, boceprevir; TVP, telaprevir. Gastroenterology 2012 142, 1373-1383.e1DOI: (10.1053/j.gastro.2012.02.011) Copyright © 2012 AGA Institute Terms and Conditions

Gastroenterology 2012 142, 1373-1383. e1DOI: (10. 1053/j. gastro. 2012 Copyright © 2012 AGA Institute Terms and Conditions

Gastroenterology 2012 142, 1373-1383. e1DOI: (10. 1053/j. gastro. 2012 Copyright © 2012 AGA Institute Terms and Conditions

Gastroenterology 2012 142, 1373-1383. e1DOI: (10. 1053/j. gastro. 2012 Copyright © 2012 AGA Institute Terms and Conditions

Gastroenterology 2012 142, 1373-1383. e1DOI: (10. 1053/j. gastro. 2012 Copyright © 2012 AGA Institute Terms and Conditions