REVERSAL OF HEPATIC FIBROSIS

Abstract

Hepatic fibrosis is a wound healing response to chronic liver injury, which if persistent leads to cirrhosis and liver failure. (Friedman, 1999)

Hepatic fibrogenesis may be the end result of chronic alcohol abuse, viral or parasitic infection, heavy metal over load, bile duct obstruction, or autoimmune disease (Davis & Kresina, 1996)

Exciting progress has been made in understanding the mechanisms of hepatic fibrosis. Major advances include: (i) the characterization of the components of extracellular matrix (ECM) in normal and fibrotic liver; (ii) identification of hepatic stellate cells as the primary source of ECM in liver fibrosis; (iii) elucidation of key cytokines, their cellular sources, modes of regulation, and signaling pathways involved in liver fibrogcnesis; (iv) the characterization of key matrix proteases and their inhibitors; (v) the identification of apoptotic mediators in stellate cells and exploration of their roles during resolution of liver injury. These advances have helped delineate a more comprehensive picture of liver fibrosis in which the central event is the activation of stellate cells, transformation from quiescent vitamin A rich cells to proliferative, fibrogenic and contractile myofibroblasts (Friedman, 1999)

Current management of the well compensated cirrhotic is directed towards the early detection of hepato cellular Failure. An adequate balanced diet and avoidance of alcohol are essential.