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Non invasive markers of liver fibrosis in hepatitis C

Journal Volume 67 - 2004
Issue Fasc.3 - Symposium
Author(s) M. Adler, B. Frotscher, Ph. Thiry, Th. Gustot
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(1) Medico-Surgical Department of Gastroenterology and Hepatopancreatology ; (2) Department of Clinical Chemistry, Hôpital Erasme, Brussels, Belgium.

Liver fibrosis reflects a loss of homeostasis between fibrogenesis and matrix degradation (1). In the extracellular space, matrix degradation occurs as a consequence of the action of enzymes called matrix metalloproteinases (MMPs), themselves inhibited by tis- sue inhibitors (TIMP 1-4) which are protease inhibitors. Chronic liver injury, whatever the cause (alcohol, virus, non alcoholic liver disease, biliary disease,...), lead to hepatic stellate cells activation, producing a fibrogenic environment within the liver, leading to extensive fibro- sis and cirrhosis, through a combination of extracellular matrix (including collagens, non collagenous glycopro- teins and proteoglycans) overproduction, diminished MMP activation and inhibition of active MPPs by TIMPs.

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