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Panminerva Medica 2017 December;59(4):320-31

DOI: 10.23736/S0031-0808.17.03359-6


lingua: Inglese

Liver fibrosis: the 2017 state of art

Gian P. CAVIGLIA 1 , Chiara ROSSO 1, Sharmila FAGOONEE 2, Giorgio M. SARACCO 1, 3, Rinaldo PELLICANO 3

1 Department of Medical Sciences, University of Turin, Turin, Italy; 2 Institute for Biostructures and Bioimages-CNR c/o Molecular Biotechnology Center, University of Turin, Turin, Italy; 3 Unit of Gastroenterology and Hepatology, Molinette Hospital, Turin, Italy


Liver fibrosis is a wound-healing response to a wide spectrum of chronic liver injuries. It is characterized by loss of hepatocytes and alteration in hepatic architecture following an imbalance between extracellular matrix synthesis and degradation. Irrespectively of underlying etiology, fibrosis may progress to cirrhosis and specific pathogenetic mechanisms as well as different disease patterns may be identified according to etiology. Liver biopsy is still considered the gold standard for fibrosis assessment, despite the fact that it is invasive, has poor patient compliance and is not exempt of complications. Several reliable and non-invasive tools are currently used in clinical practice, including imaging methods and surrogate serum biomarkers, commonly combined into composite scores. The main limitation of non-invasive methods is the low performance in the discrimination of intermediate stages of fibrosis. However, with the recent availability of novel treatment options, particularly for chronic hepatitis C, a precise staging of liver fibrosis is becoming clinically less relevant. Conversely, since patients with cirrhosis need to be monitored for the risk of hepatocellular carcinoma development, the accurate detection of this condition is a primary endpoint. Finally, several promising antifibrotic agents are under investigation in phase I and II trials. Nevertheless, further efforts are needed for the identification of novel potential targets for the development of antifibrotic drugs able to arrest, and possibly revert liver fibrogenesis.

KEY WORDS: Hepatitis, chronic - Extracellular matrix - Hepatic stellate cells - Liver cirrhosis

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