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This is a single-center and prospective study to identify specific biomarker in order to predict development of decompensation in cirrhotic patients.
The duration of the study is 36 months and it provides a cohort of 200 patients.
At screening, patient will have taken blood samples and performed HVPG. After randomization, patient will be seen at follow up every 3 months to do blood sample and every 12 months to undergo HVPG, according to the guidelines.
In addition, metabolomics analysis will be performed at screening and every 3 months. The results will be analyzed in relation to emergence of decompensation during follow up period, in order to identify specific metabolomics characteristics that may be able to predict decompensation.
Azienda Ospedaliera Universitaria Policlinico Di Modena
University of Modena and Reggio Emilia
Published on BioPortfolio: 2017-03-20T21:23:22-0400
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Experimentally induced chronic injuries to the parenchymal cells in the liver to achieve a model for LIVER CIRRHOSIS.
FIBROSIS of the hepatic parenchyma due to obstruction of BILE flow (CHOLESTASIS) in the intrahepatic or extrahepatic bile ducts (BILE DUCTS, INTRAHEPATIC; BILE DUCTS, EXTRAHEPATIC). Primary biliary cirrhosis involves the destruction of small intra-hepatic bile ducts and bile secretion. Secondary biliary cirrhosis is produced by prolonged obstruction of large intrahepatic or extrahepatic bile ducts from a variety of causes.
FIBROSIS of the hepatic parenchyma due to chronic excess ALCOHOL DRINKING.
Abnormal increase of resistance to blood flow within the hepatic PORTAL SYSTEM, frequently seen in LIVER CIRRHOSIS and conditions with obstruction of the PORTAL VEIN.
Liver disease in which the normal microcirculation, the gross vascular anatomy, and the hepatic architecture have been variably destroyed and altered with fibrous septa surrounding regenerated or regenerating parenchymal nodules.