Endothelial Dysfunction Correlates with Liver Fibrosis in Chronic HCV Infection

Background. Hepatitis C virus (HCV) infection can exert proatherogenic activities due to its direct action on vessel walls and/or via the chronic inflammatory process involving the liver. Aims. To clarify the role of HCV in atherosclerosis development in monoinfected HCV patients at different degree...

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Main Authors: Michele Barone, Maria Teresa Viggiani, Annabianca Amoruso, Serafina Schiraldi, Annapaola Zito, Fiorella Devito, Francesca Cortese, Michele Gesualdo, Natale Brunetti, Alfredo Di Leo, Pietro Scicchitano, Marco Matteo Ciccone
Format: Article
Language:English
Published: Wiley 2015-01-01
Series:Gastroenterology Research and Practice
Online Access:http://dx.doi.org/10.1155/2015/682174
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author Michele Barone
Maria Teresa Viggiani
Annabianca Amoruso
Serafina Schiraldi
Annapaola Zito
Fiorella Devito
Francesca Cortese
Michele Gesualdo
Natale Brunetti
Alfredo Di Leo
Pietro Scicchitano
Marco Matteo Ciccone
author_facet Michele Barone
Maria Teresa Viggiani
Annabianca Amoruso
Serafina Schiraldi
Annapaola Zito
Fiorella Devito
Francesca Cortese
Michele Gesualdo
Natale Brunetti
Alfredo Di Leo
Pietro Scicchitano
Marco Matteo Ciccone
author_sort Michele Barone
collection DOAJ
description Background. Hepatitis C virus (HCV) infection can exert proatherogenic activities due to its direct action on vessel walls and/or via the chronic inflammatory process involving the liver. Aims. To clarify the role of HCV in atherosclerosis development in monoinfected HCV patients at different degrees of liver fibrosis and with no risk factors for coronary artery disease. Methods. Forty-five patients were included. Clinical, serological, and anthropometric parameters, liver fibrosis (transient liver elastometry (fibroscan) and aspartate aminotransferase to platelet ratio index (APRI)), carotid intima-media thickness (c-IMT), and brachial artery flow-mediated vasodilatation (FMD) were assessed. Patients were divided into 3 tertiles according to fibroscan values. Results. Patients in the third tertile (fibroscan value >11.5 KPa) showed FMD values were significantly lower than second and first tertiles (4.7±1.7% versus 7.1±2.8%, p=0.03). FMD values were inversely related to liver elastomeric values. c-IMT values were normal. The risk for endothelial dysfunction development in the third tertile (p=0.02) was 6.9 higher than the first tertile. A fibroscan value >11.5 KPa had a positive predictive power equal to 79% for endothelial dysfunction. Conclusions. HCV advanced liver fibrosis promotes atherosclerosis by inducing endothelial dysfunction independently of common cardiovascular risk factors.
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spelling doaj-art-c127b133f96c4489b14af7c4b4f394092025-02-03T05:58:18ZengWileyGastroenterology Research and Practice1687-61211687-630X2015-01-01201510.1155/2015/682174682174Endothelial Dysfunction Correlates with Liver Fibrosis in Chronic HCV InfectionMichele Barone0Maria Teresa Viggiani1Annabianca Amoruso2Serafina Schiraldi3Annapaola Zito4Fiorella Devito5Francesca Cortese6Michele Gesualdo7Natale Brunetti8Alfredo Di Leo9Pietro Scicchitano10Marco Matteo Ciccone11Gastroenterology Unit, Department of Medical and Surgical Science, University of Foggia, OO. RR. Foggia, Viale Pinto 1, 71122 Foggia, ItalyGastroenterology Unit, Department of Emergency and Organ Transplantation, Ospedale Policlinico, University of Bari, Piazza G. Cesare 11, 70124 Bari, ItalyGastroenterology Unit, Department of Medical and Surgical Science, University of Foggia, OO. RR. Foggia, Viale Pinto 1, 71122 Foggia, ItalyGastroenterology Unit, Department of Emergency and Organ Transplantation, Ospedale Policlinico, University of Bari, Piazza G. Cesare 11, 70124 Bari, ItalyCardiology Unit, Department of Emergency and Organ Transplantation, Ospedale Policlinico, University of Bari, Piazza G. Cesare 11, 70124 Bari, ItalyCardiology Unit, Department of Emergency and Organ Transplantation, Ospedale Policlinico, University of Bari, Piazza G. Cesare 11, 70124 Bari, ItalyCardiology Unit, Department of Emergency and Organ Transplantation, Ospedale Policlinico, University of Bari, Piazza G. Cesare 11, 70124 Bari, ItalyCardiology Unit, Department of Emergency and Organ Transplantation, Ospedale Policlinico, University of Bari, Piazza G. Cesare 11, 70124 Bari, ItalyCardiology Unit, Department of Medical and Surgical Science, University of Foggia, OO. RR. Foggia, Viale Pinto 1, 71122 Foggia, ItalyGastroenterology Unit, Department of Emergency and Organ Transplantation, Ospedale Policlinico, University of Bari, Piazza G. Cesare 11, 70124 Bari, ItalyCardiology Unit, Department of Emergency and Organ Transplantation, Ospedale Policlinico, University of Bari, Piazza G. Cesare 11, 70124 Bari, ItalyCardiology Unit, Department of Emergency and Organ Transplantation, Ospedale Policlinico, University of Bari, Piazza G. Cesare 11, 70124 Bari, ItalyBackground. Hepatitis C virus (HCV) infection can exert proatherogenic activities due to its direct action on vessel walls and/or via the chronic inflammatory process involving the liver. Aims. To clarify the role of HCV in atherosclerosis development in monoinfected HCV patients at different degrees of liver fibrosis and with no risk factors for coronary artery disease. Methods. Forty-five patients were included. Clinical, serological, and anthropometric parameters, liver fibrosis (transient liver elastometry (fibroscan) and aspartate aminotransferase to platelet ratio index (APRI)), carotid intima-media thickness (c-IMT), and brachial artery flow-mediated vasodilatation (FMD) were assessed. Patients were divided into 3 tertiles according to fibroscan values. Results. Patients in the third tertile (fibroscan value >11.5 KPa) showed FMD values were significantly lower than second and first tertiles (4.7±1.7% versus 7.1±2.8%, p=0.03). FMD values were inversely related to liver elastomeric values. c-IMT values were normal. The risk for endothelial dysfunction development in the third tertile (p=0.02) was 6.9 higher than the first tertile. A fibroscan value >11.5 KPa had a positive predictive power equal to 79% for endothelial dysfunction. Conclusions. HCV advanced liver fibrosis promotes atherosclerosis by inducing endothelial dysfunction independently of common cardiovascular risk factors.http://dx.doi.org/10.1155/2015/682174
spellingShingle Michele Barone
Maria Teresa Viggiani
Annabianca Amoruso
Serafina Schiraldi
Annapaola Zito
Fiorella Devito
Francesca Cortese
Michele Gesualdo
Natale Brunetti
Alfredo Di Leo
Pietro Scicchitano
Marco Matteo Ciccone
Endothelial Dysfunction Correlates with Liver Fibrosis in Chronic HCV Infection
Gastroenterology Research and Practice
title Endothelial Dysfunction Correlates with Liver Fibrosis in Chronic HCV Infection
title_full Endothelial Dysfunction Correlates with Liver Fibrosis in Chronic HCV Infection
title_fullStr Endothelial Dysfunction Correlates with Liver Fibrosis in Chronic HCV Infection
title_full_unstemmed Endothelial Dysfunction Correlates with Liver Fibrosis in Chronic HCV Infection
title_short Endothelial Dysfunction Correlates with Liver Fibrosis in Chronic HCV Infection
title_sort endothelial dysfunction correlates with liver fibrosis in chronic hcv infection
url http://dx.doi.org/10.1155/2015/682174
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