Sustained virologic response prevents the development of esophageal varices in compensated, child-pugh class A hepatitis C virus-induced cirrhosis. A 12-year prospective follow-up study

Savino Bruno, Andrea Crosignani, Corinna Facciotto, Sonia Rossi, Luigi Roffi, Alessandro Redaelli, Roberto De Franchis, Piero Luigi Almasio, Patrick Maisonneuve

Research output: Contribution to journalArticle

138 Citations (Scopus)

Abstract

The incidence of de novo development of esophageal varices (EV) in patients with compensated liver cirrhosis has been determined by few studies in the short term and never in the long term. The aims of the present study were to determine the incidence and the risk factors associated with the development of EV and to assess whether antiviral treatment and achievement of sustained virologic response (SVR) may prevent de novo EV development in patients with HCV-induced cirrhosis. We studied 218 patients with compensated EV-free, HCV-induced cirrhosis consecutively enrolled between 1989 and 1992 at three referral centers in Milan, Italy. Endoscopic surveillance was performed at 3-year intervals according to international guidelines. SVR was defined as undetectable serum HCV-RNA 24 weeks after treatment discontinuation. During a median follow-up of 11.4 years, 149/218 (68%) patients received antiviral treatment and 34 (22.8%) achieved SVR. None of the SVR patients developed EV compared with 22 (31.8%) of the 69 untreated subjects (P <0.0001) and 45 (39.1%) of the 115 non-SVR patients (P <0.0001). On multivariate analysis, HCV genotype 1b (hazard ratio [HR] 2.40; 95% confidence interval [CI] 1.17-4.90) and baseline model for end-stage liver disease (MELD) score (HR 1.20; 95% CI 1.07-1.35 for 1 point increase) were independent predictors of EV. Conclusion: In the long term, the achievement of SVR prevents the development of EV in patients with compensated HCV-induced cirrhosis. Therefore, in these patients, endoscopic surveillance can be safely delayed or avoided. Genotype 1b infection and MELD score identify the subset of patients at higher risk of EV development who need tailored endoscopic surveillance.

Original languageEnglish
Pages (from-to)2069-2076
Number of pages8
JournalHepatology
Volume51
Issue number6
DOIs
Publication statusPublished - Jun 2010

Fingerprint

Esophageal and Gastric Varices
Hepacivirus
Fibrosis
End Stage Liver Disease
Antiviral Agents
Genotype
Confidence Intervals
Sustained Virologic Response
Incidence
Liver Cirrhosis
Italy
Therapeutics
Referral and Consultation
Multivariate Analysis
Guidelines
RNA

ASJC Scopus subject areas

  • Hepatology

Cite this

Sustained virologic response prevents the development of esophageal varices in compensated, child-pugh class A hepatitis C virus-induced cirrhosis. A 12-year prospective follow-up study. / Bruno, Savino; Crosignani, Andrea; Facciotto, Corinna; Rossi, Sonia; Roffi, Luigi; Redaelli, Alessandro; De Franchis, Roberto; Almasio, Piero Luigi; Maisonneuve, Patrick.

In: Hepatology, Vol. 51, No. 6, 06.2010, p. 2069-2076.

Research output: Contribution to journalArticle

Bruno, Savino ; Crosignani, Andrea ; Facciotto, Corinna ; Rossi, Sonia ; Roffi, Luigi ; Redaelli, Alessandro ; De Franchis, Roberto ; Almasio, Piero Luigi ; Maisonneuve, Patrick. / Sustained virologic response prevents the development of esophageal varices in compensated, child-pugh class A hepatitis C virus-induced cirrhosis. A 12-year prospective follow-up study. In: Hepatology. 2010 ; Vol. 51, No. 6. pp. 2069-2076.
@article{26339931bf1143bd8e5570a24fe31c29,
title = "Sustained virologic response prevents the development of esophageal varices in compensated, child-pugh class A hepatitis C virus-induced cirrhosis. A 12-year prospective follow-up study",
abstract = "The incidence of de novo development of esophageal varices (EV) in patients with compensated liver cirrhosis has been determined by few studies in the short term and never in the long term. The aims of the present study were to determine the incidence and the risk factors associated with the development of EV and to assess whether antiviral treatment and achievement of sustained virologic response (SVR) may prevent de novo EV development in patients with HCV-induced cirrhosis. We studied 218 patients with compensated EV-free, HCV-induced cirrhosis consecutively enrolled between 1989 and 1992 at three referral centers in Milan, Italy. Endoscopic surveillance was performed at 3-year intervals according to international guidelines. SVR was defined as undetectable serum HCV-RNA 24 weeks after treatment discontinuation. During a median follow-up of 11.4 years, 149/218 (68{\%}) patients received antiviral treatment and 34 (22.8{\%}) achieved SVR. None of the SVR patients developed EV compared with 22 (31.8{\%}) of the 69 untreated subjects (P <0.0001) and 45 (39.1{\%}) of the 115 non-SVR patients (P <0.0001). On multivariate analysis, HCV genotype 1b (hazard ratio [HR] 2.40; 95{\%} confidence interval [CI] 1.17-4.90) and baseline model for end-stage liver disease (MELD) score (HR 1.20; 95{\%} CI 1.07-1.35 for 1 point increase) were independent predictors of EV. Conclusion: In the long term, the achievement of SVR prevents the development of EV in patients with compensated HCV-induced cirrhosis. Therefore, in these patients, endoscopic surveillance can be safely delayed or avoided. Genotype 1b infection and MELD score identify the subset of patients at higher risk of EV development who need tailored endoscopic surveillance.",
author = "Savino Bruno and Andrea Crosignani and Corinna Facciotto and Sonia Rossi and Luigi Roffi and Alessandro Redaelli and {De Franchis}, Roberto and Almasio, {Piero Luigi} and Patrick Maisonneuve",
year = "2010",
month = "6",
doi = "10.1002/hep.23528",
language = "English",
volume = "51",
pages = "2069--2076",
journal = "Hepatology",
issn = "0270-9139",
publisher = "John Wiley and Sons Inc.",
number = "6",

}

TY - JOUR

T1 - Sustained virologic response prevents the development of esophageal varices in compensated, child-pugh class A hepatitis C virus-induced cirrhosis. A 12-year prospective follow-up study

AU - Bruno, Savino

AU - Crosignani, Andrea

AU - Facciotto, Corinna

AU - Rossi, Sonia

AU - Roffi, Luigi

AU - Redaelli, Alessandro

AU - De Franchis, Roberto

AU - Almasio, Piero Luigi

AU - Maisonneuve, Patrick

PY - 2010/6

Y1 - 2010/6

N2 - The incidence of de novo development of esophageal varices (EV) in patients with compensated liver cirrhosis has been determined by few studies in the short term and never in the long term. The aims of the present study were to determine the incidence and the risk factors associated with the development of EV and to assess whether antiviral treatment and achievement of sustained virologic response (SVR) may prevent de novo EV development in patients with HCV-induced cirrhosis. We studied 218 patients with compensated EV-free, HCV-induced cirrhosis consecutively enrolled between 1989 and 1992 at three referral centers in Milan, Italy. Endoscopic surveillance was performed at 3-year intervals according to international guidelines. SVR was defined as undetectable serum HCV-RNA 24 weeks after treatment discontinuation. During a median follow-up of 11.4 years, 149/218 (68%) patients received antiviral treatment and 34 (22.8%) achieved SVR. None of the SVR patients developed EV compared with 22 (31.8%) of the 69 untreated subjects (P <0.0001) and 45 (39.1%) of the 115 non-SVR patients (P <0.0001). On multivariate analysis, HCV genotype 1b (hazard ratio [HR] 2.40; 95% confidence interval [CI] 1.17-4.90) and baseline model for end-stage liver disease (MELD) score (HR 1.20; 95% CI 1.07-1.35 for 1 point increase) were independent predictors of EV. Conclusion: In the long term, the achievement of SVR prevents the development of EV in patients with compensated HCV-induced cirrhosis. Therefore, in these patients, endoscopic surveillance can be safely delayed or avoided. Genotype 1b infection and MELD score identify the subset of patients at higher risk of EV development who need tailored endoscopic surveillance.

AB - The incidence of de novo development of esophageal varices (EV) in patients with compensated liver cirrhosis has been determined by few studies in the short term and never in the long term. The aims of the present study were to determine the incidence and the risk factors associated with the development of EV and to assess whether antiviral treatment and achievement of sustained virologic response (SVR) may prevent de novo EV development in patients with HCV-induced cirrhosis. We studied 218 patients with compensated EV-free, HCV-induced cirrhosis consecutively enrolled between 1989 and 1992 at three referral centers in Milan, Italy. Endoscopic surveillance was performed at 3-year intervals according to international guidelines. SVR was defined as undetectable serum HCV-RNA 24 weeks after treatment discontinuation. During a median follow-up of 11.4 years, 149/218 (68%) patients received antiviral treatment and 34 (22.8%) achieved SVR. None of the SVR patients developed EV compared with 22 (31.8%) of the 69 untreated subjects (P <0.0001) and 45 (39.1%) of the 115 non-SVR patients (P <0.0001). On multivariate analysis, HCV genotype 1b (hazard ratio [HR] 2.40; 95% confidence interval [CI] 1.17-4.90) and baseline model for end-stage liver disease (MELD) score (HR 1.20; 95% CI 1.07-1.35 for 1 point increase) were independent predictors of EV. Conclusion: In the long term, the achievement of SVR prevents the development of EV in patients with compensated HCV-induced cirrhosis. Therefore, in these patients, endoscopic surveillance can be safely delayed or avoided. Genotype 1b infection and MELD score identify the subset of patients at higher risk of EV development who need tailored endoscopic surveillance.

UR - http://www.scopus.com/inward/record.url?scp=77952704228&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77952704228&partnerID=8YFLogxK

U2 - 10.1002/hep.23528

DO - 10.1002/hep.23528

M3 - Article

C2 - 20196120

AN - SCOPUS:77952704228

VL - 51

SP - 2069

EP - 2076

JO - Hepatology

JF - Hepatology

SN - 0270-9139

IS - 6

ER -