{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T19:20:09Z","timestamp":1791919209809,"version":"4.3.4"},"reference-count":27,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":1918,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2010,6]]},"abstract":"<jats:sec>\n            <jats:title\/>\n            <jats:p>\n                                 <jats:bold>The incidence of<\/jats:bold>\n                                 <jats:bold>\n                                    de novo\n                                 <\/jats:bold>\n                                 <jats:bold>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<\/jats:bold>\n                                 <jats:bold>\n                                    de novo\n                                 <\/jats:bold>\n                                 <jats:bold>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 (<\/jats:bold>\n                                 <jats:bold>\n                                    P\n                                 <\/jats:bold>\n                                 <jats:bold>&lt; 0.0001) and 45 (39.1%) of the 115 non-SVR patients (<\/jats:bold>\n                                 <jats:bold>\n                                    P\n                                 <\/jats:bold>\n                                 <jats:bold>&lt; 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.<\/jats:bold>\n                                 <jats:bold>\n                                    Conclusion:\n                                 <\/jats:bold>\n                                 <jats:bold>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. Hepatology 2010<\/jats:bold>\n                              <\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.23528","type":"journal-article","created":{"date-parts":[[2010,1,27]],"date-time":"2010-01-27T19:55:11Z","timestamp":1264622111000},"page":"2069-2076","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":164,"title":["Sustained Virologic Response Prevents the Development of Esophageal Varices in Compensated, Child-Pugh Class A Hepatitis C Virus\u2013Induced Cirrhosis. A 12-Year Prospective Follow-Up Study"],"prefix":"10.1097","volume":"51","author":[{"given":"Savino","family":"Bruno","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrea","family":"Crosignani","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Corinna","family":"Facciotto","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sonia","family":"Rossi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luigi","family":"Roffi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alessandro","family":"Redaelli","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roberto","family":"de Franchis","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Piero Luigi","family":"Almasio","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrick","family":"Maisonneuve","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"R1-24-20250312","doi-asserted-by":"crossref","first-page":"463472","DOI":"10.1053\/gast.1997.v112.pm9024300","article-title":"Morbidity and mortality in compensated cirrhosis type C: a retrospective followup study of 384 patients.","volume":"112","author":"Fattovich","year":"1997","journal-title":"Gastroenterology"},{"key":"R2-24-20250312","doi-asserted-by":"crossref","first-page":"131136","DOI":"10.1136\/gut.47.1.131","article-title":"Hepatitis C virus related cirrhosis: time to occurrence of hepatocellular carcinoma and death.","volume":"47","author":"Degos","year":"2000","journal-title":"Gut"},{"key":"R3-24-20250312","doi-asserted-by":"crossref","first-page":"744749","DOI":"10.1136\/gut.2003.020263","article-title":"Natural history of compensated viral cirrhosis: a prospective study on the incidence and hierarchy of major complications.","volume":"53","author":"Benvegnu","year":"2004","journal-title":"Gut"},{"key":"R4-24-20250312","doi-asserted-by":"crossref","first-page":"13031310","DOI":"10.1002\/hep.21176","article-title":"The natural history of compensated cirrhosis due to hepatitis C virus: a 17year cohort study of 214 patients.","volume":"43","author":"Sangiovanni","year":"2006","journal-title":"Hepatology"},{"key":"R5-24-20250312","doi-asserted-by":"crossref","first-page":"11471158","DOI":"10.1038\/ajg.2009.31","article-title":"Predicting mortality risk in patients with compensated HCVinduced cirrhosis: a longterm prospective study.","volume":"104","author":"Bruno","year":"2009","journal-title":"Am J Gastroenterol"},{"key":"R6-24-20250312","first-page":"217231","article-title":"Natural history and prognostic indicators of survival in cirrhosis: a systematic review of 118 studies.","volume":"44","author":"DAmico","year":"2006","journal-title":"J Hepatol"},{"key":"R7-24-20250312","doi-asserted-by":"crossref","first-page":"22542261","DOI":"10.1056\/NEJMoa044456","article-title":"Betablockers to prevent gastroesophageal varices in patients with cirrhosis.","volume":"353","author":"Groszmann","year":"2005","journal-title":"N Engl J Med"},{"key":"R8-24-20250312","doi-asserted-by":"crossref","first-page":"7884","DOI":"10.7326\/0003-4819-116-1-78","article-title":"A consumers guide to subgroup analyses.","volume":"116","author":"Oxman","year":"1992","journal-title":"Ann Intern Med"},{"key":"R9-24-20250312","first-page":"18","article-title":"Decisionmaking model for a noninvasive diagnosis of compensated liver cirrhosis.","volume":"25","author":"Marmo","year":"1983","journal-title":"Ital J Gastroenterol"},{"key":"R10-24-20250312","first-page":"285290","article-title":"Differential distribution of hepatitis C virus genotypes in patients with and without liver function abnormalities.","volume":"21","author":"Silini","year":"1995","journal-title":"Hepatology"},{"key":"R11-24-20250312","first-page":"983989","article-title":"Prediction of the first variceal hemorrhage in patients with cirrhosis of the liver and esophageal varices. 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