{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,10]],"date-time":"2026-07-10T22:37:06Z","timestamp":1783723026967,"version":"3.55.0"},"reference-count":50,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2014,3,12]],"date-time":"2014-03-12T00:00:00Z","timestamp":1394582400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Liver International"],"published-print":{"date-parts":[[2014,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Aims<\/jats:title><jats:p>Aim of this study was to assess if host (immunogenetic traits, age, sex), exogenous (alcohol) or viral factors (viral type, past <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content> infection) might affect the progression of chronic hepatitis C to liver decompensation or the development of <jats:styled-content style=\"fixed-case\">HCC<\/jats:styled-content> in a cohort of patients exposed to a single blood transfusion prior to the introduction of anti\u2010<jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> screening.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Two hundred and forty\u2010eight patients with a history of a single exposure to blood or blood products prior to 1990 were retrospectively considered. Patients were devoid of other risk factors of liver disease or immunosuppression and na\u00efve to antiviral therapies. Eight baseline variables were assessed: age at transfusion, sex, <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content> core antibody, immunogenetic profile (<jats:styled-content style=\"fixed-case\">DRB<\/jats:styled-content>1*11, <jats:styled-content style=\"fixed-case\">DRB<\/jats:styled-content>1*1104, <jats:styled-content style=\"fixed-case\">DRB<\/jats:styled-content>1*07), <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> genotype and alcohol consumption.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The follow\u2010up was 22 (<jats:styled-content style=\"fixed-case\">SD<\/jats:styled-content>: 11) years. Sixty\u2010eight patients (27%) progressed to hepatic decompensation over a median period of 22.5\u00a0years (<jats:styled-content style=\"fixed-case\">IQR<\/jats:styled-content>: 14\u201330) and 41 patients (16%) developed <jats:styled-content style=\"fixed-case\">HCC<\/jats:styled-content> over a median period of 31\u00a0years (<jats:styled-content style=\"fixed-case\">IQR<\/jats:styled-content>: 24\u201338). The cumulative incidence of liver failure was 0.4% (95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>: 0.1\u20133.1), 4.9% (95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>: 2.6\u20139.3) and 16.2% (95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>: 10.4\u201324.7) at 10, 20 and 30\u00a0years after blood transfusion respectively. By univariate analysis, only age at transfusion was correlated with the risk of decompensation. Stratifying the age of transfusion by tertiles, the incidence of hepatic decompensation was 0.7% per year in patients transfused at \u226424\u00a0years of age as compared to 1.2% and 1.9% per year in those transfused at 25\u201335 and &gt;36\u00a0years of age respectively (<jats:styled-content style=\"fixed-case\">HR<\/jats:styled-content>: 5.5, 95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>: 2.78\u201310.7, <jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.001). The risk of <jats:styled-content style=\"fixed-case\">HCC<\/jats:styled-content> development was correlated by univariate analysis with age at transfusion (as continuous variable, <jats:styled-content style=\"fixed-case\">HR<\/jats:styled-content>: 1.12, 95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>: 1.08\u20131.16 per year of age, <jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.001, &gt;36 compared to \u226424\u00a0years, <jats:styled-content style=\"fixed-case\">HR<\/jats:styled-content>: 10.3, 95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>: 3.9\u201326.9, <jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.001) and male sex (<jats:styled-content style=\"fixed-case\">HR<\/jats:styled-content>: 4.2, 95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>: 1.7\u201310, <jats:italic>P\u00a0=\u00a0<\/jats:italic>0.001). Multivariate analysis confirmed age at transfusion and male sex as independent predictors of <jats:styled-content style=\"fixed-case\">HCC<\/jats:styled-content> development [<jats:styled-content style=\"fixed-case\">HR<\/jats:styled-content>: 1.12 per year (95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>: 1.08\u20131.16), <jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.001 and <jats:styled-content style=\"fixed-case\">HR<\/jats:styled-content>: 5.4 (95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>: 2.2\u201313.2), <jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.001 respectively].<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>In patients with transfusion\u2010acquired HCV infection, age at transfusion affects the risk for hepatic decompensation. Age at transfusion and male sex are independent risk factors for HCC development.<\/jats:p><\/jats:sec>","DOI":"10.1111\/liv.12502","type":"journal-article","created":{"date-parts":[[2014,2,17]],"date-time":"2014-02-17T11:26:57Z","timestamp":1392636417000},"source":"Crossref","is-referenced-by-count":5,"title":["Prognostic factors of hepatic decompensation and hepatocellular carcinoma in patients with transfusion\u2010acquired HCV infection"],"prefix":"10.1111","volume":"34","author":[{"given":"Claudio","family":"Zavaglia","sequence":"first","affiliation":[{"name":"Struttura Complessa di Gastroenterologia ed Epatologia \u2018Crespi\u2019 Ospedale Niguarda  piazza Ospedale Maggiore 3 20162 Milano Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Enrico","family":"Silini","sequence":"additional","affiliation":[{"name":"Unit\u00e0 di Anatomia Patologica Azienda Ospedaliero\u2010Universitaria di Parma  viale Gramsci 14 43100 Parma 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