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Prognostic factors of hepatic decompensation and hepatocellular carcinoma in patients with transfusion‐acquired HCV infection
Author(s) -
Zavaglia Claudio,
Silini Enrico,
Mangia Alessandra,
Airoldi Aldo,
Piazzolla Valeria,
Vangeli Marcello,
Stigliano Rosa,
Foschi Antonella,
Mazzarelli Chiara,
Tinelli Carmine
Publication year - 2014
Publication title -
liver international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.873
H-Index - 110
eISSN - 1478-3231
pISSN - 1478-3223
DOI - 10.1111/liv.12502
Subject(s) - medicine , hepatocellular carcinoma , decompensation , blood transfusion , immunosuppression , univariate analysis , incidence (geometry) , hepatitis c , gastroenterology , liver transplantation , cumulative incidence , cohort , transplantation , multivariate analysis , physics , optics
Aims Aim of this study was to assess if host (immunogenetic traits, age, sex), exogenous (alcohol) or viral factors (viral type, past HBV infection) might affect the progression of chronic hepatitis C to liver decompensation or the development of HCC in a cohort of patients exposed to a single blood transfusion prior to the introduction of anti‐ HCV screening. Methods Two hundred and forty‐eight 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 naïve to antiviral therapies. Eight baseline variables were assessed: age at transfusion, sex, HBV core antibody, immunogenetic profile ( DRB 1*11, DRB 1*1104, DRB 1*07), HCV genotype and alcohol consumption. Results The follow‐up was 22 ( SD : 11) years. Sixty‐eight patients (27%) progressed to hepatic decompensation over a median period of 22.5 years ( IQR : 14–30) and 41 patients (16%) developed HCC over a median period of 31 years ( IQR : 24–38). The cumulative incidence of liver failure was 0.4% (95% CI : 0.1–3.1), 4.9% (95% CI : 2.6–9.3) and 16.2% (95% CI : 10.4–24.7) at 10, 20 and 30 years 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 ≤24 years of age as compared to 1.2% and 1.9% per year in those transfused at 25–35 and >36 years of age respectively ( HR : 5.5, 95% CI : 2.78–10.7, P < 0.001). The risk of HCC development was correlated by univariate analysis with age at transfusion (as continuous variable, HR : 1.12, 95% CI : 1.08–1.16 per year of age, P < 0.001, >36 compared to ≤24 years, HR : 10.3, 95% CI : 3.9–26.9, P < 0.001) and male sex ( HR : 4.2, 95% CI : 1.7–10, P = 0.001). Multivariate analysis confirmed age at transfusion and male sex as independent predictors of HCC development [ HR : 1.12 per year (95% CI : 1.08–1.16), P < 0.001 and HR : 5.4 (95% CI : 2.2–13.2), P < 0.001 respectively]. Conclusions In patients with transfusion‐acquired HCV infection, age at transfusion affects the risk for hepatic decompensation. Age at transfusion and male sex are independent risk factors for HCC development.