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Hepatic steatosis at one year is an additional predictor of subsequent fibrosis severity in liver transplantation recipients with recurrent hepatitis C virus |
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Brandman D, Pingitore A, Lai J, Roberts J, Ferrell L, Bass N, Terrault N. Liver Transpl. 2011 Jul 18. doi: 10.1002/lt.22389. [Epub ahead of print] |
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Source University of California San Francisco, 513 Parnassus Ave, Box 0538, San Francisco, CA 94143.
Recurrent hepatitis C virus (HCV) is the most common cause of graft loss among HCV-infected liver transplant (LT) recipients. Diabetes (DM) has been associated with increased rates of fibrosis progression but whether steatosis affects post-LT outcomes, independent of DM, is unclear. Using a retrospective cohort of HCV-infected LT recipients, we determined the prevalence of hepatic steatosis and evaluated the relationship between steatosis on index biopsy at one year post-LT (±6 months) and severity of subsequent fibrosis. A total of 152 HCV LT recipients were followed for a median follow-up after the index biopsy of 2.09 (range 0.13-6.17) years, with a median number of biopsies/patient after the index biopsy of 2 (range 1-6). Steatosis (≥5%) was present in 45 (29.6%) individuals in the 1-year index biopsy post-LT; steatosis was mild (grade 1) in 80%. In multivariate analysis, presence of steatosis at 1-year post-LT was positively associated with genotype 3 (OR= 3.60, p=0.02), older donor age (OR= 1.03, p=0.04), and pre-LT hypertension (OR= 3.29, p=0.009). At 3 years post-LT, the cumulative rate of significant fibrosis (F2-4 Ludwig-Batts scale) was 49% in those with steatosis at 1 year versus 24% in those without steatosis (p=0.003). In multivariable analysis, steatosis at 1-year was an independent predictor of subsequent F2-4 fibrosis (OR= 2.20, p=0.008). Steatosis was a stronger predictor of fibrosis in the setting of sirolimus use (HR 9.38, 95% CI 1.37, 64.16; p=0.02). We conclude that steatosis is frequent in the early post-LT period, and that steatosis within the 1 year post-LT is a marker of higher risk of fibrosis progression in HCV-infected patients.
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