Data from a randomly generated split-sample of 50 (60%) patients were used to estimate the model, and data from the remaining 34 (40%) patients were used to validate the model. A predictive model was constructed by modeling the values of the independent variables and their regression coefficients. Each of the variables included in the model was analyzed to rule out any significant differences between the estimation and the validation groups. Bootstrapping was used to perform an additional internal validation by generating 10,000 resampling BGB324 in vivo sets with replacement. The results of the internal bootstrap validation gave estimates for the area under the receiver operator

characteristic (AUROC) curve with the median (5th percentile-95th percentile). The diagnostic accuracy of LSM (at each time point) and of the predictive model (at 6 months) to identify patients at risk to develop significant fibrosis (F ≥ 2) and portal hypertension (HVPG≥ 6 mmHg) at 1 year after LT were assessed using the AUROC curve. The optimal LSM and score cutoff values were selected on the basis of sensitivity (S), specificity (Sp), positive predictive value (PPV), and negative predictive value

(NPV) to identify significant fibrosis PF-02341066 price and portal hypertension. We used SAS version 9.1.3 software (SAS Institute Inc., Cary, NC) for the MMRM analysis. All other analyses were done with SPSS 12.0 (SPSS Inc., Chicago, IL). From August 2004 to January 2008, 84 LT recipients with HCV infection and MCE公司 19 with other etiologies were included. The cause of LT in non–HCV-infected patients was: alcoholic cirrhosis (n = 10), primary biliary cirrhosis (n = 2), Caroli’s disease (n = 2), familial amyloid polyneuropathy (n = 2), autoimmune hepatitis (n = 1), and cryptogenetic cirrhosis (n = 2). The baseline characteristics (donors

and recipients) of all patients (n = 103), including histological and hemodynamic data 1 year after LT, are summarized in Table 1. All HCV-infected patients showed histological signs of chronic hepatitis C recurrence. Acute rejection was carefully investigated and not detected in any of the liver biopsies performed at 12 months. Liver biopsy in the five patients not infected with HCV showed mild steatosis without Mallory hyaline (n = 1), minimal sinusoidal dilatation (n = 1), and unspecific mononuclear infiltration (n = 3). Of the liver biopsies, 41 (46%) were percutaneous and 48 (54%) were transjugular. The median of total length was 17 mm (8–23 mm) in percutaneous biopsies and 16 mm (6–36 mm) in transjugular biopsies (P = 0.602), with 91% of specimens ≥ 10 mm, 68% ≥ 15 mm, and 32% ≥ 20 mm. We found a good correlation between significant fibrosis and portal hypertension (kappa = 0.62) including liver biopsies < 15 mm (kappa = 0.75) and < 10 mm (kappa = 1.0). A total of 335 valid LSM were available during the first 12 months after LT.