Sarah Bos

54 CHAPTER 4 SynthaSil forAPTT, factordeficientplasmaforFII andQFAthrombinforFI) andprotocols from the manufacturer (Instrumentation Laboratory, Breda, the Netherlands). Edoxaban-calibrated Anti-Xa levels We estimated edoxaban plasma levels by edoxaban-calibrated anti-Xa assays. The anti-Xa assay was assessed on the ACL 300 TOP (Werfen, Breda, the Netherlands) with BIOPHEN heparin (LRT) purchased from Nodia (Amsterdam, the Netherlands). This was calibrated with the BIOPHEN Edoxaban calibrator from Nodia (Amsterdam, the Netherlands). Statistical analysis A difference of 20% in the reduction of thrombin generation following edoxaban between patients and controls was considered relevant. This difference could be detected with an alpha of 0.05, a standardized power of 0.80, and a two-sided sigma of 20% in both groups using 16 subjects per group. Data are expressed as means (with standard deviations (SDs)), medians (with ranges), or numbers (withpercentages) as appropriate. Twogroupswere compared by Student’s t-test or Mann-Whitney U test as appropriate. Multiple groups were compared using One-way ANOVA (with the Bonferroni posttest) or Kruskal-Wallis H test (with Dunn’s posttest) as appropriate. The Wilcoxon signed rank test was used to assess differences between time points within a single group. P values of 0.05 or less were considered statistically significant. GraphPad Prism (San Diego, USA) and IBM SPSS Statistics 23 (New York, USA) were used for analyses. Results Patient characteristics Sixteen patients and 16 healthy subjects were included. The median age of patients was 60 [48-65] years versus 49 [42-58] years for the healthy subjects. Mean BMI was similar between patients and healthy subjects as shown in table 1. Fifteen patients had Child Pugh A cirrhosis and one had Child Pugh B cirrhosis. None of the patients was decompensated. Etiologies of cirrhosis were distributed as follows: 4 cholestatic liver disease (1 primary biliary cholangitis, 2 primary sclerosing cholangitis (PSC), 1 small duct PSC), 2 non-alcoholic steatohepatitis (NASH), 4 alcoholic steatohepatitis (ASH), 2 auto-immune hepatitis (AIH), 1 hepatitis C virus (HCV), 1 hemochromatosis and 2 overlap syndromes (1 PSC/AIH and 1 NASH/ASH/AIH).