5 mg/dL, and T3/4 stage were

associated with RFS on univariable analysis (Supporting Table 4). Active HCV infection and albumin <3.5 mg/dL were associated with OS on univariable analysis. There was no significant difference in OS after transplantation between NASH and HCV/ALD MLN0128 research buy patients (3-year 83.3% versus 71.1%; P = 0.204; Supporting Fig. 2). T3/4 stage was independently associated with RFS on multivariable analysis (Exp B, 3.291 [1.116-9.705]; P = 0.032). Though not significant, both active HCV infection (Exp B, 2.252 [0.891-5.688]; P = 0.087) and albumin <3.5 mg/dL (Exp B, 2.316 [0.967-5.544]; P = 0.061) were independently associated with OS on multivariable analysis. Among those with NASH, differences in RFS (median, 60 months versus not reached; P = 0.364) and OS (median, 64 months versus not reached; P = 0.155) between patients with and without bridging fibrosis or cirrhosis were not significant (Supporting Figs. 3 and 4). Seven of twenty-three NASH patients with metabolic syndrome (30.4%) and 9 of 29 (31.0%) without metabolic Angiogenesis inhibitor syndrome died at last follow-up. Causes of death among patients with metabolic syndrome included HCC progression without liver failure (n = 1), liver failure resulting from HCC progression (n = 2), liver failure without HCC recurrence

(n = 2), and coronary artery disease (n = 2). Corresponding causes of death among NASH patients without metabolic syndrome included HCC progression without liver failure (n = 2), liver failure resulting from HCC progression (n = 4), and liver failure without HCC recurrence (n = 3). Causes of death among HCV/ALD patients included HCC progression without liver failure (n = 27), liver failure from HCC progression (n = 10), liver failure without HCC recurrence

(n = 27), and other causes (n = 13). In this retrospective study, NASH patients with HCC had less-severe background liver disease at tumor diagnosis compared to HCV MCE and/or ALD counterparts. Among all patients who underwent curative treatment of HCC, 17.2% had NASH—a volume higher than that noted in other series.25, 31 In agreement with other reports, HCC/NASH patients were more often female, were older at HCC diagnosis, had larger BMI, and more often had components of or the diagnosis of metabolic syndrome compared to HCV/ALD patients.1, 9, 18-20, 23, 24, 28, 38-40 Similarly, NASH/HCC specimens also had more-severe steatosis, lobular inflammation, and hepatocyte ballooning (Table 1). Though clinical and individual histopathological findings should not be used as surrogates for an overall pathologic diagnosis of NASH,7, 15, 41-46 these differences reflect the accuracy of pathologist diagnosis of NASH in this patient cohort. Uniquely, this study shows that NASH patients have better synthetic liver function (as measured by serum bilirubin, albumin, and INR), less often had ascites, and had lower MELD scores compared to HCV/ALD counterparts at HCC diagnosis.