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A S L D A b st ra ct s were included in the study. Hemoglobin less than 14.0g/dl at W1 and W2 of treatment was associated with subsequent decrease in ribavirin dose (p = 0.0005 and 0.0002, respectively), and addition of erythropoietin (p = 0.0145 and 0.0001, respectively). Drop in hemoglobin of.2g/dl from baseline atW2was also significantly associated with addition of erythropoietin (p = 0.0005). Hemoglobin at W1 or W2 was not associated with requirement for blood transfusion or with extended rapid virological response (eRVR), end of therapy response (ETR) or sustained virological response (with 4, 12 and 24 week follow-up; SVR4, SVR12 and SVR24 respectively). Undetectable viral load at W2 was associated with eRVR (p = 0.0025), ETR (p = 0.027), SVR4 (p = 0.037) and SVR12 (p = 0.0007). Undetectable viral load at W1 was not significantly associated with eRVR (p = 0.08), ETR or SVR4, SVR12 and SVR24. Conclusions In patients being treated with P, R, PI for CHC, undetectable viral load at W2 is associated with eRVR, ETR, SVR4 and SVR12. Early anemia (at W1 or W2) is associated with subsequent ribavirin dose reduction and addition of erythropoietin. Early monitoring of hemoglobin at W1 and W2 and of HCV RNA at W2may be helpful in patient management.

Background: Hepatocellular carcinoma (HCC) in nonalcoholic steatohepatitis (NASH) has been increasingly reported as the concept of NASH has received wide acceptance among clinicians in the intervening years. Moreover incidence of NASH itself is expected to increase reflecting age of gluttony. However it does not make sense from a cost-effectiveness point of view to screen HCC frequently in all patients with NASH because patients with NASH make up around 1% in overall Japanese population. Aim: This study was designed to assess risk factors for HCC in patients with NASH to develop effective screening methods. Patients and Methods: Our study included all the patients who were consecutively diagnosed at Gunma University Graduate School of Medicine and its affiliated hospitals as having NASH between 2000 and 2006, were followed up for at least 24 months. We evaluated incidence of HCC to date. We compared clinicopathological features (physical findings, laboratory findings, histological features and complications) between patients with HCC (HCC group) and patients without HCC (non-HCC group). The criteria for the diagnosis of NASH were compatible liver histology. We confirmed the diagnosis of HCC by ultrasonographic scanguided tumor biopsy except the treatment-resistant ascites or absence of informed consent in which an angiography or computed tomography showed typical characteristics of HCC. Results: The overall sample included 79 patients (26 men and 53 women, median age 63 years). The follow-up period ranged from 30 to 138 months with an average of 52 months. Fourteen patients (9 men and 5 women, median age 63 years) developed HCC. As for histological stage due to Blunt's classification, 1 and 16 had stage 1, 2 and 23 had stage 2, 3 and 12 had stage 3, and 8 and 14 had stage 4 in HCC group and non-HCC group, respectively. All cases accompanied either obesity or diabetes mellitus. Univariate analysis showed age, sex, histological stage, prothrombin time, serum total cholesterol level, and serum uremic acid level were significant different between HCC group and non-HCC group. Multiple logistic analysis showed male sex (odds ratio: 44.09, 95% Confidence interval: 3.564-545.4, p=0.032) and elder age (odds ratio: 1.134, 95% Confidence interval: 1.0181.265, p=0.029) were significant risk factors for HCC in patients with NASH. Conclusions: Though preliminary results, male sex and elder age were significant risk factors for HCC in patients with NASH and these patients have to be regularly monitored for early detection of HCC. At the same time, we should increase the sample size and follow-up periods and confirm our hypothesis in the near future.