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Hepatocellular carcinoma (HCC) may still develop in chronic hepatitis B (CHB) patients treated with lamivudine. Whether HCC rates are comparable in patients treated with the current first-line antivirals remains uncertain. We estimated the incidence and evaluated predictors of HCC in a large nationwide prospective cohort (HepNet.Greece) of HBeAg-negative CHB patients treated with entecavir. HBeAg-negative CHB patients from the same cohort who were initially treated with lamivudine were used as controls. We included 321 patients treated with entecavir for a median of 40 months and 818 patients treated initially with lamivudine for a median of 60 months. In the entecavir group, HCC developed in 4 of 321 (1.2%) patients at a median of 1.5 (range: 1.0-4.5) years, while the cumulative HCC incidence was significantly higher in cirrhotics than noncirrhotics (1, 3, 5 years: 0%, 3%, 9% vs 1%, 1%, 1%; P = 0.024) and in older patients (P = 0.026). Entecavir compared with lamivudine group patients had lower HCC incidence (1, 3, 5 years: 0.3%, 1.2%, 2.8% vs 0.7%, 3.8%, 5.6%; P = 0.024). However, in multivariable Cox regression analysis, the HCC risk was independently associated with older age (P < 0.001), male gender (P = 0.011) and cirrhosis (P = 0.025), but not with the initial agent. In conclusion, our large nationwide study indicates that the HCC risk remains increased in entecavir-treated HBeAg-negative CHB patients with cirrhosis, particularly of older age, at least for the first 5 years. The HCC risk does not seem to be significantly reduced with entecavir compared with antiviral therapy starting with lamivudine.

In HBeAg-negative chronic hepatitis B patients treated with peginterferon alfa-2a, HBsAg decline >10% at 24 weeks is significantly associated with SR. The combination of the PARC rule and week 24 decline in HBsAg can identify almost two-thirds of patients who are unlikely to achieve SR. Clinicaltrials.gov identifier: NCT01283074.

Nonalcoholic fatty liver disease (NAFLD) is closely related to insulin resistance and the metabolic syndrome and might be an important cardiovascular (CV) risk factor. Epicardial adipose tissue (EAT) has been implicated in the pathogenesis of obesityrelated CV disease. In an NAFLD population, we investigated EAT thickness and its possible relations to NAFLD and cardiac structure and function. This was an observational study of 57 patients with NAFLD and 48 age-matched controls. Patients with NAFLD had significantly higher body mass index (P < .0001), waist circumference (P < .0001), and high-sensitivity C-reactive protein (P ¼ .005), whereas high-density lipoprotein cholesterol (P ¼ .01) and adiponectin (P ¼ .005) levels were significantly lower. The EAT was not thicker in NAFLD but was positively related to indices of impaired glucose tolerance and inflammation, with diabetes being an independent predictor of EAT thickness (b* ¼ 0.29, P ¼ .04). No relations were found between EAT and cardiac structure and function. In conclusion, this study confirms a pathologic phenotype of NAFLD. Epicardial fat was not significantly related to NAFLD per se, but diabetes, glucose metabolism, and inflammation were closely related to its thickness.

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