Hepatocellular carcinoma risk in HBeAg-negative chronic hepatitis B patients with or without cirrhosis treated with entecavir: HepNet.Greece cohort.

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.

Association of antiviral therapy with reduced disease progression in chronic Hepatitis B patients: Results from a nation-wide cohort study.

BACKGROUND AND AIMS: Although effective treatment in terms of inducing virological and biochemical response for chronic hepatitis B (CHB) is available, its effect on the clinical course of the disease has not yet been accurately estimated. Objective of this study was to evaluate the effect of antiviral therapy and its type [interferon +/- nucleos(t)ide analogs (NAs) vs. NAs] on the occurrence of a clinical event (liver decompensation, liver transplant, hepatocellular carcinoma and death from a liver-related cause) in CHB patients. METHODS: The study population was derived from the HEPNET-Greece, a nationwide cohort study aimed to evaluate the current epidemiological course of viral hepatitis. To account for time-dependent confounding, Cox marginal structural models were used to analyze data. RESULTS: Thirty out of 2,125 eligible patients experienced a clinical event during their follow-up. When comparing treated to untreated individuals, the hazard ratio (HR) for a clinical event was 0.39 (95% CI: 0.16-0.98; p =0.044) in the whole sample, whereas there were indications of a more intense effect in the subgroup of patients with cirrhosis at presentation (HR =0.16, 95% CI: 0.02-1.21; p =0.075). The effect of Interferon initiated treatment was not significantly different of that of NAs. There was some evidence, albeit not statistically significant, of a protective treatment effect on hepatocellular carcinoma development (HCC). CONCLUSIONS: Data from observational studies can provide useful inference, provided they are analyzed appropriately. The current study has shown that the available treatment options for CHB offer a significant clinical benefit to CHB infected individuals. Hippokratia 2016, 20(3): 214-221.

Atorvastatin therapy is associated with improvement of oxidized low-density lipoprotein cholesterol levels, which correlates with the degree of stenosis in patients with carotid atheromatosis with and without prior angioplasty.

AIM: Oxidized low-density lipoprotein (oxLDL) is a pivotal factor of the atheromatous process. Statins reduce atheromatosis and cardiovascular risk. The aim of the present study was to investigate the effect of statin therapy on circulating oxLDL and the possible impact of such effect on stenosis due to carotid artery atheromatosis. METHODS: A total of 100 patients (76 males, median age 68 years) with carotid atheromatosis were enrolled. Those with stenosis >70% (n=50) were pre-treated with carotid angioplasty, whereas those with <70% were treated conservatively. Both groups were given low-dose atrorvastatin, tittered to maintain LDL cholesterol <100 mg/dL. Anthropometrics, complete lipid profile, and oxLDL were obtained in 1, 3, 6 and 12 months. Stenosis was evaluated by ultrasonography at baseline and 12 months. RESULTS: Lipid profile significantly improved at 12 months and oxLDL fell from 62.26+/-22.03 mg/dL at baseline to 44.49+/-21.75 mg/dL at 12 months (P<0.001). In the invasively pretreated group no restenosis was noticed; in the conservatively treated group a significant reduction of stenosis was demonstrated (47.6+/-13.2% vs 37.7+/-15.7%, P<0.001). The decrease of oxLDL correlated with the reduction of stenosis (r=0.17, P=0.018). In multivariate analysis, oxLDL was an independent risk factor for re-stenosis (hazard ratio=4.319, P<0.001). CONCLUSION: A marked reduction of oxLDL was shown in patients with carotid atheromatosis treated with low-dose atorvastatin. Moreover, oxLDL could be a measure of the degree of stenosis in such patients.