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Background and aim: Patients with genotype 4 (G4) chronic hepatitis C (CHC) are considered a difficult to treat population, although current data on G4 treatment responsiveness and duration are controversial. Greece represents a country with an intermediate prevalence of G4 infections, offering an opportunity to compare treatment outcomes by genotype and to identify potential prognostic factors for sustained virologic response (SVR). Methods: All CHC patients from the HepNet.Greece, an ongoing nationwide cohort study on viral hepatitis, with known hepatitis C virus (HCV) genotype who received treatment with Peg-IFNa and ribavirin were analyzed. Results: From 4443 patients, 951 (61.7% males, 78.4% Greeks, median age 40.6 years, 10% cirrhosis) fulfilled the inclusion criteria. G4 was found in 125 (13.1%) patients. Genotype distribution was not significantly different between Greeks and immigrants. Patients with G4 had similar odds of SVR compared to G1 but significantly lower compared to G2/G3. Age, treatment discontinuation, presence of cirrhosis and previous history of HCV-treatment were associated with lower probabilities of SVR. Ethnicity did not affect SVR for all genotypes while response to treatment was similar between Greek and Egyptian patients groups (35.7% vs 40.9%, p=0.660%) with G4 infection. The relation between SVR and genotype did not substantially change after adjustment for age, gender, cirrhosis, treatment interruption and history of HCV-treatment. Conclusions: The findings of this large cohort of CHC patients with a well balanced genotype distribution further supports the idea of considering G4 as a difficult to treat genotype. Further investigation is needed to identify genotype specific prognostic factors. [ABSTRACT FROM AUTHOR]

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., (© 2014 John Wiley & Sons Ltd.)

Objective: To evaluate the risk and predictors of hepatocellular carcinoma (HCC) in HBeAg-negative chronic hepatitis B patients of the large HEPNET.Greece cohort study who received long-term oral antivirals starting with lamivudine monotherapy., Design: Retrospective analysis of HCC incidence in HBeAg-negative chronic hepatitis B patients from a retrospective-prospective cohort who were treated with nucleos(t)ide analogue(s) starting with lamivudine monotherapy for ≥12 months., Setting: A nationwide network of liver centres., Patients: 818 patients were included: 517 with chronic hepatitis B only; 160 with compensated cirrhosis; 56 with decompensated cirrhosis; 85 with unclassified disease severity., Interventions: All patients were treated with nucleos(t)ide analogue(s) starting with lamivudine monotherapy., Main Outcome Measures: Development of HCC., Results: During a median follow-up of 4.7 years, HCC developed in 49 (6.0%) patients. The 5-year cumulative incidence of HCC was higher in patients with cirrhosis than in those with chronic hepatitis B only (11.5% vs 3.2%, respectively; p<0.001). HCC developed in 0.7%, 6.7% and 11.7% of patients <50, 50-60 and >60 years old, respectively (p<0.001). Virological on-therapy remission did not significantly affect the incidence of HCC in all patients or those with cirrhosis, but it showed a trend for lower HCC incidence in patients with chronic hepatitis B only (p=0.076). In multivariate analysis, age, gender and cirrhosis were independently associated with HCC risk regardless of virological remission., Conclusions: Long-term therapy with nucleos(t)ide analogue(s) starting with lamivudine monotherapy does not eliminate HCC risk in HBeAg-negative chronic hepatitis B. The risk of HCC is particularly high in patients with cirrhosis, who should remain under HCC surveillance even during effective therapy. Older age and male gender remain independent risk factors for HCC, while virological on-therapy remission does not seem to significantly reduce the overall incidence of HCC.

Aim: To investigate the long-term outcome and the risk of progression to chronic hepatitis B in inactive hepatitis B surface antigen carriers., Material and Methods: A total of 307 HBsAg (+)/HBeAg (-)/antiHBe (+) subjects with initially normal alanine aminotransferase (ALT) levels and undetectable/ low serum HBVDNA with hybridization assay and later with PCR (10(5) copies/ml), were followed-up every 6 months for a period of 3 to 21 years (7.45 +/- 3.75 years)., Results: 234 out of the 307 HBsAg (+) patients (76.2%) had persistently normal ALT and undetectable / low (10(5) copies/ml) HBVDNA during follow-up. In 73 patients (23.8%), a reactivation of the disease with elevated ALT and positive HBVDNA (> (10(5)copies/ml) was recorded during the follow up. Thirty-five out of 73 patients underwent liver biopsy, while 22 of them received treatment. Twenty-four patients (7.8%) lost HBsAg after a mean of 7.4 +/- 3.6 years. Regarding the complications of chronic hepatitis B, only one patient developed compensated cirrhosis and no one developed HCC., Conclusions: Our results show that in almost 24% of inactive chronic hepatitis B carriers reactivation of the disease may occur even after many years. However the risk of liver-related complications is very low in these subjects.

The prevalence of hepatitis C virus (HCV) infection and the mother-to-child transmission of HCV were studied in 2408 pregnant women. Positive antiHCV were detected in 47 women (1.95%), 21 of whom (44.7%) were HCVRNA(+), but only seven had abnormal aminotransferases. Three/21 HCVRNA(+) women had an abortion. We lost contact with other 10 women. Thirty-four babies were tested for antiHCV, HCVRNA and levels of aminotransferases at birth and at the age of 6 and 12 months. AntiHCV were detectable in all babies at birth and these maternally acquired antibodies disappeared by the age of 12 months in all but two of who were infected with HCV. HCVRNA was detected at birth in one (6.25%) baby born out of 16 HCVRNA(+) mothers and this baby also had abnormal aminotransferases. However, HCVRNA was undetectable and aminotransferases returned to normal levels by the age of 6 months. In another baby born also from an HCVRNA(+) mother, the HCVRNA was detected for the first time at the age of 12 months. The HCV genotype from both babies was the same as their mother's. These results show that (a) the high prevalence in the group of pregnant women studied can possibly be attributed to the fact that 311/2408 (12.91%) of them came from the former eastern countries, where disposable syringes were not used but lately or were ex-drug addicts and (b) there is a low risk of perinatal mother-to-child transmission of HCV and this risk is related to the presence of HCVRNA in the carrier mother.