Occult hepatitis B virus infection as a risk factor for hepatocellular carcinoma in patients with chronic hepatitis C in whom viral eradication fails.

AIM: Recent studies have suggested that an occult hepatitis B virus (HBV) infection negative for HBsAg but positive for HBV-DNA contributes to hepatocellular carcinoma (HCC) development in patients with chronic hepatitis C. Some follow-up studies have suggested the clinical importance of occult HBV infections in HCC development even after interferon (IFN) therapy, but a recent study denies the significance of the impact of occult HBV infection. Focusing on HCC development in patients in whom hepatitis C virus (HCV) eradication by interferon (IFN) therapy had failed, we conducted this study in order to assess the impact of occult HBV infections on HCC development in these patients. METHODS: We enrolled 141 patients with chronic hepatitis C (histological stage F2 or F3) who were seropositive for HCV-RNA even after IFN therapy. Serum HBV-DNA was assayed using the real-time polymerase chain reaction. During follow-up, ultrasonography and/or computed tomography (CT) were performed at least every 6 months to monitor HCC development. RESULTS: The cumulative incidence rates of HCC were 8.9%, 25.7% and 53.7% at 5 years, 10 years and 15 years, respectively, after IFN therapy. Multivariate analysis indicated that low platelet counts (<12 x 10(4)/mm(3)), occult HBV infection, high ALT levels (>/=80 IU/L) after IFN therapy and the staging of liver fibrosis were important independent factors affecting the appearance of HCC. CONCLUSIONS: Occult HBV was a risk factor for HCC development in patients with chronic hepatitis C in whom HCV eradication had failed. Therefore, patients with chronic hepatitis C with occult HBV should be monitored carefully for HCC after IFN therapy.

Radiofrequency ablation of hepatocellular carcinoma: correlation between local tumor progression after ablation and ablative margin.

OBJECTIVE: To identify the determinants of tumor progression, we examined the ablation zones and patterns of local progression of small single primary hepatocellular carcinomas after radiofrequency ablation. MATERIALS AND METHODS: Eighty-five patients with single primary hepatocellular carcinoma less than 3 cm in diameter underwent complete tumor ablation. Clinical and biochemical features, tumor characteristics, tumor location within 5 mm from intrahepatic vessels, needle biopsy before treatment, and presence of ablative margin of 5 mm or more were statistically analyzed as determinants of local tumor progression. The Kaplan-Meier method and a Cox model were used for the analyses. Patterns of local tumor progression were examined by image analysis. RESULTS: During a median observation period of 30.3 months, 14 (16.5%) of the 85 patients had local tumor progression. The results of the log-rank test showed that the presence of vessels contiguous with the tumor (p = 0.0292) and the absence of an ablative margin of at least 5 mm (p = 0.019) significantly correlated with local tumor progression. Cox regression analysis showed that the absence of an ablative margin of at least 5 mm was an independent factor (p = 0.04). The most common pattern of local tumor progression was a single viable outgrowth from the side of the ablated area when the ablative margin was less than 5 mm. Multiple viable outgrowths were observed in one case despite the presence of an ablative margin greater than 5 mm. CONCLUSION: An ablation zone with an ablative margin of 5 mm or greater was the most important factor for local control of hepatocellular carcinoma.

Severe chronic active Epstein-Barr virus infection associated with multiple necrotic lesions in the liver.

We report an atypical presentation of a chronic active Epstein-Barr virus (EBV) infection with multiple nodular coagulation necrosis in the liver, that appeared as hypodense areas on a CT scan. The patient, a 26-year-old man, was hospitalized following over 2 years of intermittent fever, weight loss and liver abnormalities after contracting infectious mononucleosis. We diagnosed his illness as a chronic active EBV infection (CAEBV) because of the high antibody titers against EBV and the histological evidence of organ disease with demonstration of EBV mRNA. A liver biopsy revealed EBV-infected T-cell infiltration with hemophagocytosis and marked hepatocytolytic necrosis. The patient developed multiple coagulation necrosis with well-defined borders surrounding T-cell aggregation in the liver 8 months later. He died of respiratory failure due to interstitial pneumonitis. The analysis of EBV-genome termini demonstrated a clonal proliferation of T-cells harboring EBV, but no T-cell antigen receptor (TCR) gene rearrangement was observed. We speculate that the pathogenesis of this disease was an atypical expression of organ damage as a result of an aberrant T-cell response to EBV infection.