The objective of this study was to assess the relationship between adherence to telaprevir based-regimen and antiviral effect in 94 Japanese patients with genotype 1 and high viral titer chronic hepatitis C. We included recently identified predictive factors such as IL28B polymorphism (rs8099917). Patients with rs8099917 TT genotype (n=50) treated with telaprevir based-regimen achieved a high SVR rate (94.0%, 47/50). In patients with rs8099917 TG/GG genotype (n=44), the SVR rate for treatment-naïve patients and relapsers and non-responders to previous treatment was 50.0%, 90.9%, and 30.4%, respectively, and efficacy in treatment-naïve and non-responder patients was considered inadequate. Importantly, adherence to telaprevir based-regimen should be maintained over a period of 24 weeks for treatment-naïve patients and relapsers with rs8099917 TG/GG genotype. In addition, prolonged therapy with telaprevir based-regimen may be considered for treatment-naïve patients and non-responders with rs8099917 TG/GG genotype.

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In Sapporo and its surrounding areas, we encountered 11 successive cases of acute sporadic hepatitis E between late September and late October in 2009. Surprisingly, the HEV strains, obtained from the patients, segregated to a compact cluster in genotype 4, suggesting that the epidemic was caused by the propagation of single source strain. In addition, these HEV strains were closely related not only to "Sapporo strain" previously reported, but also to "Kitami/Abashiri strain", which caused acute hepatitis several years ago in Kitami and Abashiri regions, located far away from Sapporo. Despite intensive surveillance by the Hokkaido Study Group for Hepatitis E, neither a common infection source nor precipitating event for epidemic could be identified. The advanced system for food distribution may have spread the HEV strains, thereby complicating identification of the source of HEV infection. "New Sapporo strains" should be carefully monitored in the future.

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A 70-year-old Japanese man underwent posterior segmentectomy of liver in order to treat hepatocellular carcinoma occurred after 2 years follow-up for presumed inactive carrier of hepatitis B virus with complication of nonalcoholic fatty liver disease. Depending upon precise histological assessment for underlying liver disease using the sample obtained by surgery, pathological diagnosis both chronic hepatitis B and nonalcoholic steatohepatitis (NASH) with grade 1 and stage 0 were confirmed. The current report is the first one in which minute clinical, virological and pathological characteristics are described for hepatocellular carcinoma developed in mild chronic hepatitis B caused by HBV genotype Ae and NASH with no fibrosis.

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The first case was a male in his 30's who was taking an antiepileptic agent for the treatment of lifelong epilepsy. He was being treated at a local clinic but developed severe liver dysfunction and lowered consciousness. Prothrombin time activity was less than 40% with grade II hepatic encephalopathy. He was diagnosed with acute liver failure due to hepatitis C virus (HCV). The route of infection was uncertain. The second case was a male in his 30's. He had been infected with HCV tainted blood and developed acute hepatitis type C (AHC). After admission, low prothrombin activity continued, and icterus was prolonged. Both cases were done with immediate multidisciplinary therapy including interferon (IFN), leading to significant improvement. After overcoming the acute stage IFN was continued for 24 weeks and persistent HCV infection was prevented in both cases. It was suggested that IFN was a useful treatment for acute liver failure due to HCV or AHC.

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It was reported that elevated serum CA19-9 levels in chronic liver injuries decreased in proportion to the improvement of the liver injuries after treatment. Case 1 was 48-year-old woman with chronic hepatitis B. Case 2 was 69-year-old man with hepatitis C virus (HCV)-related cirrhosis. Case 3 was 75-year-old man with chronic hepatitis C. In the present 3 cases, serum CA19-9 levels significantly decreased after successful antiviral treatment for viral hepatitis. These results indicate that liver injury might induce significant elevation of serum CA19-9 without malignant diseases.

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[in Japanese]

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