AIM:To elucidate risk factors contributing to the development of hepatocellular carcinoma (HCC) among patients with sustained viral response (SVR) after interferon (IFN) treatment and to examine whether HCV-RNA still remained in the liver of SVR patients who developed HCC. METHODS:Two-hundred and sixty-six patients, who achieved SVR, were enrolled in this study. We retrospectively reviewed clinical, viral and histological features of the patients, and examined whether the development of HCC depends on several clinical variables using Kaplan-Meier Method. RT-PCR was used to seek HCV-RNA in 3 out of 7 patients in whom liver tissue was available for molecular analysis. RESULTS:Among the enrolled 266 patients with SVR, HCC developed in 7 patients (7/266; 2.6%). We failed to detect HCV-RNA both in cancer and non-cancerous liver tissue in all three patients. The cumulative incidence for HCC was significantly different depending on hepatic fibrosis (F3-4) (P = 0.0028), hepatic steatosis (Grade 2-3) (P = 0.0002) and age (≥ 55) (P = 0.021) at the pre-interferon treatment. CONCLUSION:The current study demonstrated that age, hepatic fibrosis, and hepatic steatosis at preinterferon treatment might be risk factors for developing HCC after SVR.

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Aim: Patients with chronic liver diseases (CLD) suffer from a variety of subjective symptoms, and the assessment of healthrelated quality of life (HRQOL) is crucial. The Chronic Liver Disease Questionnaire (CLDQ) is the first liver disease-specific instrument for this purpose. In this study we aimed to develop the Japanese version of CLDQ and to assess its validity and reliability in Japanese patients with chronic viral hepatitis.Methods: The participants included 135 Japanese patients chronically infected with hepatitis B or C virus. The Japanese version of the CLDQ was developed according to the standard "back-translation" method. In addition to the Japanese version of the CLDQ, we asked the patients to fill out two other selfreport questionnaires: the Japanese versions of the 36-Item Short Form Survey (SF-36) and Hospital Anxiety and Depression Scale (HADS). Then, the internal consistency, convergent and discriminant validity of the Japanese version of CLDQ were statistically examined.Results: Cronbach's alpha of the Japanese version of the CLDQ was acceptable. The mean score was lower in emotional domains of the CLDQ, compared with those in somatic domains. Pearson correlations between Japanese CLDQ and SF-36 and HADS were significant. The mean of the CLDQ scores decreased in all domains in patients with liver cirrhosis compared with those in patients with chronic hepatitis. Conclusion:The Japanese version of the CLDQ is a reliable and valid instrument for assessment of the HRQOL of Japanese patients with chronic viral hepatitis. The results also suggest that the HRQOL of Japanese patients is mainly impaired by emotional factors rather than somatic symptoms, and significantly worsened by progression of the disease.

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It still remains unclear how antimitochondrial autoantibodies (AMA) are involved with immunopathogenesis of primary biliary cirrhosis (PBC). We have suggested the potential role of IgA-AMA in damage to epithelial cells in PBC. In the current study, we investigated whether IgA-AMA were detectable in sera and saliva of PBC patients, to examine the association between detectable IgA-type autoantibodies in sera or saliva and progression of liver diseases. Fifty-three patients with PBC were enrolled, and IgA-AMA in sera and saliva were sought by immunoblotting using pork heart mitochondria as antigens. The progression of PBC was determined as Scheuer's classification consisting of four histological stages. We found IgA-AMA, IgA-anti-PDC-E2, and IgA-anti-E3BP in 43/53 (81%), 37/53 (70%), and 35/53 (66%) sera of patients with PBC, but none of controls. The progression of PBC was statistically associated with presence of IgA-anti-PDC-E2 (P = 0.0124), but neither with IgA-AMA (P = 0.1296) nor anti-IgA-E3BP (P = 0.5973). In saliva, detectable IgA-AMA, IgA-anti-PDC-E2, and IgA-anti-E3BP were noted in 12/26 (46%), 6/26 (23%), and 11/26 (42%), respectively. Detection of IgA-anti-PDC-E2 was strongly associated with progression of PBC (P = 0.0002), whereas detection of IgA-AMA and IgA-anti-E3BP were not associated (P = 0.2145 and P = 0.5118). The current findings suggest that the presence of IgA-anti-PDC-E2 in sera or saliva might be associated with progression of PBC, although a prospective study with PBC patients with detectable IgA-anti-PDC-E2 at early stages will be required to conclude the contribution of IgA-anti-PDC-E2 to the progression of PBC.