The present investigation compared the histological ®ndings in the liver of chronic hepatitis C patients who were or were not co-infected with TT virus (TTV) to determine the histological and clinical characteristics of TTV infection. One hundred eighty patients with chronic hepatitis or liver cirrhosis type C were included in this study. Serum samples were tested for the presence of TTV DNA by a nested polymerase chain reaction. The liver biopsy specimen of each patient was examined, and scores were assigned to indicate the severity of each of the following features: in¯ammatory cell in®ltration in the periportal, parenchymal, and portal areas; ®brous stage; lymphoid reaction in the portal area; portal sclerotic change; perivenular ®brosis; pericellular ®brosis; damage of bile duct; and irregular regeneration of hepatocytes. Sixty-four (34.4%) of the 180 patients were positive for TTV DNA. The histological features of the liver and the blood biochemical parameters of the TTV DNApositive and TTV DNA-negative patients, did not differ signi®cantly except for the score of irregular regeneration (IR) of hepatocytes. Among those in the F4 stage of ®brosis, the score of IR of the TTV DNA-positive patients was signi®-cantly higher than that of the TTV DNA-negative patients. In conclusion, chronic TTV infection does not modify the biochemical features of chronic hepatitis type C patients. TTV may be a risk factor, however, for the development of hepatocellular carcinoma in patients with type C liver disease in the F4 stage.

Our data suggest that chronic HGV coinfection worsens the histological features of liver disease.

Objective: We investigated the background clinical factors of patients with hepatocellular carcinoma (HCC) diagnosed at our institute and, from these results, determined those factors important for evaluation of a population at high risk of HCC. Methods: This study comprised 250 patients diagnosed with HCC from 1990 through 1995 in the Nihon University Itabashi Hospital. Background clinical factors, such as the results of blood chemistry at the time of the first angiography, were examined. Results: Markers of viral hepatitis in the 250 cases were as follows: type B (B-HCC), 29 (11.6%), type C (C-HCC), 201 (80.4%); type B+C, 3 (1.2%), and non-B, non-C (NBNC-HCC), 17 (6.8%). Approximately 35% of B-HCC and NBNC-HCC cases, but only 6% of C-HCC cases, exhibited platelet counts (PLT) equal to or more than 200,000/ml. On the other hand, 56.5% of the C-HCC cases exhibited PLT less than 100,000/ml, in contrast to less than 30% of the B-HCC and NBNC-HCC cases. Irrespective of the etiology of HCC, male sex and a history of smoking were characteristic risk factors. The percentages of abnormal results in combinations of tests in the B-HCC, C-HCC and NBNC-HCC subsets were: 69, 97 and 70% in the aspartate aminotransferase (AST) + PLT group (group A); 83, 98 and 70% in the group A + alanine aminotransferase (ALT) group (group B), and 86, 98 and 100% in the group B + γ-glutamyl transpeptidase (γ-GTP) group (group C), respectively. When hepatitis B surface antigen (HBsAg) and hepatitis C antibody (HCV-Ab) were also taken into account, abnormal results were found in every case in all of the HCC groups. Conclusion: C-HCC was found predominantly in cases with liver cirrhosis, whereas B-HCC and NBNC-HCC were observed more frequently in cases without liver cirrhosis. Testing for HBsAg and HCV-Ab, in addition to AST, ALT, PLT and γ-GTP, is considered necessary when screening for HCC.