HBV markers and antibodies (anti-C100 and anti-Core) to HCV were tested in 774 cases in an endemic area for liver diseases. Out of 774 cases, 97 cases (12.5%) were positive for HBsAg and 94 cases (12.1%) were positive for antibodies to HCV. Ten (10.3%) among 97 cases positive for HBsAg were superinfected with HCV.
In 132 cases negative for HBsAg and with elevated ALT, 39 cases (29.5%) were positive for antibodies to HCV.
HBV markers which reflect the HBV replication such as HBsAg titer, frequency of HBe antigenemia, DNA-P levels and inhibitory rate of anti-HBc titers were lower in the cases of superinfection than in HBV carriers negative for antibodies to HCV.
These results suggest that HCV may reduce the replication of HBV in the cases of superinfection.

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A seroepidemiological survey of four hepatitis C virus (HCV) relative antibodies was conducted among 1062 inhabitants who lived in an endemic area for non-A, non-B hepatitis in Gifu prefecture Japan, and were older than 30 years. Each seropositive rate of HCV relative antibodies was as follows: anti C100-3 antibody 15.3%, anti CP-9 antibody 36.0%, anti CP-10 antibody 33.3% and anti GOR antibody 22.3%. 482 of 1062 (45.4%) inhabitants were seropositive for anti C100-3 antibody and/or anti CP-9 antibody and/or and CP-10 antibody, who were considered to have been infected with HCV previously. Remarkably, 91 of 918 (9.9%) inhabitants with normal serum level of ALT (<36IU/l) were seropositive for anti C100-3 antibody.

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Genomes of hepatitis C virus (HCV) have been reported to have divergence among nations or individuals. We cloned and sequenced the structural regions of HCV isolated from 5 Japanese patients with liver cirrhosis and hepatocellular carcinoma, and compared those with other clones reported in Japan and in the United States. The 5' non-coding region is very conserved and the core region is relatively conserved among the all clones. In contrast, the envelope region (E1, NS1/E2) was not so conserved between Japanese clones and American's clone. Furthermore, we recognized two hypervariable regions (HV1, HV2) in NS1/E2. The hydrophobicity analysis of these regions, however, showed that there are almost idenitcal hydrophilic portions in HV1 and HV2. The secondary structure analysis of the proteins showed that all isolates have identical turn structure in the portions.
These data suggested that the regions may play an important role in the immunoreactions as reported in human immunodeficiency virus.

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Pathophysiology after simultaneous interruption of each branch of hepatic artery (A), portal vein (P), and bile duct (B) in the 40% areas of the liver was investigated with and without penicillin (Pc) administration. Main cause of death within one week was hepatic failure. Liver damage was observed histologically in both ligated and nonligated hepatic lobes.
In the group of 40% APB interruption without Pc administration, severe hepatic dysfunction and systemic endotoxemia were disclosed. Considerable elevation of lipid peroxide and marked decrease of hepatic microcirculation were also observed. However, in the groups of 40% APB interruption with Pc administration and of hepatectomy of the ligated hepatic lobe 6 hours after 40% APB interruption without Pc administration, those changes were significantly less and the long-term prognosis was notably improved.
Consequently, pathogenesis of liver damage in the nonligated hepatic lobe after 40% APB interruption may be caused by decreased microcirculation and promoted by lipid peroxidation following marked systemic endotoxemia originating in the ligated hepatic lobe.

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Effect of dibutyryl cyclic AMP (DBcAMP) and glucagon on liver adenine nucleotide metabolism in hepatitis induced by D-galactosamine (GalN) was investigated. In normal rats, after the administration of two stimulators, hepatic ATP level decreased slightly and transiently, with concomitant increased in ADP and AMP. It was posturated that both stimulators enhanced ATP-utilizing metabolic processes such as gluconeogenesis.
Reduction of all adenine nucleotides level occurs in liver tissue severly damaged by GalN; this reflects the marked loss of viable hepatocytes. However, the level of all adenine nucleotides was restored by DBcAMP and glucagon administration in GalN treated rats. Different metabolic response was recognized between DBcAMP and glucagon. DBcAMP brought about higher level of hepatic ATP than glucagon in GalN treated rats.
Thease findings suggested that DBcAMP was more effective than glucagon especially on liver energy metabolism in GalN treated rats.

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An ultrastructural study was performed using supersaturated model bile systems to partially explore the mechanisms whereby apolipoprotein (apo) A-1 inhibits cholesterol crystal nucleation. Various lipid particles; vesicle, micelle, and non-micellar, non-vesicular discoidal particle, in model bile systems in the absence or presence of apo A-1 were consistently separated by gel permeation chromatography. Apo A-1 coeluted with discoidal particles. Discoidal particles without apo A-1 showed rapid transformation, i.e., multilamellar formation, followed by microcrystal nucleation, whereas those with apo A-1 showed very little transformation. In conclusion, apo A-1 stabilizes discoidal particles, consequently inhibiting cholesterol crystal nucleation.

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The Liver Cancer Study Group of Japan analyzed statistically 9564 patients with primary liver cancer diagnosed from Jan. 1, 1986 to Dec. 31, 1987 in 601 hospital throughout the country. In 3263 cases, a histological diagnosis was available. They comprised 2982 cases of hepatocellular carcinoma, 173 of cholangiocellular carcinoma, 25 of mixed carcinoma, 19 of hepatoblastoma, 8 of sarcoma and 56 others. In this article, the results from the 9th survey including diagnosis, treatment and clinicopathological features of primary liver cancer were reported. Furthermore, the survival rates of the HCC and CCC patients receiving hepatic resection were calculated based on follow-up from January 1, 1978 to December 31, 1987. Survival rates were also correlated with the factors indicating the histologic features and the stage of the tumor.
This survey will provide a lot of significant information to understand the clinicopathological features of primary liver cancer in Japan and to estimate the prognosis after surgical treatment.

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Two patients of autoimmune hepatitis manifested by clinico-pathological features of acute hepatitis were reported. They were 60- and 48-year-old females with abrupt appearance of jaundice as an initial symptom (patient 1 and 2, respectively). Blood chemistry examined on admission revealed highly elevated serum transaminases, being decreased in a short term by administration of glycyrrhizin in both patients. Initial liver biopsies revealed compatible findings with acute hapatitis. Transaminases reelevated twice in both patients and promptly responded to oral prednisolone in each time but repeat biopsies carried out in the second relapse revealed histological progression to chronic active hepatitis. In patient 1 hyper-γ-globulinemia and positive ANF were detected as early as in the initial episode, but in patient 2 autoimmunity indicated by positive LE cells, LE test, anti-DNA antibody and anti-smoothymuscle antibody as well as hyper-γ-globulinemia developed during relapses. These data contains valuable suggestions for insight into the development and progression of autoimmunity in this disease with acute onset.

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Histological changes of the liver were observed at the early stage and after the death of the course of acute hepatic failure in a patient with adult T cell leukemia (ATL). A fifty-three year-old Japanese male had been followed as chronic ATL for six years. Liver dysfunction had not been noticed during these years. Ten days before admission, the patient had general fatigue, jaundice and skin eruption. On admission, serum total bilirubin showed 10.6mg/dl, GOT 4167IU/l and LDH 4501IU/l. The peripheral blood leukocyte count was 18, 900/mm³, consisting of 75% abnormal lymphocytes with convoluted or lobulated nuclei. Serum anti-HTLV-I antibody was positive, but anti-HAIgM, antiHBcIgM and anti-HCV antibodies were negative. Aspiration liver biopsy revealed massive infiltration of mononuclear cells including ATL cells mainly in the portal areas. Glucagon-Insulin therapy, Interferon, methylprednisolone and plasma exchange therapies were started. However, the patient died of hepatic failure. Autopsy disclosed yellow atrophic liver. Pathological examination revealed massive hepatic necrosis and hemorrhage without infiltration of ATL cells, which was considered to be caused by a Schwartzman mechanism.

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A 75-year-old man of hepatocellular carcinoma (HCC) with solitary bone metastasis was reported. In April, 1983, he complained of the pain of left humerus, and the tumor and fructure of it were found. A histological study of the tumor and high serum levels of AFP (14000ng/ml) revealed bone metastasis of HCC. There were no other metastatic lesions and amputation of the left humerus was performed. Hepatic angiography was performed one month after amputation, and arterial chemotherapy was carried out for a small tumor stain suggesting HCC. Additionally, three times of arterial chemotherapy, and two times of TAE treatment were performed for four years following operation. He died of advanced HCC in January, 1990. Long survival of six years and nine months after diagnosis of solitary bone metastasis from HCC was obtained because of good therapeutic effects by combination therapies such as amputation of the metastatic lesion, arterial chemotherapy, and TAE treatment.

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We reported a case of congenital hepatic fibrosis (CHF) with huge cornal varix. A 36-year-old female complained precordial pain and X-ray films of the chest showed a round tumor shadow of 7×9 cm in size near the discending aorta. Imaging diagnostics revealed the tumor shadow as a cornal varix running to the azygos vein.
In the course of the examinations of the tumor shadow, findings suggesting portal hypertension were obtained in imaging diagnostics. In that, giant splenomegaly, dilated portal system, large portal systemic collaterals and dilated splenic artery were shown in ultrasonography, X-ray computed tomography and antiography. Mosaic pattern of the liver parenchyma in ultrasonography and the stretched hepatic artery in angiography suggested the progressed fibrosis in the liver. Laparoscopic examination revealed a masked-melon appearance of the live surface.
Needle biopsy specimen of the liver showed enlarged portal area of mature collagen fiber without inflammatory cell infiltration, neither hepatocellular change nor lobular rearrnagement. These findings were compatible with those of CHF.
No other abnormalities such as renal cysts (which) accompained in high incidence in the case of CHF were found in this case.

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