Correlation of serum IgM class anti-HBc with other serum HBV markers and presence of HBcAg or HBV core particles in the liver was studied in 25 patients with HBsAg-positive chronic liver disease. Sera were assayed for IgM class anti-HBc by both radioimmunoassay (Dainabot) and enzymeimmunoassay (Abbott). Liver biopsies were studied for HBcAg immunocytochemically using peroxidase labeled antibody method and for core particles by electron microscopy.
IgM class anti-HBc was positive in 7 patients with acute exacerbation and 2 patients with continuously high level of serum transaminase. Relationship between IgM class anti-HBc and other serum HBV markers was unclear. In liver biopsies from the patients with serum IgM class anti-HBc, HBcAg-positive hepatocytes and naked core particles in sinusoidal lumen and Disse space were detected more frequently than without serum IgM class anti-HBc. These findings suggest that in type B chronic liver disease the presence of serum IgM class anti-HBc correlates with increased production of HBcAg and release of core particles from hepatocytes.

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Comparative histopathological studies were performed among type A, type B and type non-A, non-B (NANB) hepatitis using needle biopsied specimens of the livers which were taken from patients with acute hepatitis (A 16, B 20, NANB 42), persistent hepatitis (B 40, NANB 21) and chronic active hepatitis (B 56, NANB 57). Some features characteristic to NANB heaptitis were obtained. They included (1) a poor regenerative activity and an indistinct boundary between regenerating area and necro-inflammatory area in acute hepatitis (2) a relatively loose cobblestone appearance of hepatocytes in persistent hepastitis and (3) a conspicious araphnoid and pericellular fibrosis, a vague nodularity of the parenchyma, a diffusely distributed mild to moderate necroinflammatory activity and small numbers of dysplastic cells in chronic active hepatitis. These caracteristics of NANB hepatitis are probably derived from a poor regenerating activity of hepatocytes.

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To investigate whether the anti-HBs response to the hepatitis B vaccine is genetically determined or not, the HLA antigens were examined in 167 vaccine recipients. The vaccine recipients were divided into five groups according to the time of acquiring of anti-HBs (early responder: 41 cases, late or no responder: 36 cases, no responder: 23 cases) and the titer of antiHBs (high responder: 32 cases, low or no responder: 41 cases).
Bw39 (22.0%) and Cw7 (43.9%) in the early responder were statistically significant in frequency (Pc<0.02 and Pc<0.007 respectively). The frequency of Bw52 and DRw9 in the late or no responder and also in the no responder were found to be significantly higher than that in normal controls. B7 (34.4%) Cw7 (46.8%) and MT1 (93.7%) in the high responder were statistically significant in frequency (Pc<0.002 Pc<0.007 Pc<0.03 respectively). The frequency of Bw52 in the low responder was found to be higher than that in normal controls.

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As a preliminary approach to the clinical application of interferon (IFN) on hepatocellular carcinoma (HCC), the effect of human IFN-β on the growth of a human HCC cell line, PLC/PRF/5, was studied. The cell growth in vitro was inhibited dose-dependently. when IFN was given at the concentrations of 30 to 1, 000IU/ml. When the effect of IFN was examined on several cloned sublines of PLC/PRF/5 cells, heterogeniety in susceptibility to the growth-inhibitory effect was shown. Moreover, when human IFN was given to cultures in vitro at a concentration of 100IU/ml or to transplanted tumors in nude mice at a dose of 20, 000IU/day, the antiproliferative or the antitumor effect disappeared within the first one or two weeks of treatment period. It is thus suggested that there are IFN-resistant sublines of PLC/PRF/5 cells. In the author's opinion, if the tumor growth was observed in patients with HCC during the treatment with IFN, other therapies should be carried out.

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We investigated the influence of galactosamine (Gal N) or Gal N and Endotoxin model in rats in which the RES was normal or stimulated by OK-432. Results, 1) The mortality of the rats administrated Gal N 1.2g/kg or Gal 0.5g/kg and Endotoxin 0.5mg/kg was 100%. On the other hand, the RES stimulated rats by OK-432 were survived more than one month after administration of Gal N or Gal N and Endotoxins. 2) The pretreatment of OK-432 inhibited the increase of S-GOT, S-GPT and bilirubin concentrations in serum after 24 hours and so on. 3) Histological studies revealed the massive liver necrosis in Gal N treated rats at 48 hours after Gal N administration. On the other hand, pretreatment of rats with OK-432 revealed only focal necrosis, but not massive necrosis. 4) The Gal N liver injury was inhibited by the pretreatment of rat with OK-432.

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Oxygen delivery and utilization in liver were investigated in 38 patients with alcoholic liver injuries by organ-reflectance spectrophotometry during peritoneoscopy. The regional hepatic blood volume (ΔEr_569-650) decreased significantly with progress of fibrosis of liver and fatty metamorphosis. The estimated oxygen saturation level of hepatic blood hemoglobin (estimated SO²) decreased significantly in liver cirrhosis, and it was lower in liver fibrosis than in nonspecific change of liver. The in vivo hepatic oxygen consumption (VO²) decreased significantly with progress of fibrosis of liver, and it was lower in patients with fatty metamorphosis than in those without fatty metamorphosis. The in vivo hepatic oxygen consumption decreased concomitantly with the decrease in the regional hepatic blood volume. It is concluded that the disturbance of oxygen delivery and utilization in liver could play an important role in the progress of alcoholic liver injury.

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The purposes of this study is to evaluate diagnosis, causative drugs, clinical and histological features and treatment in the 211 patients with drug-induced liver disease.
The result leads to the following conclusions:
1) The coincidence of positivity between the challenge tests and the immunological tests was 68.2%. 2) All cases of follow up study of LMT became negative. The shortest term was 8 days, the longest was 210 days and the mean was 87.4±67.8 days. 3) Of all causative drugs in the cases, cardiovascular agents were the most commonly encountered (32.0%) with drugs acting on the central nervous system (29.2%) and antibiotics (18.8%) next. The order of frequency of individual drugs was as follows; ajmaline, halothane, cefems and triopronine. Specific clinical and histological findings were observed with all of the drugs. 4) The factors to determine the prognosis were degree of jaundice, liver histological findings and causative drugs. 5) The clinical course in nine cases was prolonged, and six were accompanied by hypogammaglobulinemia. 6) Eight patients died and three of them had halothane hepatitis. 7) Steroid therapy was not so effective for the treatment of the drug-induced liver disease.

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In order to establish the respective roles of halothane metabolites and hypoxia in the rat model of halothane hepatotoxicity, experiments were designed with special reference to blood gas. After pretreatment with phenobarbital (80mg/kg, i.p) for four consecutive days, rats were exposed to 1.0% halothane under a mildly hypoxic condition (FiO₂=14%) for two hours. Since halothane anesthesia caused a significant decrease in PaO₂ levels, rats exposed to highly hypoxic atmosphere (FiO₂=10%) in which PaO₂ levels were comparable to those in halothane group served as controls. In the halothane group, marked centrilobular necrosis and elevation of SGPT activity were observed, whereas neither significant hitological lesion nor elevation of transaminase activity was noted in the highiy hypoxic grollp. Although phenobarbital treatment did not further decrease the PaO₂ levels during halothane anesthesia, serum fluoride level which appears to quantitatively reflect the reductive pathway of halothane metabolism remarkably increased. From these results, we conclude that halothane metabolites rather than hypoxia per se play a major role in the development of halothane induced liver injury in the rat model.

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Portal blood flow (PBF) can be measured quantitatively by using a B-mode combined pulsed Doppler (BCD) system. Blood flow velocity determined by the Doppler spectrogram and vascular cross-sectional area measured from the B-mode tomographic image enables us to calculate blood flow volume quantitatively.
Using this system, PBF was measured in 88 healthy adults, 13 patients with acute hepatitis (AH), 16 with chronic inactive hepatitis (CIH), 45 with chronic active hepatitis (CAH), 81 with cirrhosis (LC), 16 with idiopathic portal hypertension (IPH) and 39 with hepatoma (HCC).
In patients with CAH, LC, IPH and HCC, the cross-sectional area of the portal vein was larger than normal and the blood flow velocity of the portal vein was smaller than normal. However, in the blood flow volume through the portal vein, there was no significant difference between normal subjects and patients with liver diseases (AH, CIH, CAH, LC, IPH and HCC).

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Laser Doppler velocimetry (LDV) is a technique for continuous estimation of fluctuating blood flow in the surface of the tissue and does not require invasion of the circulation. This technique is based upon the Doppler principle that a shift in the frequency of an electromagnetic wave emitted or reflected from a moving object is proportional to the velocity of the oblect.
The regional hepatic blood flow measurement by the LDV was carried out in 10 anesthetized dogs, comparing with that by the hydrogen gas clearance technique and electromagnetic flowmeter. The laser Doppler flow signal and that absolute hepatic blood flow by the hydrogen gas clearance technique and by the electromagnetic flowmeter were highly correlated with statistical significance. And the flow measurement by the LDV was reproductible in the same dog as long as the probe was pressed lightly against the same point of liver surface. Especially, the LDV had a great advantage of a continuous measurement of the blood flow in a small localized liver surface, subtly and simultaneously responding sensitively to a minor change of the hepatic blood flow.

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In the present study, we assessed the clinical significance of the determination of the direction of splenic venous flow by the doppler flowmetry in relation to hepatic encephalopathy in 21 patients with a large splenorenal shunt. Clearly, the direction of blood flow in the splenic vein assessed by the pulsed doppler flowmetry differentiated patients with a history of chronic hepatic encephalopathy or patients in whom hepatic encephalopathy subsequently occurred from those without hepatic encephalopathy in extensive splenorenal shunting.

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A radionuclide angiography as a non-invasive method in 148 cases for measuring a portal component of the total circulation.
The results were as follows; The portal circulation in healthy adults (n=17) was 70.8±3.51% of the total liver blood flow, whereas that of patients with hepatic cirrhosis showed very low portal perfusion such as 38.5±16.4% (n=103). Portal components in patients of hepatic cirrhosis without varices are calculated to be 50.0±16.0%, whereas patients with Varices showed a clear reduction of portal components to 30.6±13.7%. The portal components were correlated well with the levels of serum albumin, cholinesterase and ICG R-15.

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A 53-year-old male with amebic liver abscess was diagnosed with serologic test and treated successfully with metronidazole.
He was admitted to our hospital complaining of fever and pain in the right hypochondrium. Ten months previous to the admission, he had been to Korea. Clinical examinations suggested the presence of the amebic liver abscess in the right hepatic lobe. Definitive diagnosis was made with the positive latex agglutination test (Entamoeba hystolytica). After ten days of metronidazole treatment, his symptoms resolved completely. He returned an active life after one and a half month-hospitalization. The lesion was absent on the follow-up hepatic CT-scan done after 80 days later.

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Bile duct necrosis due to transcatheter arterial embolization (TAE) in two patients with hepatocellular carcinoma were reported.
Preoperative TAE were carried out in 29 patients and bile duct necrosis was experienced in two out of 29 (7%). In these two patients, gelfoam powder was used as the embolus. Among 29, four were embolized with gelfoam powder. Therefore, incidence of bile duct nectosis after TAE with gelfoam powder was 50%.
Because of the hazards of severe complications such as bile duct necrosis, we conclude that the gelfoam powder should not be used except for the TAE of one segment or smaller area of the liver.

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A 29-year-old man developed thrombosis of the superior mesenteric vein whose onset occurred in October 1980 with epigastralgia and underwent an extensive enterectomy. Thereafter he had several bouts of hematemesis and melena and was diagnosed to have congenital AT III deficiency 3 years and 6 months after the initiatory symptom appeared. Later, while he was on anticoagulant could successfully be arrested then with the administration of fresh blood and fresh frozen plasma.
In January 1984, he was admitted with hematemesis, hepato-and splenomegaly. A through examination revealed esophagogastric varices and extensive portal occlusion with resultant cavernous transformation of portal vein.
This case was thought to represent a rare instance in which, in the presence of congenital AT III deficiency as underlying pathology, repeated recurrences of superior mesenteric venous thrombosis led to selected occlusion of the splenic vein and portal trunk without causing generalized venous thrombosis since, to our knowledge, such a case has not been reported in the world literature.

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The liver cancer study group of Japan analysed statistically 4658 cases of primary liver cancer diagnosed from Jan. 1, 1980 to Dec. 31, 1981 in 584 hospitals throughout the country. In 2286 cases, a histological diagnosis was available. They comprised 2038 cases of hepatocellular carcinoma, 146 of cholangiocarcinoma, 33 of mixed carcinoma, 30 of hepatoblastoma, 6 of sarcoma, and 33 others. Other 2372 cases had no histological diagnosis.
The survey included histological features of the tumors, pathology in noncancerous portions of the liver, modality of metastasis, gross features of the tumors, degree of the tumor extension to the surrounding tissue, past medical history, initial symptoms and signs, AFP level at the time of diagnosis made, radiographic (angiogram, scintiscan, computed tomography) and ultra-sonographic features, surgical procedures, and survival rates, etc.

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