We have carried out a clinical study of 59 patients with fulminant hepatitis who ranged in age from 18 to 80 years (male 25, female 34). Fifty-nine percent of the patients wereabove the age of 40 and the age distribution of the 34 women showed an increased incidence in both the younger and older age groups. Furthermore, significant preexisting disease or complication was present in 30 of 59 patients. The development of the disease may relate to host factors such as age, sex, hormonal status and general resistence, The etiology of the disease was presumed to be viral in 47 patients who included 17 following blood transfusion within the preceding six months and drug reaction in the remaining 12. Thevalue of different laboratory date was analysed for early diagnosis of fulminant hepatitis. Most patients had progressive elevations of total bilirubin with a relative increase of unconjugated bilirubin, fluctuating levels of GOT and GPT (GOT>GPT) with abrupt falls of the serum transaminase near the come, lowered concentrations of albumin and cholinesterase, slightly to striking elevations of alkaline phosphatase and LDH and leucocytosis. However, the most consistent markers of the severity or early diagnosis of the disease were prothrombin time, α-fetoprotein and acute rapid turnover proteins such as haptoglobin, α₁-acidglycoprotein with short half-life time which were produced in the liver cells really.

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Immune complexes (I.C.) in the sera of various kinds of liver diseases were examined by means of a Clq solid-phase radioimmunoassay. Positive I.C in sera with amounts of 2.0 μg/ml or more were detected in 17 of 73 sera (23.3%): 7 of 27 liver cirrhosis (25.9%), 6 of 24 chronic hepatitis (25.0%) and 4 of 22 acute hepatitis (18.2%). Amounts of I.C in liver disease sera were less than 10.0 μg/ml except one serum of liver cirrhosis (12.0μg/ml), and they were almost one tenth of amounts of S L E sera.
The mean complement levels and the mean amounts of Clq in the I.C positive sera were 20.7 CH50 and 46.0μg/ml respectively and they were less than 25.2 CH50 and 51.8μg/ml Clq of the I.C negative sera. However, there were no correlation between amounts of I.C and complement levels or amounts of Clq.
In 17 I.C positive sera, 5 showed low complement levels less than 10.0 CH50, 6 had anticomplementary activity and 5 were positive for HBs antigen. In the I.C positive sera, complement levels correlated inversely with anticomplementary activity of sera. TheI.C positive sera did not show any particular clinical course nor complications such as nephritis or angitis.

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In order to elucidate the defence mechanism of hepatitis B Virus (HBV) infection, nonspecific anti-viral substances were studied using sera of 36 normal adults and 92 patients with HBV infection. Interferon. could not be detected in all of these sera, but a new factor, anti-viral substance (AVS) was found. The serum AVS level in acute hepatitis was correlated with the titer of HBsAg. In chronic active hepatitis and liver cirrhosis, serum level of AVS was higher than those of asymptomatic HBsAg carrier and chronic inactive hepatitis. Therefore it was thought that the serum levels of AVS reflected the significance for the activity and chronicity of the histological findings of the liver.
AVS was heat labile substance. The molecular weight was calculated as about 800, 000 from the data of Sepharose 4B column chromatogram. It did not show any species and virus specificity. Its inactivating effect against virus was thought to work exclusively in extracellular fluid.

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Since only one fourth of chronic alcoholics develop liver cirrhosis, it has been suggested that, in addition to an extreme amount of alcohol intake, other factors play a role for the pathogenesis of cirrhosis in alcoholics. To see whether a genetic predisposition is significant for progression to cirrhosis, histocompatibility antigens were determined in 37 alcoholics whose daily alcohol intake was over 70g of ethanol for more than 10 years.
Subjects included 13 without liver damage, 7 with alcoholic fatty liver or hepatitis andwith alcoholic cirrhosis. According to the total amount of alcohol consumed, alcoholic cirrhosis subjects subdivided into two groups, i.e., high alcohol in take (37.6g/kg/day x years, 6 cases) and low (15.0g/kg/day x years, 11 cases). In patients with cirrhosis and low intake of alcohol, the frequency of HLA-B12 was high (57.1%) compared to alcoholics without liver damage (0%). The presence of RA factor was also high (75%) in cirrhosis with low intake of alcohok.
These results sugest that, in patients with alcoholic cirrhosis whose total amount of alcohol consumed were relatively low, a genetic factor plays, at least in part, a role for progression to cirrhosis.

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Mitochondrial function of the rat liver in biliary obstruction was studied. Respiratory parameters of mitochondria such as RC, P/O, S₃, ATP synthesis, and mitochondrial cytochrome a, c were reduced with the prolongation of bile duct obstruction. Latent ATPase activity was elevated in early stage of jaundice but decreased in long term obstruction. DNP stimulated ATPase showed same changes as latent ATPase and the ratio of latent ATPase to DNP stimulated ATPase was increased with the prolongation of biliary obstruction, which indicated the deterioration of injury of mitochondrial membrane.
The role of bile acids as one of the respiratory inhibitors was examined in vitro; free CDCA inhibited most remarkably, conjugated CDCA did next and both free and conjugated CA did less.
In hypotension induced in jaundiced rats by exanguination, mitochondrial respiration was inhibited more prominently than that without hypotension.

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The present investigation was conducted to determine Whether the leucocyte adherence inhibition (LAI) test is useful for the diagnosis of hepatocellular carcinoma (HCC) and serve as an immunological parameter of HCC progress.
LAI test using a tissue extract from liver of HCC as the antigen was conducted on leucocytes from the patients with HCC, liver cirrhosis and the other GI cancer. The rates of nonadherence index were 37, II and -2.3 percent, respectively. Thus, The LAI test Was proved to be useful for the diagnosis of HCC, and was also speoific to HCC When the tissue extract from HCC was used as the antigen.
The LAI test using α-fetoprotein (AFP) as the antigen failed to get leucocyte adherence to glass, therefore, it was concluded that AFP was not the substance which may cause LAI phenomenon.

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In 15 patients with unresectable primary hepato-cellular carcinoma, the authors performed trans-catheter arterial embolization therapy in which under fluoroscopic control the feeding artery of tumor is superselectively catheterized and occluded with the injection of Gelfoam particles soaked in Mitomycin C solution.
Apparent tumor regression was observed in 11 of 15 patients and 2 of 11 survivors have been alive for more than 15 months after the therapy. AFP value decreased markedly in all of 9 patients who had had its high level before the therapy.
On the follow-up angiography which was perfbrmed in 7 patients, all of them showed not only a marked reduction of the tumor size but also an obvious decrease of the tumor vascularity, and especially in 5, almost complete disappearance of the "tumor vessels" and "tumor stain " was observed, although the embolized hepatic artery was already recanalized.
Thus, the transcatheter arterial embolization can be regarded as an almost specific therapy of unresectable epatoma.

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Plasma clearance and biliary excretion of an iv injected ^99mTc-pyridoxylideneisoleucine (Pi) were compared in control rats and in rats excreting sulfobromophthalein (BSP) into the bile at a maximal rate (Tm). Both plasma clearance and biliary excretion of ^99mTc were delayed in rats made in a BSP Tm state compared with control rats. However, when the data were compared with the results previously reported for ^99mTc-N-2, 6-(dimethylphenylcarbamoylmethyl) iminodiacetic acid (HIDA, K. Kitani, et al., Jap. J. Nucl. Med. 15: 999, 1978), the inhibitory effect of BSP was less prominent on biliary excretion and conversely, more striking on plasma clearance for ^99mTc-Pi.

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A 24-year-old woman had pruritus and jaundice which recurred during each of two pregnancies. Liver function tests showed an excretory dysfunction with conjugated hyperbilirubinemia, elevated serum alkalin phosphatase and indocyanin green retention, but γ-glutamyl transpeptidase level was within normal range.
Following delivery the patient became asymptomatic, and liver function tests returned to normal. The same clinical pictures with pruritus, jaundice and abnormal liver function tests were induced when the patient was challenged with synthetic estrogen, ethinyl estradiol.
These results suggest that estrogen may be important in the pathogenesis of intrahepatic cholestatic jaundice of pregnancy.

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A 59 year-old male patient with chronic rheumatoid arthritis was treated with Dpenicillamine in a dose of 0.5 g per day.
Two weeks after starting therapy, jaundice was observed and accompanied by pruritus, fatigue and slight eosinophilia. Serum bilirubin rose to 9.4mg/dl, GOT to 52u/dl, GPT to 41 u, and alkaline phosphatase to 27.7 K.A. units. The examination of E.R.C.P. revealed no ob struction of the biliary tracts.
Liver biopsy specimen showed the cholestasis in the areas of central vein. Parenchymal chahge and cell infiltration in the portal tracts were slightly recognized. The patient had jaundice for about four months. These observations indicate a drug-induced intrahepatic cholestasis caused by D-penicillamine.

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