Each glucocorticoid affected suppressively, relating to added dosis (0.05-50μg/ml), on the growth of established cultured cells such as liver cell (Chang) and fibroblast (3T3, NRK, L, ), respectively, and also inhibited the growth of the fibroblastoid cells originated from adult rat liver. But the effect was not shown on the epithelioid cells from rat liver. In the cell lines, the Chang cells were most sensitive to glucocorticoids, highest Betamethasone followed by Prednisolone and Hydrocortisone. Contrary, it might be shown, the fibroblast cell lines were affected by Hydrocortisone efficiently followed by Prednisolone and Betamethasone. From these results, it should be concerned, for the treatment to hepatic diseases, about the inhibitory effect of glucocorticoids on the growth of liver cells and the differences of the acting effect of these medicaments.

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The localization of α-fetoprotein (AFP) in rat liver by immunofluorescence was studied on D-galactosamine induced liver injury.
D-galactosamine (gal) was administered to male rats by intraperitoneal injection in a single dose of 400 or 750mg/kg body weight. After gal injection, PAS positive granules appeared in the liver cell and were most prominant at 6 hour after gal administration. The value of serum GPT and liver tissue damage reached the maximum at 48 hour. The highest value of mitotic indices in liver cells was observed at 72 hour. Serum AFP was detected by means of Ouchterlony method in gal (750mg/kg body weight) administration at later than 96 hour. At 96 hour after gal (400 or 750mg/kg body weight) administration, AFP was detected in liver cells by immunofluorescent technique. The AFP-positive liver cells were interspersed in gal (400mg/kg body weight) administration, and gathered around the central or hepatic vein in gal (750mg/kg body weight) administration.
These results are suggested that the production of AFP in D-galactosamine induced hepatic injury is related to the regeneration of liver cells.

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Out of 201 residing Japanese people in Suez area, Egypt, 7 people developed hepatitis sporadically from August 1976 to February 1977. These cases showed a typical clinical picture and course of acute viral hepatitis and it was suspected to be acute hepatitis type A from the serological investigation of hepatitis type A and type B. The route of infection was supposed to be from the intake of contaminated food owing to their living environment and occupational conditions. The infected patients were males aged from 20 to 32 with an average age of 25. The frequency ratio of the sample cases classified by their ages to the population was 6.1% in the 20's, 1.6% in the 30's and 0% above 40 years of age. Their residing periods up to the onset of the disease were 63 days at the shortest and 354 days at the longest with an average of 242 days.
The tropical and sub-tropical areas are regarded as wide-spread areas of hepatitis virus type A. The risk degree of infection and morbidity of the residing Japanese people in these districts differ according to such factors as age, occupation, hygiene and environment. Taking these facts in consideration, we must consider preventive measures as soon as possible.

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In order to elucidate the mechanism of α-naphthylisothiocyanate (ANIT) induced cholestasis in rats, some hepatic changes after administration of ANIT 80mg/kg BW were examined With the lapse of time.
For the purpose of clarifying changes of the bile production system, bile flow, concentration of bile acid and bicarbonate and sodium in bile were measured after infusion of secretin and taurocholic acid. Canalicular bile flow was estimated by measuring the biliary clearance of erythritol-C¹⁴. As for the evaluation of hepatocellular injury, levels of cytochrome P-450 in the microsome of hepatocyte and protein synthesis in the liver were estimated.
Consequently. it seems that ANIT was activated in drug metabolising system through cytochrome P-450 in the liver, and a significant change was produced in both bile acid metabolism and its transport system. Bile acid independent bile flow in the canaliculus was inhibited, too. Thereafter, bile ductule and even bile duct were disturbed functionally and histrogically.

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Clinical and splenoportographic studies were made on 6 cases with repeating hepatic encephalopathy without episodes of alimentary tract hemorrhages. In all cases spleno-renal shunt was found. There were 2 cases with esophageal varices and 5 cases with gastric varices. There was 1 case without gastric and esophageal varices. The caval vein in 4 cases and the heart in 2 cases were radioopacified by contrast medium through the spleno-renal shunt. These caval venographies and cardiographies were thought to be the evidences of higher shunt ratio of spleno-renal collateral. In the patients with repeating hepatic encephalopathy, there was a great possibility of the presence of splenorenal shunt.

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Methods: Ten mCi of 99mTcO4- solution was instilled into the upper part of rectum. Scintigrams were taken sequentially at 15-second interval by time-lapse camera and radioactivities were recorded with VTR.
Results: In 4 patients without hepatic diseases and 10 cases with chronic hepatitis, the scintigrams visuahzed the portal system, liver and heart succesively. In 24 of 26 cases with hepatic cirrhosis however, the scintigrams clearly visualized the heart earlier than the liver.
In chronic hepatitis, appearance-time of radioactivities at the liver sequentially followed VTR was earlier than that at the heart. But, in 24 of 26 cases with hepatic cirrhosis, appearance-time at the liver was later than that at the heart.
Portal shunt index was 0% to 10% in normal subjects, 8% to 24% in chronic hepatitis. The index was more than 25% in all cases with hepatic cirrhosis.
In conclusion, our per-rectal portal scintigraphy is a non-invasive, useful method for analysing the portal circulation.

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A 46 year-old male with severe liver cirrhosis, who has a heavy alcohol intake over 25 years, showed persistent hemolytic anemia and haemorrhagic tendency. Under microscopic and scanning electron microscopic studies, approximately 60% of erythrocyte showed spiculated form. It was considered that spur cell was caused by decreased serum lecithin: cholesterol acyltransferase level and elevated cholesterol/phospholipid ratio of erythrocyte membrane. Severe haemorrhagic tendency, decreased coagulation factors and hyperfibrinolysis were seen during hemolysis and 131Ifibrinogen half life was shortened in the patient. Haemorrhagic tendency was related, not only to cirrhosis, but also to chronic DIC which induced by severe impairment of hepatic reticuloendothelial system and persistent hemolysis. DIC was improved according as hemolysis decreased. The patient is still alive one year after admission and spur cell was decreased to about 2% of erythrocyte count.

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