In the rats treated with chenodeoxycholic acid (CDCA) hepatic injury in females is more extensive than that in males. In order to clarify the mechanism underlying the appearance of such sex difference, 200mg/day of CDCA was orally administered to male and female rats for 8 weeks and sex differences in the composition of bile acid in portal blood and bilejuice and changes in concentration of lipids in plasma and the liver were investigated.
As to the composition of bile acid, the CDCA levels in female rats were 1.8 times higher in portal blood and several times higher in bile juice than those in males.
Such sex differences are considered to be due to the difference in 6β-hydroxylase system of bile acid in the liver. It is suggested that the protective mechanism of the female rat against hepatotoxicity caused by bile acid is inferior to that of the male rat.
As to the lipid levels in the liver and plasma, in male, no remarkable change was noticed, while in female, an increase of cholesterol and triglyceride in the liver and a decrease of triglyceride in plasma were observed.
Such change in lipid levels suggested that inhibition of cholesterol synthesis by CDCA in females is less than in males and the transport system of triglyceride from the liver to blood is hindered in females.

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To raise Shwartzman reaction in the liver of rabbits, endotoxin of E. coli was injected into the liver through the common bile duct as a preparative injection. 24 hours later, the same endotoxin was injected into marginal vessels of the ear. Shwartzman reaction thus produced was localized chiefly in the liver and only mild influence was seen in the other organs of the body. Macroscopically marked widespread hemorrhagic necrosis of the liver was observed. Microscopically the picture of this hemorrhagic necrosis resembled that of human fulminant hepatitis. Single injection of E. coli endotoxin caused only mild spotty necrosis of the liver. When the above reaction was provoked repeatedly marked liver fibrosis which sometimes could be called cirrhosis was brought about. The result of this experiment shows some importance of Shwartzman reaction as a part of pathogenesis of acute liver necrosis in man.

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1. There were seen about 20 cases of constitutional direct hyperbilirubinemia in T. village, K. Island, Okinawa Prefecture and they seemed to have been inherited.
Among them 3 icteric patients were investigated in our hospital including laparoscopy and liver biopsy and it was confirmed that one case was suffering from Rotor's syndrome and the other two from Dubin-Johnson syndrome. Besides 6 cases of Rotor's syndrome and 3 cases of Dubin-Johnson syndrome were found by ICG test.
2. In this isolated village, all 12 icteric cases mentioned above were found only in four families. The type of jaundice which was found in the three out of the four families proved to be either Rotor's syndrome or Dubin-Johnson syndrome, but in the fourth family in which the pedigree of both types of jaundice were mixed, it was confirmed that father and daughter were affected with Dubin-Johnson syndrome and son with Rotor's syndrome. These are very important and interesting facts that have never been reported in established cases.
3. Both Dubin-Johnson syndrome and Rotor's syndrome in this village seem to beinherited as an autosomal incomplete dominant trait.

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It has been postulated that cellular autoimmune reaction directed against cell membrane of hepatocyte is responsible for the pathogenesis of chronic liver disease. To test this hypothesis, inhibition rate of leucocyte migration was determined using an organspecific antigen of human liver and purified HBsAg according to Sobørg's method. The specific antigen was obtained by the isolation and the purification from solubulized liproprotein of normal human hepatocyte membrane. Specificity of the isolated antigen was confirmed by the Ouchterlony's gel diffusion technique. Among 39 patients with chronic liver disease, the cellular antibody against the specific antigen was observed in 16 cases (41%). The cellular antibody against purified HBsAg was seen 14 cases (36%). It was noteworthy, however, that a high frequency of serum HBsAg or/and cellular antibody against HBsAg was detected in patients with positive cellular antibody against the specific antigen (14 out of 16 cases). The cellular immune reactivity to the specific antigen was found to be correlated well with the severity of hepato-cellular necrosis. By contrast, no correlation was observed between the reactivity to HBsAg and any histological abnormalities. These findings suggest that cell-mediated autoimmune response to the specific antigen plays, at least in part, a significant role of chronic hepato-cellular necrosis.

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Percutaneous transhepatic portography was carried out by a modified method of Lunderquist et al. in 13 patients mostly with liver cirrhosis. The needle (27cm in length) sheathed with a catheter (outer diameter 1.35mm, inner diameter 0.94mm) was introduced through the 7th or 8th intercostal space in the midaxillary line toward the right intrahepatic portal branch. A guidewire was introduced through the catheter, passed into the portal vein, and then the catheter was advanced with the guidewire into the splenic or superior mesenteric vein. It was successful in 10 out of 13 cases to opacify the portal vein. There was no serious complication caused by this procedure. One of the patients was diagnosed to have a small hepatocellular carcinoma and in another a hepatic tumor was denied by this method. The value and merits of this method are discussed in comparison with the other various prodedure of portal venography.

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Here is reported a clinicopathological course of an interesting case of acute hepatitis type-B (a d r). The case was a 25-year old male who appeared to be infected in the laboratory where a large amount of the HBs antigen positive blood treated. He was turned to be positive for HBs antigen by the routine periodic examination, and at this stage his liver function tests were quite normal. When he was admitted to the hospital and observed, typical hepatitic symptoms and abnormal liver functions were found out. HBs antigen showed the peak about 10 days prior to the peak of S-GPT, and also disappeared about 10 days, preceding S-GPT normalized. S-GPT remained abnormal for about 40 days successively. e antigen was detected transient around the peak time of HBs antigen; anti HBc was detected about 10 days prior to the negative change of HBs antigen, and a rather low titer was continuously kept. According to the orcein stained samples obtained by the liver biopsy at the active stage and the recovery stage of hepatitis, HBs antigen was mainly observed in the cytoplasm of liver cells, distributed mostly in the middle and peripheral zones of liver lobulus, and was focal distribution type.

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Two patients with hepatocellular carcinoma, associated with hypoglycemia, are described. First case is a 60-year-old male who had a history of posttransfusion hepatitis fifteen years ago, progressed into cirrhosis of the liver and eventually to hepatoma, and died of gastrointestinal bleeding one month after admission. Second case is a 61-year-old male with liver cirrhosis who progressed to hepatoma during the course of following his clinical course by periodical examinations for eleven years. Hypoglycemia developed at terminal stages of the disease on both cases. Parenteral glucose load revealed low responses of insulin and glucagon. Moderate increase in blood lactic acid was found during hypoglycemic episode (second case). A marked decrease of glucose-6-phosphatase activity with elevated hexokinase level in tumor tissue was found upon examination of the necropsy material on the second case. Autopsy examination of these cases disclosed that almost all of the livers were replaced by tumor masses and no islet cell hyperplasia of the pancreas was observed.
Data obtained indicate the possibility that the mechanism of hypoglycemia of these patients is due to the unbalance existing between glucose utilization and synthesis resulting from the enhanced glycolysis of substantially grown hepatoma tissues and from the lack of gluconeogenic capacity due to virtual loss of residual liver tissues.

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