In order to know any morphological changes of the ducts which are associated with their destruction, serial sections of 6 cases of late PBC (autopsy livers) were carefully examined.
Three types of the morphological changes were found just before complete disappearance of the bile ducts on the serial sections: 1. periductal cellular reaction, 2. periductal edema, and 3. periductal mild fibrosis or non-significant changes. Type 1 and 2 were relatively pronounced in the scarring stage of PBC (2 cases) and type 3 in cirrhosic stage (4 cases).
These morphological changes were occasionally associated with cystic dilatation or narrowing of the lumina of the bile ducts.

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hepatitis, 7 of subacute hepatitis, 53 of liver cirrhosis and 33 of hepatoma) in the period from 1958 to 1975. Hepatic coma of liver cirrhosis was divided into three types due to S. Sherlock's classification, that is, 40 of acute type, 10 of chronic type and 3 of the other.
1. Acute type had ascites and/or jaundice more than 3mg/dl of serum bilirubin, and low serum choline esterase activity less than 0.60ΔpH by Shibata's method. On the other hand, chronic type had no ascites within one year before the first attack of hepatic coma, and more than 0.60ΔpH of serum choline esterase activity.
2. Blood ammonia concentration showed high level at the onset of hepatic coma in about half of the total cases, but in only 15% of acute type during April to August.
3. 59% of patients with hepatic coma showed alkalosis, whereas some cases of hepatoma showed acidosis.

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Serum γ-glutamyl transpeptidase (γ-GTP) activity was elevated in all cases of 31 patients with alcoholic hepatitis. The subjects were subdivided into two groups, with and without cirrhosis. In the group without cirrhosis (17 cases), the raised values reverted to normal within 3 weeks after abstention from alcohol, while in the other group with cirrhosis the high levels had not returned to normal for more than 6 weeks.
Histochemically, sufficient γ-GTP activity was demonstrated in both the cytoplasm of liver cells and the cell membranes adjacent to the lumen of bile canaliculi. Marked enzyme activity was observed on alcoholic hyalines and along pericellular fibers around the balloonshaped liver cells.
These results suggest that the serum y-GTP elevation results from hepatic enzyme induction and has some relation to liver cell degeneration and fiber formation in alcoholic hepatitis.

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Serum alkaline phosphatase (ALP) activity of patients with hepatocellular carcinoma is higher than normal controls. To clarify the matters, serum ALP activities and isoenzymes were compared in sera of the patients with several types of hepatocellular carcinoma as to size, numbers and the localization of the tumor, using RI-scanning of the liver.
As the results, a tendency of an increase in ALP activity and incidence of detection of macromolecular ALP was observed in the following occasions. A) When tumors were more multipie, B) when the localization of tumor was more toward hilus than periphery and C) when tumors was larger than smaller.
These results indicate that ALP activity and/or incidence of detection of macromolecular ALP are related to the extent of the cholestatic area of the biliary system within the liver.

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A 58-year-old male with pyothorax had liver biopsy because of an abnormality found in liver scan. The histological findings of the specimen suggested acute viral hepatitis. Three days after, positive HB-Ag was revealed, and the patient's clinical course was that of a typical acute hepatitis.
Microscopically, scattered liver necrosis, either single cell or focal, was found throughout the lobuli, with the dissociations of hepatic cell cords. All the features of necrosis, including eosinophilic cell degeneration, acidophilic bodies and ballooning cells, were found. The infiltrated inflammatory cells consisted mainly of lymphocytes, but a few neutrophilic and eosinophilic leukocytes were also found in the parenchyma and portal triad. Ductulitis was present in portal area.

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A 49 year-old male with severe hepatic failure and hemolytic anemia associated with striking acanthocytosis is described. For about 30 years he had a heavy alcohol intake. Physical examination revealed intense jaundice, ascites, splenomegaly and hemolytic anemia with spur-shaped red blood cells. The peculiar spur cells of this disorder are so named because of their "burr", "spiculated" morphology.
Hemolytic anemia with "alcoholic" cirrhosis of the liver was diagnosed clinically. Severe hemolytic anemia persisted for about 4 months despite therapy with steroid hormone and the patient lapsed into hepatic coma and died.
The cause of the spur cell formation is unknown. However it is considered likely that spur cell formation and hemolysis may be due to some factors in the patient's plasma.
The pathological specimen of the liver showed micronodular cirrhosis (precirrhotic stage) with cholestasis and no fatty infiltration.

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