Intrahepatic distribution and intracellular localization of pre-S₂ antigen was studied in 87 liver biopsy specimens from 79 patients with chronic type B hepatitis. Of 87 biopsy specimens, pre-S₂ antigen was observed in 70, HBsAg in 71 and HBcAg in 49 subjects, respectively after staining with peroxidase-anti-per-oxidase technique. Intracellular pre-S₂ antigen was stained in three patterns, that is, cytoplasmic diffuse pattern, inclusion pattern and membranous pattern. pre-S₂ antigen was stained in 70 of 71 specimens demonstrated HBsAg in their liver tissue, and 69 of those 70 specimens showed similar staining pattern to HBsAg. HBcAg was observed in the liver in relation to serum HBe antigenemia and DNAP activities. In contrast to HBcAg, detection of pre-S₂ antigen and HBsAg in the liver was not associated with serum HBeAg or DNAP activities.

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In order to clarify the prophylactic effects of HB vaccine to HBV contamination and the duration of antibody response, 200 subjects who had received HB vaccine were followed up for 47 months. The following results were obtained. 1) Anti-HBs response was noted in 55 of 59 (93.2%) male recipients and 117 of 121 (96.7%) female recipients by PHA or RIA. 2) Mean anti-HBs titers (PHA) reached a peak at 11 months in male recipients and 6 months in females, with titers (2^N) of 6.4 and 8.0, respectively. 3) Sharp rise of anti-HBs titer within one month was noted in the recipients possesing low titer anti-HBs only detected by RIA. 4) Revaccination was undertaken 46 months after the first innoculation in six subjects. One month later, all six subjects showed anti-HBs titers higher than 25 by PHA, suggesting a booster effect following the revaccination.

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A study was made a comparison of a histochemical examininations of γ-GTP, serum γ-GTP and isoenzyme Pattems. In zymograms, most of cases with GT₂ (comparable to fraction of α₂-globulin) and GT₃ (that of β-globulin) were found in patients of chronic active hepatitis (C.A.H.) and liver cirrhosis (L.C.).
A marked activity of this enzyme was ohserved in swollen of Kupffer cells in cases of acute hepatitis, while that in hepatic lobules and marked proliferation of bile ductules in C.A.H. and L.C.. As the results of correlation between γ-GTP activity in liver cells·bile canaliculi and the epithelium of bile ducts and serum γ-GTP isoenzyme patterns, augmetation of GT₃ fraction was found in cases with the increase γ-GTP activity of that, significantly more increasing than GT₁ and GT₂ fractions. Furthermore, most of cases with GT₃ fraction were patients of C.A.H. or L.C.,
It is reasonable to presume that the pregress ef liver damage may causes the increase of serum γ-GTP and γ-GTP activity in the liver, moreover GT₃ ffaction was accompanied with the increasing of γ-GTP activity in liver cell·bile canaliculi and the epithelium of bile ducts.

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To investigate the possible mechanislns of elevation of serum IgA level in alcoholic liver disease (ALD), serum secretory IgA (SIgA) and dimeric IgA (D-IgA) were studied in 74 cases with various types of ALD. SIgA and D-IgA were significantly increased in ALD compared with control subjects, and there was a significant correlation between serum IgA and D-IgA, SIgA and D-IgA (%). SIgA level was significantly correlated with values of sGOT, sGPT and/or γ-GTP. In the immunohistochemical study of IgA, the number of IgA containing cells in the lamima propria of colon was significantly increased in the elevated cases of serum IgA level in ALD, Moreover in ALD, D-IgA level was significantly correlated with the number of IgA containing cells in the lamina propria. These results conclude that the mechanism of elevated serum IgA in ALD is partly derived from excessively produced D-IgA in the Colonic mulcosa.

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Much remains to be elucidated with regard to classification of hepatic encephalopathy (HE). Recently, Italian Association for the Study of the Liver has proposed a new clinical entity; acute episodic encephalopathy in addition to acute encephalopathy and chronic recurrent encephalopathy.
In order to distinguish these three clinical patterns of HE from each other, theory of quantification was applied, using cases typical for each clinical entity and the discrimination score for HE was calculated.
When this score was applied to individual cirrhotic patients with coma, the HE, except for chronic recurrent encephalopathy, was unable to be classified appropriately. Hence, it was conceivable that HE due to liver cirrhosis was practically to be divided into two types; one, chronic recurrent type and the other, end stage coma type which prognosis was grave.
In conclusion, we now propose the clinical classification of HE as follows; 1) Acute type which is typical for fulminant hepatitis, 2-a) End stage coma type and 2-b) Chronic recurrent type both of which are seen in liver cirrhosis. This classification was found to be useful, in paticular for therapeutical intervention of HE including Fischer's solution.

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Eighty one (sixty cases) electrocardiograms were recorded and studied during injection sclerotherapy with ethanolamine oleate for esophageal varices.
Frequency of abnormal ECG in limb-lead was below: premature atrial contraction 9.9%, premature ventricular contraction 13.6%, ST depression 7.4%, bradycardia 1.2%, which was similar to usual upper gastroendoscopy.
In 12-leads monitoring, sixty percent of cases showed abnormal ECG during intravariceal injection of sclerosant. Abnormal ECG appeared in two cases at a time of inflating balloon attached endoscope or hemostatic balloon.
These ECG changes were transient, but noteworthy.

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The effect of TAE (Transarterial embolization) on the tumor growth rates was studied in 26 patients with hepatocellular carcinoma (RCC) whose AFP levels were over 400 ng/ml before TAE. The growth rate in each case was expressed as the doubling time of serum AFP level (T₂AFP) and classified into three growth types; rapid≤60 days, 60<intermediate≤120 days, 120 days<slow: and compared them before and after TAE in each of them.
The results were the followings: (1) After the first TAE, the growth rate became more rapid in 12 cases (46.2%), and it became slower in 6 cases (23.1%). (2) The survival time was depended upon the T2AFP following TAE, but not upon the growth rate before TAE, particularly the prognosis in the rapid growth type after TAE was poorer than that of intermediate or slow growth type. (3) It seemed to be effective and necessary to give additional theraoy during AFP reduction period after TAE. (4) It was suggested that the biological characteristics of HCC might be changed by the first TAE, thus it is important to have strict indication of the therapeutic modality in the cases with slow or intermediate growth rate.

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Significance of intra operative angio-echography under CO₂ gas injection into hepatic artery, for diagnosis of small intrahepatic metastasis in cases of HCC, were investigated. 23 cases of HCC were studied, whose resected specimen were exactly confirmed if there were small satellite nodules smaller than 10mm or not. 9 cases among these 23 cases, had 16 nodules. 14 cases had not any nodules. Picture of angio-echography were divided into three types. There are positive enhance, negative enhance, and non enhance. 13 nodules among 16 nodules are recognized as positive enhance, 3 nodules are also ecognized as negative enhance. 5 nodules among them had not detected by plain echo and these are ruled out only by angio-echo. Smallest one among these nodules are 4mm diameter, On the other hand, there are 14 cases, who had not any satellite nodules. In 4 cases of them, it was suspected to have some sateilite nodules, by plain echo. Rut angio-echo showed non enhance in all 4 cases, then existence of satellite nodules are denied. Sensitivity both true positive and true negative are 100% about the diagnosis of small intrahepatic metastatic nodules.

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We examined the expression of nine cellular oncogenes in liver samples from seventy patients with various liver disease. With c-K-ras, four RNA bands (5.6-, 2.1-, 1.5-, and 1.2-kilobase RNA species) were detected in all the liver tissue examined without significant variation in the relative intensities of the bands. Expression of c-fos was also detected in the human liver tissue, but its expression level was very low. Expression of other oncogenes was not detected.
Our results indicate that (1) there may be little correlation between liver regeneration in the human liver disease and the expression of oncogenes examined; (2) the constant expression of c-K-ras in the human liver may be linked to essential hepatocellular function rather than carcinogenesis. The significance of c-K-ras expression in the human liver remains to be determined.

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In order to examine three dimentional changes on hepatocyte cytoskeleton of obstructive jaundice liver, we observed the hepatocytes in common bile duct ligated rats by quick freezing and deep-etching replica method as well as conventional transmission electron microscopy. Networks of bile canalicular microfilaments (BCMF) proliferated around dilatated bile canaliculi and spread to the surroundings of neiboring junctional complexes. BCMF attached directly to bile canalicular membrane in one end and similar (end-to-membrane) to the proliferated intermediate filaments (IF) and vesicles in another. Predominantly increased IF ran parallel and attached directly to junctional complexes, and seemed to reinforce them. IF also increased extremely at the peripheral cytoplasm of hepatocytes sometimes in bundle forms. It is suggested that these findings are the adaptation of hepatocyte cytoskeleton to remarkably increased bile duct pressure and cholestasis. To the contrary, arrangement of organelle and cytoskeleton at the cytoplasm near nucleus were preserved almost intact on three dimentional architecture.

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A case of idiopathic portal hypertension (IPH) associated with SLE was reported. A 46-year old female had been diagnosed and treated with SLE 4 years ago. She was admitted for rupture of esophageal varices on October 1986. Her preoperative examination showed IPH associated with SLE. Transabdominal esophageal transection and splenectomy were performed. Histological specimen of wedge biopsied liver showed chronic active hepatitis and no cirrhosis. Therefore, we diagnosed that IPH associated with SLE and lupoid hepatitis. It was difficult to solve IPH, because there were two theories which were viral hepatitis and autoimmune disease. Furthermore, portal hypertension was rapidly progressive on the clinical stage, so that this case was interesting on etiology of IPH.

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A 76 year-old man with past history of syphilitic disease 30 years before was reffered to our hospital because of hepatomegaly. Clinical features of this patient included hepatomegaly, ascites, proteinuria, elevated serum biliary tract enzyme values and increased value of ICG R15.
Hepatic scintigram and whole body CT revealed hepatomegaly with no space ocupying lesions.
Gastrointestional endscopy showed low grade esophageal varices at lower part of the esophagus, and it suggested that portal hypertension was present. Liver biopsy specimen showed amyloid deposition chiefly in the Disse space and its substance compressed hepatocytes. This substance was proven to be AL protein because of resistance to permangate treatment by Wright method, so primary amyloidosis was diagnosed.
A case of hepatic amyloidosis with marked hepatomegaly, ascites and portal hypertension without splenomegaly and with renal failure was reported.

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A case of drug-induced toxic epidermal necrolysis (TEN) with severe liver injury diagnosed by the lymphocyte stimulation test (LST) and the patch test was reported. A 35-year-old man was given tiopronin because of liver injury in a dose of 300mg daily for 43 days. Exanthema and jaundice appeared at 10 days and 20 days after the start of tiopronin administration, respectively, And then, bullae of various sizes leaving erosions appeared all over his body. Serum bilirubin and GOT/GPT elevated to 32.5mg/dl and 518/543 IU/l, respectively. A diagnosis of drug-induced TEN with intrahepatic cholestasis was made based on his clinical course and skin lesions. After suspected drugs were discontinued and dexamethasone was strated, skin lesions and joundice improved gradually. Tiopronin was identified as a causing agent by LST and patch tests. This is the first report of a case of tiopronin-induced TEN with intrahepatic cholestasis.

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A 29-year-old woman was admitted to our hospital with complaints of upper abdominal pain in August 1984. Hematological examination showed anemia and thrombocytopenia. Other data revealed along prothrombin time and bleeding time. Alpha-fetoprotein was negative. Her case was diagnosed as cavernous hemoangioma of the liver and spleen by abdominal arteriogram, but these lesions were suspected of angiosarcoma because bone metastasis was found. We failed in the trial of liver biopsy under laparoscopy because of sever bleeding on the surface of the liver tumor. Finally, the definite diagnosis of hepatic and splenic angiosarcoma was taken from histological findings of the surgically resected liver. She died of hepatic failure in March 1985. Autopsy disclosed of the angiosarcoma of the liver, spleen and bone, but the origin was unknown. It is difficult to take antemortem diagnosis of hepatic angiosarcoma. Especially, this disease must be differentiated from cavernous hemoangioma and cystic lesion of liver. If suggestive of hepatic angiosarcoma, liver biopsy under laparotomy or surgical liver resection should be performed.

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