Some cases of acute hepatitis B are known to be infected by horizontal infection, especially child-parent or parent-child infection. In order to study when and how the infant is infected with HB virus and the development of chronic carrier of HBs antigen, HBs antigen and anti-HBs of infants whose mother had sufferd from acute hepatitis B were followed.
Of 34 mothers with acute hepatitis B, 26 (76.5%) cases had children with HBs antigen. Of 60 children, 33 cases had HBs antigen (55.5%).
As regards the age distribution of the children with HBs antigenemia, none of them abve 11 years of age were HBs antigen positive and only one was anti-HBs positive. In addition, 27 (81.8%) of 33 cases children under 3 years of age had HBs antigen and none of them had anti-HBs. Six (26.1%) cases of 23 children in the range of 4 to 10 years of age had HBs antigen, 4 were anti-HBs positive and 2 cases were identified without HBs antigen or and-HBs but became anti-HBs positive after several months.
From follow up studies, 22 (84.4%) out of 27 infants under 3 years were HBs antigen positive and only 2 (33.3%) of 6 HBs antigen positive infants between 4 and 10 years developed chronic carriers of HBs antigen.
This led us to postulate that infection with HB virus under 2-3 years of age might lead to a high frequency in the development of chronic HB virus carrier.
There was a difference in the value of transaminase between transient and persistent HBs antigen positive children. The value of S-GPT showed over 200 U in the former and under 100 U inthethe latter in the period of observation.

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Radioimmunoassay of carcinoembryonic antigen (CEA) was carried out in various liver diseases, particularly in liver tumors, and its clinical significance was discussed.
In primary cancer of the liver, thirty-one out of 88 cases with hepatoma (35.2%) and two out of 5 cases with cholangioma (40.0%) showed a CEA titer more than 2.5ng/ml, and the percentage of elevated CEA was also lower than in other entodermally derived malignant tumors. No obvious of cirrhosis, AFP levels and HBsAg. Serial CEA determinations have not so usefulness for evaluation of prognosis in these liver malignancies.
On the other hand, twenty-nine out of 51 metastatic liver cancers (56.9%) showed a strongly liver cancers could be elevated by the combination of both CEA and AFP assays.
Increased CEA levels were also observed in patients with hepatitis and with cirrhosis. Therefore, the presence of benign hepatic disease must be considered in evaluating CEA levels, and the differential diagnosis between liver cirrhosis and hepatoma could not be made on the basis of the CEA levels.

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Serum concentrations of 3, 3', 5'-triiodothyronine (reverse T₃, rT₃), 3, 3', 5-triiodothyronine (T₃), thyroxine (T₄), free T₄ index, TBC index and thyroid stimulating hormone (TSH) were studied in groups of various hepatic disorders with euthyroid state (69 cases) and a group of normal subjects (61 persons).
In this study, hepatic disorders were classified in acute hepatitis (7 cases), chronic persistent hepatitis (7 cases), chronic aggressive hepatitis 2A (11 cases), chronic aggressive hepatitis 2B (5 cases), compensated hepatic cirrhosis (31 cases), decompensated hepatic cirrhosis (6 cases) and hepatoma with hepatic cirrhosis (2 cases).
The mean serum rT₃ concentration of decompensated hepatic cirrhosis group was 64.4 ng per 100ml, which was significantly greater than the mean normal value of 30.3 ng per 100ml. In other groups of hepatic disorders, however, the mean serum rT₃ concentrations were slightly higher than the normal value.
The mean serum concentration of T₃ of 90.8 ng per 100 ml in patients with decompensated hepatic cirrhosis was significantly lower than the normal mean of 151.9 ng per 100ml. On the contrary, the mean serum concentrations of T₃ of other groups of hepatic disorders were considerably above the normal.
The mean serum concentration of T₄ of all groups with hepatic disorder were above the normal with or without statistical significance, respectively.
The mean rT₃/T₃ value of 1.27 in a group of decompensated hepatic cirrhosis was markedly higher than that of 0.20 in normal subjects. In other groups of hepatic disorders, the mean rT₃/T₃ values were similar to normal value.
Correlative studies of thyroid hormon levels and liver function tests were carried out simultaneously in all cases with hepatic disorders. The rT₃/T₃ value was correlated with value of icterus index (r=0.372, P<0.01), alkaline phosphatase (r=0.367, P<0.01), LDH (r=0.315, P<0.01) LAP (r=0.273, P<0.05), ICG tolerance test (r=0.375, P<0.01), prothrombin-time (r=0.359, P<0.01), cholinesterase (r=-0.255, P<0.05), total protein (r=-0.347, P<0.01) and Albumin (r=-0.370, P<0.01).
These findings suggested that marked alterations of peripheral conversion of T₄ to T₃, rT₃ were recognized only in decompensated hepatic cirrhosis. The correlative results of rT₃/T₃ with liver function tests might suggest that rT₃/T₃ value would be an useful indicator for the severity of the hepatic damage of terminal stage.

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In order to clarify the origin from which increased serum GOT in chronic alcoholics derives, serum mitochondrial GOT (m-GOT) and other conventional serum enzyme activity was measured. Sixty percent of chronic alcoholics (n=63) showed elevated GOT levels, whereas GPT, γ-GTP, CPK and Al-Pase activity were increased in 43, 67, 7 and 51% respectively. M-GOT was separated by using DEAE Sephadex columnchromatography and measured by UV-assay system. M-GOT activity in healthy controls (n=15) was 1.8±o.6 U. (Mean±SEM), whereas cirrhotics (LC: 12.5±1.3U.), in 21 cases of chronic hepatitis (CH: 9.9±l.2U) and in 9 cases of acute hepatitis (AH: 25.4±4.2U.). Moreover, when m-GOT was expressed as m-GOT/GOT ratio in patients with total GOT values being more than 50 U., the increased m-GOT activity in chronic alcoholics became more striking, that is 19.3±2.3% in chronic alcoholics (n=21), 14.2±1.7% in LC (n=17), 12.2±2.0% in CH (n=13) and 5.3±1.0% in AH (n=9). In chronic alcoholics there were no significant correlations between the activity of m-GOT vs. CPK and m-GOT vs.γ-GTP respectively.
In the present study, we have shown that m-GOT/GOT ratio was higher in chronic alcoholics followed by LC, CH and AH. These results suggest that increased m-GOT activity in chronic alcoholics may reflect, at least in part, mitochondrial injury of hepatocytes by ethanol.

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By using the enzymatic method devised by Nagasaki and Akanuma, plasma lecithin-cholesterol acyltransferase (LCAT) activity was examined in 96 patients of hepatobiliary diseases. Plasma LCAT activity of 24 normal controls was 80.7±20.59 units (nmoles/ml/hr) and the activity was low especially in liver cirrhosis, liver cancer and malignant biliary tract obstruction. LCAT activity was less than 40 units in most of liver cirrhosis and more than that in the majority of chronic hepatitis, which seemed to enable the differentiation of both diseases possible by measuring LCAT activity alone. LCAT activity correlated well with serum choline esterase, albumin, R15ICG, bilirubin and alkaline phosphatase and could reflect the degree of hepatocellular impairment or biliary tract obstruction. In acute hepatitis, LCAT activity recovered with convalescence of clinical course and during the course, while LCAT activity showed progressive decrease in liver cancer. LCAT activity also correlated well with maximal osmotic fragility of erythrocytes, which suggested the close relation between the increment of cholesterol content of erythrocytes and impaired LCAT activity.

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Patients with hepatobiliary disease were fbund to have an increased urinary excretion or coproporphyrin.
Erythrocytes from the patients had an increase o. uroporphyrinogen-1-synthase activity, coproporphyrin contents and Heinz body formation which were correlated with urinary coproporphyrin excretion
These results suggest that secondary coproporphyrinuria in hepatobiliary diseases was at least partly due to an increased cOproporphyrin synthesis probably through hemolytic processes.

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Splenoportography was carried out in 121 patients in the past decade in our department and affiliated hospitals. Portograms of 13 subjects that were confirmed to have the primary hepatocellular carcinoma were retrospectively studied for the changes of portal veins. Portograms of 13 cases with hepatoma were able to be divided into four types, (1) Thrombus formation, (2) Displacement, (3) Mixture of (1) and (2), and (4) No changes. Of 13 cases, portal vein thrombi were demonstrated in 6 cases (46 per cent), and a lot of informations about the obliterative extent and status of collaterals caused by these thrombi were obtained. There were 4 cases which showed no changes (31 per cent). A diagnosis of hepatoma could not be made by means of splenoportography. In portograms, no portal branches in the space occupying lesions were demonstrated, and there was no changes in the portal vein shape which could suggest the infiltrative invasion of carcinoma.

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Two cases of lupoid hepatitis were reported which showed several different findings in clinical picture, hepatic histology and serological tests. One case was a mature female with an acute onset. She had Several abnormal findings on liver function tests with high titers of anti-nuclear antibody and anti-smooth muscle antibody. Her liver biopsy specimen showed a finding similar to the subacute hepatitis (Tisdale). Corticosteroid reduced promptly her symptoms and titers of the antibodies with improved liver functions. The second biopsy of liver showed a marked reduction of the inflammatory change.
The other case was a menopausal female with gradual onset. She had been suffering from rheumatoid arthritis fbr 10 years with high titer of rheumatoid factor and anti-nuclear antibody but without anti-smooth muscle antibody. Histological examination of her liver showed an infiItration of a large number of plasma cells. The treatment on corticosteroid improved her symptoms and liver function but did not reduce sufficientiy titers of anti-nuclear antibody and rheumatoid factor with elevated blood sedimentation rate. She developed Sjogren's syndrome one years later. The liver biopsy done at that moment showed still a moderate infiltration of the inflammatory cells into portal and sinusoidal areas.

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A case of Cruveilhiel-Baumgarten syndrome was presented with special reference to the serum bile acids as an indicator of portal-systemic shunt. Total serum bile acid concentration was enzymatically determined in the hepatic vein and other various sites of systemic vein by selective catheterization.
Serum bile acid concentration was lowest in the hepatic vein and elevated in the inferior and superior vena cava. The elevation of the serum bile acid concentration suggested the existence of portal-systemic shunt.
The presence of shunt in the elevated sites of serum bile acid concentration was confirmed by angiographical finding. This case is the first to utilize serum bile acid concentration for the detection of the portal-systemic connection site.

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A 70 year-old woman had a sudden onset of severe epigastrlc pain without any provoking cause during hospitalization because of hyperthyroidism. A fist-sized smooth tender mass was palpated in the epigastrium. By ultrasonography, hepatic scintigraphy, selective celiac arteriography and peritoneoscopy, solitary hepatic cyst was diagnosed. Liver function tests showed abnormal high levels of Al-P and LDH contrary to normal levels of serum bilirubin and transaminase. Echinococcal hepatic cyst was denied for the reason of negative data of serological test. The hepatic cyst measurlng about 10×9×6.5cm was excised by left lateral segmentectomy. The contents of the cyst were brownish-yellowish fluid whose sediment contained much red cells and blood coagula attached to the inner surface of the wall. The biochemical components of the fluid were almost same as that of the serum.
Microscopically, the wall of the cyst consisted of the thick collagen band, whose inner surface was partly a layer of collumnar epithelium with somewhat compressed brush border. There were hemorrhage and deposition of hemosiderin in the cystic wall.

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