To see if UDP accelerates the metabolism of ethanol, Wistar female rats weighing about 200g were given UDP (100mg/kg b.w.) intragastrically prior to a single dose of ethanol (3g/kg b.w.) ingestion.
1) UDP pretreatment accelerated blood ethanol disappearance rate (Widmark's β60 value) by 64%.
2) The hepatic triglyceride concentrations 6 hours and 20 hours after ethanol administration increased by 260% and 290% respectively. When UDP was given prior to ethanol administration, these increases were only 180% and 130% respectively suggesting the lipotropic effect of UDP.
3) UDP pretreatment did not affect the activities of alcohol dehydrogenase and microsomal ethanol oxidizing system, and cytochrome P450 content in liver.
4) The ratio of lactate to pyruvate in liver 6 hours after ethanol did not differ from control. UDP pretreatment did not change the ratio either.
5) There were significant increases in hepatic ATP content and the size of adenylate pool by UDP pretreatment, while the adenylate energy charge was unchanged as compared with cthanol-fed and control groups. These data suggest that UDP may enhance ethanolmetabolism by stimulating ATP metabolism.

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Morphologic changes of perisinusoidal stellate cell (fatstoring cell) in the liver with various stages of hepatic fibrosis were studied electron-microscopically in 20 patients with chronic alcoholic liver injury: 5 patients with mild hepatic fibrosis (group I), 6 with moderate fibrosis (group II), and 9 with severe fibrosis (group III).
In the group I, the numbers of stellate cell were essentially normal and stellate cell had no significant changes in organelle. By contrast, stellate cell was increased in number and had well developed RER and large lipid droplets in the group II, especially where the cell had contacted with increased collagen fiber bundles. Similarly, the outstanding changes of stellate cell were observed in group III, particularly in the central zone of the parenchymal nodule. In the peripheral zone of the nodule, however, stellate cell contained no lipid droplets.
These findings suggest that stellate cell plays, at least in part, a role for fibrogenesis of alcoholic liver disease.

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We will report the role of phosphatidylcholine (PC) in lipoprotein-X (LP-X) formation. LP-X contents in the serum were positively correlated with serum phospholipid-tocholesterol ratio in obstructive jaundice.
Among serum phospholipids, mainly PC increased in obstructive jaundice. The substance, which was formed by adding PC liposome to serum, was almost identical with LP-X observed in obstructive jaundice.
When red blood cells (RBC) were incubated with PC-added serum, cholesterol of RBC was leached out to incorporate into the LP-X-like substance.
When the bile duct of rat was ligated, serum phospholipid concentration increased first, and then an elevation of serum cholesterol, a decrease in cholesterol of RBC and an appearance of LP-X took place simultaneously.
In PC-liposome-infused rat, serum cholesterol elevated and about 60% of elevated cholesterol were found in LP-X-like substance. Hepatic cholesterogenesis was also enhanced by the infusion of PC-liposome.
These results strongly suggest that the regurgitation of bile PC to serum is the initiating factor of LP-X formation and the cause of the enhanced hepatic cholesterogenesis in obstructive jaundice.

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Study was conducted to investigate abnormal metabolism of serotonin (5-hydroxytryptamine; 5-HT) in hepatic encephalopathy, with special regard to assessment of tryptophan (Trp) and 5-hydroxyindoleacetic acid (5-HIAA) levels in the cerebrospinal fluid (CSF) of patients with cirrhosis and fulminant hepatitis. In contrast to control subjects, Trp in CSF was increased significantly in cirrhosis with and without encephalopathy and fulminant hepatitis. 5-HIAA in CSF was increased significantly in cirrhosis with encephalopathy, but no significant increase was observed in cirrhosis without encephalopathy as compared with control. As compared with cirrhosis without encephalopathy, however, only Trp level was significantly elevated in CSF of cirrhosis with encephalopathy. Significant correlation between Trp and 5-HIAA in CSF was observed. During clinical course in two out of three patients with hepatic encephalopathy, both Trp and 5-HIAA levels changed in parallel to the development of encephalopathy.
Experimental study on acute ischemic hepatic failure in rats revealed that Trp and 5-HIAA levels were increased in almost all brain regions, but 5-HT levels were increased significantly only in midbrain, hypothalamus, medulla pons and striatum.
In conclusion, these results strongly suggest that brain serotonin metabolism is enhanced in patients with hepatic encephalopathy, being mediated through plasma amino acid imbalance.

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The sera of 41 cases of acute hepatitis A were examined serologically to detect the changes of antibody to HAV (anti-HAV) by both RIA (HAVAB) and IAHA methods. By IAHA method anti-HAV increases rapidly of 5 weeks after the onset of the disease.
Therefore it needs the paired sera to determine the increase of anti-HAV. However, this method has two ploblems as follow: the first; the diagnosis can be made only retrospectively. The second; it's difficult to detect anti-HAV without puried HA antigen adequitely. By RIA method anti-HAV can be detect positively at the beginning of the disease. Applied the phenomenon, i.e.; IgM fraction increases at the beginning and IgG fraction increase at the convalscent stage of acute infectious illness, to hepatitis A. The ratio, M-ratio index, between IgM fraction treated by 2-ME and not treated one make more reliable diagnosis of hepatitis A through one point serum check.
These results suggest that the paired sera treated with IgM fraction give more efficient diagnosis for patients with acute hepatitis A than one point serological examination.

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From seventy-one cases of post-transfusion hepatitis (PTH) recorded over seven years (1972 to 1978), it is observed that the incidence of Type B PTH has fallen off sharply while Type non-B PTH has gradually increased. Incubation periods of 40 to 120 days were noted in 9 cases of Type B PTH and 14 to 150 days in 61 cases of Type non-B. The differences suggest that at least two causative agents are involved in Type non-B PTH. Incidences of intial symptoms, jaundice and of remarkable SGPT elevation (greater than 1500IU/L) were statistically lower in Type non-B PTH than in Type B hepatitis. Biochemical recovery within 10 weeks from the onset, however, was much lower in Type non-B PTH (31%) than in Type B hepatitis (91%). Moreover, prolongation of more than 24 weeks of abnormal SGPT was found in 36% of the Type non-B PTH cases, and when observed only in non-icteric cases the prolongation rate was 57%. These findings suggest that non-icteric hepatitis was more prone to persist in Type non-B PTH.
Nine out of 10 liver biopsy specimens from patients, in whom abnormal SGPT persisted for more than 6 months, revealed chronic persistent hepatitis or chronic aggressive hepatitis. To resolve the problem of whether chronic non-B PTH develops cirrhosis of the liver and eventually produces hepatocellular carcinoma, long-term observations of many cases are needed.

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Plasma exchange therapy for hepatic coma in fulminant hepatitis was evaluated from our experiences of five patients. All the cases were fulminant type of post-transfusion hepatitis. Plasma exchanges were performed by using an intermittent or continuousflow centrifuge, and 2.4-3.2 liters of patient's plasma were exchanged with fresh frozen plasma in two to three hours in one exchange.
In two of the five patients (75 year-old male and 67 year-old female), in whom the procedure was started in Stage III coma, complete recovery was recognized, and symptoms and biochemical data were improved; one awakened after two exchanges and the other after three exchanges following one charcoal hemoperfusion. However, their jaundice increased gradually, and eventually they died from recurrence of hepatic failure added to a desperate complication, such as intra-abdominal abscess and renal insufficiency, respectively. In the remaining three patients, any responses were not recognized following plasma exchanges.
From the results, plasma exchanges were considered to have therapeutic effects almost equal to those of exchange transfusion for hepatic coma in fulminant hepatitis.

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It is known experimentally that glucagon and insulin have synergistically promotive effect of liver cell regeneration, which are called hepatotrophic factors in portal venous blood. On this basic assessment, we applied clinically glucagon and insulin infusion in the treatment of acute liver failure. 1 mg glucagon and 10 units regular insulin were dissolved in 500ml of 5% glucose solution and aromatic aminoacids-free aminoacid solution Was continuously administered.
Clinical assessment, blood chemistry, hepaplastin test, rapid turnover proteins, and alphafetoprotein were examined on admission, at the beginning and the end of this therapy. Among 15 patients of acute liver failure, 5 patients have been relieved and the other 2 patients have recovered from hepatic coma.
In the early diagnosis of acute liver failure, hepaplastin test and rapid turnover proteins were good parameters, while alpha-fetoprotein was valuable parameters of liver regeneration, so far.

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By the study of serum alkaline phosphatase (ALP) in liver diseases, it is well documented that intestinal ALP is increased in liver cirrhosis (LC) whereas in hepatocellular carcinoma (HC) hepatic ALP is increased appreciably. The present report describes the results of investigations which were performed to know how ALP isoenzymes change during development of HC from other liver diseases.
(1) Study of ALP isoenzymes with agar gel electrophoresis disclosed that intestinal ALP in 17.65% of 51 patients with acute hepatitis, in 15.78% of 38 paticnts with chronic inactive hepatitis, in 34.68% of 49 patients with chronic active hepatitis and 44.83% of 29 patients with LC (but without HC) whereas in 101 patients with HC it was detected only 14.55% in spite that all the patients had LC. Almost the same tendency was observed in bone ALP isoenzyme of serum of patients with those diseases. (2) Follow-up study showed that, in all of 10 patients with LC later developed HC, the activity of intestinal ALP as measured by polyacrylamide gel electrophoresis decreased progressively and hepatic ALP increased towards malignant change. In 6 cases, decrease of intestinal ALP was noted before alphafetoprotein became positive (higher than 400ng/ml).
The fact that intestinal and bone ALP decrease during development of HC is pathophysiologically interesting and it can be utilized for early diagnosis of HC although the mechanism is still unknown.

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Serum ferritin concentration in patients with hepatocellular carcinoma (HCC) and liver cirrhosis (LC) was measured by using radioimmunoassay.
Serum ferritin is elevated above the normal range (less than 200ng/ml) in 33 of 50 patients with HCC and 8 of 30 patiehts with LC. A mean value of 507.4±662.8 (S.D.) ng/ml in HCC was significantly higher than that of 151.8±142.3ng/ml in LC (p<0.01). No obvious correlation existed between serum ferritin and α-Fetoprotein (AFP) levels in HCC. However, it is noteworthy that elevated serum ferritin levels were observed in 85% of AFP low producing HCC (AFP less than 400ng/ml). In 70% of AFP low producing cases, serum ferritin levels were over 400ng/ml in contrast to 6.7% of LC. Serum ferritin levels were also found to be raised in 4 of 5 cases with minute hepatocellular carcinoma. Theses observations suggest that serum ferritin is a useful marker for HCC, particularly in AFP low producing cases.
On the other hand, serum ferritin levels did not correlated with HBsAg or the size of tumor.
Furthermore, changes of serum ferritin before and after hepatic resection or anticancer chemotherapy (one shot injection) in cases with HCC were discussed.

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Of 173 autopsy and operation cases of hepatocellular carcinoma (HCC) for the past 6 years from 1972 to 1977 at Kurume University Hospital, 25 cases of HCC without cirrhosis were seen and clinicopathological studies were carried out. Among HCCs with or without liver cirrhosis, there were many differences of age, sex, clinical course, cause of death, metastasis, frequency of intrahepatic tumor thrombus and serum HBsAg.
Serum HBsAg was positive in only 2 of the 21 cases (9.5%) of HCC without cirrhosis. On the other hand, it was positive in 45 of the 104 cases (43.3%) of HCC with cirrhosis.
In general, differentiation of the HCC tissue tended to parallel to the degree of fibrosis in non-cancerous area. In the cases with slight fibrosis, HCC showed poor differentiation. On the other hand, in the cases with dense fibrosis, HCC showed well differentiation.

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A man aged 26 with HBs·Ag positive liver cirrhosis suffered from acute type A hepatitis. There was sudden onset of fever, associated with increase in serum IgM concentration and appearance of atypical lymphocyte in peripheral blood in this patient. These symptoms are usually characteristic to acute type A hepatitis.
Infection on this patient with acute type A hepatitis was confirmed by serial detection of hepatitis A antibody.
It is interesting that titer of HBs·Ag in this patient transiently decreased by simultaneous infection of type A virus and returned to original level after recovery of type A hepatitis.

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Three cases of primary biliary cirrhosis were reported. Histopathologic proof of primary biliary cirrhosis was possible only by means of serial sections of surgical liver biopsy specimens. For the diagnosis of primary biliary cirrhosis needle biopsies had limited diagnostic value. Needle biopsy findings of each case were those of chronic active hepatitis, micronodular liver cirrhosis and intrahepatic obstructive jaundice, respectively. The patients were 29, 59 and 29 year old females. The most common presenting symptoms were chronic jaundice and itching. Serum bilirubin, alkaline phosphatase and cholesterol concentration were elevated. Hypergammaglobulinemia and increase of IgM were recorded. Antimitochondrial antibody were present. Findings of serial sections of wedge biopsies.-In case 1, damaged interlobular bile ducts were surrounded by lymphocytes and plasma cells. In Glisson's capsules the interlobular bile ducts were decreased or frequently absent. Case 2 showed the complete loss of interlobular bile ducts and septal bile ducts even in serial sections of wedge liver tissues. Lymphoid aggregates were found frequently in the Glisson's capsules. Also in case 3, the characteristic findings were the decrease or loss of interlobular bile ducts as well as septal bile ducts. A dense lymphocytic infiltration and granuloma of epithelioid cells and giant cells were seen around the damaged bile ducts.

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