Liver specimens, from rats with cirrhosis induced by long term administration of CCI₄ and from man with cirrhosis, were examined under scanning (SEM) and transmission (TEM) electron microscopies.
SEM revealed cirrhotic liver sinusoids, in man and rat, to become narrow by compression due to regenerated hepatocytes, hypertrophied Kupffer cell, and distend space of Disse with abundunt proliferated celluler components and collagen fibers. Furthermore, pores of the sinusoidal endothelium were partly reduced in number.
On the other hand, TEM disclosed a development of basement membrane within the space of Disse and the endothelial cell layer appeared to be continuous in part.
It could be concluded from these data that these changes represent the circulatory disadvantage to the hepatocytes, resulting in further hepatocellular injury in cirrhosis.

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Banti's disease, supposedly a disease entity in Japan, is characterized by presence of portal hypertension (splenomegaly and esophageal varices) and hypersplenism (anemia, leucopenia and thrombocytopenia). The etiology is unknown, and similar cases with portal hypertension and hypersplenism due to an apparent etiology (e.g. schistosomiasis and cirrhosis) are excluded. The underlying pathological features are either liver fibrosis or early cirrhosis (Miyake's B'). Pathogenesis of portal hypertension is thought to be narrowing and/or occlusion of terminal branches of portal veins (intrahepatic). In cases, however, those findings are not so conspicuous, and to the contrary markedly dilated vessels are remarkable findings. In this study, microscopic observation of these vessels on serial sections disclosed dilated abnormal inletvenules located at the periphery of Glisson's sheath which connect proliferated arterioles in Glisson's sheath and dilated sinusoids and central veins. We suspect this abnormal flow or shunt, apparently different from the normal hepatic vascular system, play an important role on pathogenesis of portal hypertension in Banti's disease.

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A new method was presented for morphometrical examination of the intrahepatic bile ducts designed upon a view that the hepatic arterial branches and the bile ducts run parallel in the portal tiad. The present experiment was carried out using the method to know the level and extent of the intrahepatic bile duct destruction in the livers of PBC. It was shown that in PBC livers (23 cases) the bile ducts with diameter below approximately 70-80 μ were destructed and the smaller the duct, the more the destruction. The destruction of intrahepatic bile ducts was neither so extensive in the 1st stage of PBC nor progressive in further stage of PBC, even in cirrhotic liver.
It was suggested that this marked destruction of intrahepatic bile duct (especially smaller bile ducts) might be an important factor for occurrence of chronic intrahepatic cholestasis and apparently progressive and fatal course of PBC.

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In the liver of male rats which were administered D-galactosamine-HCL (350mg/kg)for 4 weeks on alternate days, the focal necrosis in liver lobules, the proliferation of Kupffer cells as well as the periportal inflammation and ductular proliferation in portal tracts were prominent, but the periportal fibrosis was not recognized. Histochemical observations on the above liver tissues revealed that the increased activity of y-glutamyl transpeptidase (γ-GPT) was observed in the canalicular membrane of periportal parenchymal cells, in the epithelium of bile ducts and ductules, and in some inflammatory cells within periportal fields. The biochemical determination of the activity of γ-GPT in the plasma and in the hepatic tissue of rats demonstrated that it was significantly increased after D-glactosamine-HCl administration. In the histochemical study on biopsy specimens of patients with chronic hepatitis who showed an elevated serum γ-GPT activity, the localization of γ-GPT was found to be similar to that seen in the liver of rats which were administered D-galactosamine-HCl. From these findings, it is concluded that the serum γ-GTP activity in patients with chronic hepatitis probably reflects the degree of the inflammatory process in the liver.

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Impaired glucose tolerance were observed in patients with chronic hepatitis treated with glucocorticoid, but not observed in patients without liver disease receiving glucocorticoid.
Increment of insulin response to oral glucose were obsurved in patients with chronic hepatitis treated with glucocorticoid or not, liver cirrhosis, and patients without liver disease receiving glucocorticoid.
Either ΔIRI or Δglucose increased in patientswith chronic hepatitis and liver cirrhosis but ΔIRI in patients without liver disease receiving glucocorticoid, extremely elevated, and glucose level was same as control. In patients with chronic hepatitis treated with glucocorticoid decrement of ΔIRI and increment of glucose were observed.
The elevation of fasting FFA level were observed only in patients with liver cirrhosis.
The increment of triglyceraid level were observed in patients without liver disease receiving glucocorticoid.
These results indicate that there are hormonal disturbance and different mechanism of glucocorticoid effects in chronic liver disease.

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Quantitative determinations of serum alpha-fetoprotein (AFP) in 96 hepatoma patients have demonstrated three distinct patterns in the changes of AFP levels. In 50 patients weekly changes in serum AFP levels were more than about 10μg/ml or more (Group A). In the second group of 27 patients, a change of approximately 1000ng/ml in 3 to 4 months in AFP levels (Group B) was observed. The last group of 19 patients showed changes less than 200ng/ml in AFP levels throughout the course of the study (Group C). The survival time in Group A hepatoma patients was less than 6 months and from 6 to 18 months in Group B. Group C was composed of both, ones with long survival time from 24 to 40 months, and ones with short survival time less than 5 months. Histology revealed poorly differentiated cancer cells in Group A, moderately differentiated cells in Group B, and well differentiated cells as well as anaplastic cells in Group C.

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Two adult cases with hyperammonemia and recurrent episodes of disturbance of consciousness were reported.
Both cases were 23 year-old men. Physical and histological examination showed no apparent sign of chronic liver diseases. Laboratory examination revelaed high blood ammonia level and low blood urea nitrogen level. In electroencephalogram slow waves were dominant. Portal venography did not reveal a portal-systemic shunt. Ammonia tolerance test was abnormal and urinary excretion of urea decreased. Analysis of serum free amino acids in case 1 showed that citrulline slightly decreased and glutamic acid increased. In case 2 citrulline increased 10 time more than normla value.
These data strongly suggest that case 1 and 2 are belonged to inherited hyperammonemia probably through partial deficiency of ornithine carbamolytransferase and argininosuccinate synthetase respectively.

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An autopsy case of a 38-year-old male who had pathologically intrahepatic gallstones and severe atrophy of the left lobe of the liver after cholecystectomy and choledo-chojejunostomy 5 years before death was reported.
Histopathological study revealed that the obstruction and dilatation resulted from hepatolithiasis of the left biliary trees with coincident narrowing of the lumen of the left branch of the portal vein might be attributed to the significant atrophy of the left lobe of the liver.
Although it is still unknown why the stenosis and dilatation of the bile duct of the left lobe of the liver occurred, congenital anomaly of the biliary tree of the liver was suggested.

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