[Histological studies on the livers with intrahepatic gallstones (author's transl)].
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Biomedical subjects
Publications and source records attributed to G Ohta.
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Statistical investigations indicate that disappearance of bile ducts, estimated by a histometric method, was more extensive in symptomatic than in asymptomatic patients with primary biliary cirrhosis. The extent and degree of intrahepatic bile duct disappearance in PBC is related to the degree of copper granule deposition in the hepatocytes, the degree of atypical ductular proliferations and the fibrous septa formation. Bile plug formation and chemically determined copper content are not so well related to the bile duct disappearance, while periportal lymphoid cell infiltration is not related to the degree or extent of bile duct disappearance at all.
A 72-year-old-man had severe portal hypertension, refractory ascites, and granulomatous liver disease involving the small tributaries of the hepatic and portal veins. Granulomatous lesions were found neither in the hepatic parenchyma nor in the other organs. The diminished lumina of the affected veins and periportal fibrosis that probably resulted from the granulomatous vascular lesions seem to cause portal hypertension and refractory ascites.
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The case of a 78-year-old man with the characteristic clinical and pathologico-anatomic pictures of the Cronkhite-Canada syndrome associated with sigmoid cancer is reported. He died ten months after the onset of his disease. Autopsy findings of the patient are described in detail. The other fifty three cases of the syndrome are reviewed, and clinical and pathologico-anatomic features of the Cronkhite-Canada syndrome are discussed.
The morphological characteristics of orcein positive granules in hepatocytes from 11 patients with chronic intrahepatic cholestasis and from 2 newborn normal livers were studied. Histochemical investigations revealed their protein nature and many sulphydryl and/or disulphide groups. Copper was demonstrated in the granules by histochemical techniques and electron X-ray micronalysis. No difference was observed in the hepatic distribution and appearance of the granules between the livers of those with chronic cholestasis and the newborn. Ultrastructurally, a variety of electron dense granules were seen at the site of orcein positive granules in the hepatocytes of the patient with primary biliary cirrhosis. Some had a single-layered membrane and seem to be lysosomal derivatives. It is suggested that the copper in lysosomes seen in both chronic cholestasis and normal newborn livers, need not to be cytotoxic.
An autopsy case of sarcoidosis with chronic intrahepatic cholestasis for 2 and a half years was presented. Generalized distribution of noncaseating epithelioid granulomas and positive Kveim test were consistent with sarcoidosis. Histological examination of the liver revealed extensive bile duct destruction similar to that seen in the liver of primary biliary cirrhosis. Destructive cholangitis found in the liver appeared to be responsible for long term intrahepatic cholestasis, and no sarcoid granulomas in the liver were found to destroy any bile duct. The possible relation in pathogenesis of the bile duct destruction between primary biliary cirrhosis and sarcoidosis was discussed.
Histometric examinations, based on the assumption that hepatic arterial branches and bile ducts run parallel within the portal tracts, suggest that in primary biliary cirrhosis bile ducts with a lumen (the smallest diameter between the subepithelial basal membranes) below 70--80 micron are destroyed. The smaller the ducts, the more they destroyed. Extensive destruction of the ducts was seen more frequently in the nonfibrotic stage of primary biliary cirrhosis than in later stages. Serial sections of the intrahepatic bile ducts in primary biliary cirrhosis revealed three types of periductal lesions preceding the disappearance of bile ducts: (A) periductal cellular reaction including features of chronic nonsuppurative destructive cholangitis, (B) periductal edema, and (C) periductal fibrosis. In the nonfibrotic stage, types A and C were frequent, whereas in the fibrotic stage types A and B were increased, and type C was predominant in the cirrhotic stage.
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Seventeen autopsy cases with occlusion of the circle of Willis were examined clinicopathologically. These patients ranged in age from 8 years to 64 years and consisted of 6 males and 11 females. The following results were obtained. 1. Fresh and massive intracerebral hemorrhage was confirmed in 13 of 17 patients and cerebral infarct in 4 of 17 patients. 2. Among these 13 patients, massive hemorrhage was found in basal ganglia, thalamus and hypothalamus of 9 patients, and in thalamus, cerebral peduncle and midbrain of 4 patients. 3. Rupture of the dilated muscular-type arteries was noted in the thalamus and basal ganglia in 2 of 13 patients. Ruptured arteries with organization of the lumen were found in the old hemorrhagic foci in one of them. 4. Overgrown and dilated arteries, branching off from the circle of Willis, were confirmed in 11 patients. These arteries consisted of "perforating" arteries well developed as collateral circulation. 5. No ruture in these arteries of the subarachnoidal spaces was found in 11 patients. In one of them, a small saccular aneurysm was found. These findings strongly suggest that in patients with occlusion of the circle of Willis intracerebral rupture of overgrown "perforating" arteries as collateral circulation may be the main cause of intracranial hemorrhage and intracerebral hemorrhage due to rupture of the arteries may be repeated.
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Microcytotoxicity assay revealed that peripheral bloof lymphocytes from patients with chronic active hepatitis were cytotoxic against cultured rat liver cells established by Coon in 1968. Non E-rosette forming cells were cytotoxic in 26 of 28 patients (93%) with chronic active hepatitis, whereas E-rosette forming cells were cytotoxic in only 1 of them. Either an addition of 10 microgram/well of aggregated IgG to non E-rosette forming cell culture or a preincubation of non E-rosette forming cells with 100 microgram/ml of aggregated IgG significantly reduced the cytotoxicity from 62.9 +/- 12.8% to 32.8 +/- 11.6% or to 25.6 +/- 11.3% (p less than 0.001). An addition of antihuman IgG/Fc also reduced the cytotoxicity to 37.4 +/- 17.2%. Significant cytotoxicity of positively selected EA-rosette forming cells was observed in 4 of 10 patients with chronic active hepatitis and that of positively selected EAC-rosette forming cells was demonstrated in 3, whereas in any of these patients neither non EA-rosette forming cells nor non EAC-rosette forming cells were cytotoxic. Cultured liver cells used in this study were seen to possess insoluble liver specific antigen on their surface membranes, but not soluble liver specific lipoprotein of Meyer zum Büschenfelde, by using an indirect immunofluorescence technique. These results suggested that effector cells are Fc-receptor-bearing cells and that the mechanism of the reaction may be mediated in an antibody-dependent cell-mediated reaction directed against insoluble liver specific membrane antigen(s) rather than soluble one.
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