Sclerosing hepatic carcinoma (SHC) is composed of slender cords or small nests of tumor cells with peripheral palisading, and abundant intervening sclerosis. The tumor seems to have the histologic features of both hepatocellular carcinoma (HCC) and cholangiocarcinoma. To evaluate the phenotypic expression of SHC and to investigate its cellular origin, immunohistochemical studies on three cases of SHC were performed. In all cases, the tumor cells showed positive staining for cytokeratins AE1, AE3 and 19, carcinoembryonic antigen (CEA) and epithelial membrane antigen (EMA). The expressions of cytokeratins AE1 and 19 were stronger in the palisading cells than the interior of the cords and nests. Conversely, CEA and EMA were expressed mainly in the inner portion. Alpha-fetoprotein was expressed in only one case, mainly in the palisading cells. In summary, SHC has the histological as well as the immunohistochemical profiles intermediate between HCC and cholangiocarcinoma, and the immunohistochemical profile suggests that SHC arises from primitive hepatoblast with a tendency of differentiation to the bile duct epithelium.
Carcinoma, Hepatocellular

Transforming growth factor-beta (TGF-beta) plays an important role in hepatic fibrogenesis. It is thought to inhibit regeneration of the hepatocytes. The aim of this present study was to clarify the correlation of TGF-beta, collagen type III (PIIINP) and the regenerating activity of hepatocytes, and the effect of prostaglandin E2 (PgE2) on them in acute liver injury. Two hundred and sixteen male Sprague-Dawley rats, weighing 200g on average, were divided into six experimental groups and two control groups; group I-CCl4 only administration, group II-partial hepatectomy(PH) only, group III-PH following CCl4 administration, group IV-olive oil only administration, group V-sham operation, group VI-CCl4 administration with pretreatment of PgE2, group VII- PH with pretreatment of PgE2, and group VIII- PH following CCl4 administration with pretreatment of PgE2. Five rats were sacrificed at 12, 24, 36, 48, 96 and 168 hours after the administration of CCl4 or PH in each experimental group. The liver was tested with immunohistochemical stain for proliferating cell nuclear antigen (PCNA) and in situ hybridization for TGF-beta. Radioimmunoassay for serum PIIINP was also performed. The results were as follows: TGF-beta was expressed mainly in the perisinusoidal cells and periportal mesenchymal cells. The TGF-beta positive cells were most numerous in the combined group of CCl4 plus PH. TGF-beta expression tended to have an inverse relation, with the PCNA index in all experimental groups. The PCNA index was highest in the CCl4 only group and lowest in the combined group of CCl4 plus PH. The PH only group showed a peak PCNA index at 48 hours. In the CCl4 only group and the combined group of CCl4 plus PH, serum PIIINP appeared to increase at 12 hours or more after the expression of hepatic TGF-beta. Pretreatment of PgE2 revealed that TGF-beta precipitously disappeared at 48-96 hours after insult. PgE2 influenced the vanishing period, not the emerging time of TGF-beta and had a remarkable effect on the amount of TGF-beta especially in the PH following CCl4 administration group, which resulted in significant accentuation of PCNA indices. In conclusion, PH of the prior injured liver induces a marked increase of TGF-beta followed by a significant suppression of regeneration of the remaining liver, and PgE2 overtly suppresses the expression of TGF-beta.
Male ; Humans ; Rats ; Animals

A case of hepatic fascioliasis misdiagnosed as metastatic carcinoma was reported. The patient was a 22-year-old woman who had had rectal adenocarcinoma (Duke stage C2), and had been treated by Mile'operation 8 months ago. A computed tomogram(CT) demonstrated multiple low density nodules in the liver suggesting a metastatic tumor. A partial liver lobectomy was performed. The resected liver showed multiple necrotic nodules, which appeared to be abscesses containing eggs of the Fasciola species. Parasitic infection should be considered as one of the possible etiologies of hepatic nodules which mimic metastatic carcinoma either clinically or radiologically.
Female ; Humans ; Adenocarcinoma ; Neoplasm Metastasis

Primary cystic neoplasia of the liver is rare. We report a cystadenoma with mesenchymal stroma (CMS) and a cystadenocarcinoma, and make a review of literature with particular reference to their histogenesis. The CMS has many similarities to the ovarian mucinous cystadenoma; occurring almost exlusively in female, being lined by mucus-secreting epithelial cells, and containing dense ovarian-like stroma. These features suggest that CMS may arise from the ectopic ovarian tissue within the liver. Cystadenocarcinoma may have its origin in CMS or cystadenoma without mesenchymal stroma of CMS. Cholangiocarcinoma arising from the congenital hepatic cysts can be differentiated only when it contains benign epithelia.
Female ; Humans ; Cysts

We reported a case of Wilson's disease, which was histologically confirmed by liver biopsy in a 15 year-old boy and made a comprehensive analysis on the sum of 22 cases reported in Korean literature. Although Wilson's disease is still rare, it should be included in the differential diagnosis of chronic liver diseases particularly in children of 5 to 15 years old. For the clinical diagnosis of Wilson's disease, changes in serum ceruloplasmin, plasma copper and urine copper values are most important as well as Kayser-Fleischer ring and family hestory. The serum level of GOT, when elevated, were always higher than GPT. This atypical transaminase profile may be a clue for diagnosis of hepatic diseases by a metabolic derangement. Among various histologic changes of the liver in Wilson's disease, what have diagnostic importance are anisonucleosis, nuclear glycogenosis and Mallory body, all of which may appear in any stages of the disease. In 3 cases only neurologic symptoms such as dysarthria and athetosis were found. Hemolytic anemia was another rare complication.
Child ; Male ; Female ; Humans ; Diagnosis, Differential ; Biopsy

This is a case report of idiopathic intestinal lymphangiectasia occurring in a 3-year-old boy. Idiopathic intestinal lymphangiectasia is believed to be a part of the generalized congenital disorder of lymphatic system. The present case revealed markedly ectatic lymphatics in the lamina propria of duodenal villi with lymphorrhagia. Clinical features were typical of the protein-losing enteropathy; hypoalbuminemia, hypocalcemia, chylous ascites, edema of the lower extremities and mild lymphocytopenia. This case indicates that serious protein loss may ensue, even in cases of intestinal lymphangiectasia without abnormalities of extraintestinal lymphatics.

No abstract available.
Epinephrine* ; Facial Nerve* ; Paralysis* ; Rabbits*

No abstract available.
Evoked Potentials, Auditory, Brain Stem* ; Rabbits*

Retroperitoneum is often the site of occurrence of schwannoma, but reports on schwanoma of the adrenal gland is exceptional and only 4 cases have been documented in the literature. This report is to add one such case occurred in a 53 year-old male who had anorexia, nausea and indigestion for one month. Whole body bone scan and abdominal CT scan revealed a 10 cm sized solid mass at upper pole of the left kidney. Under the impression of renal cell carcinoma, an operation was performed. The tumor was well encapsulated and appeared not to involve the kidney. The cut surfaces were light yellow and seemed to be composed of several hard lobules with areas of mucoid, cystic and calcific changes. No adrenal gland was identified grossly. But microscopically, the tumor was found to be partly surrounded by a small portion of adrenal cortical tissue. Histologically the tumor was a typical schwannoma with Verocay bodies, although modified in some extents by mucoid degeneration, cystic change, hyaline change and focal calcification. It is worthwhile to remember that the retroperitoneal schwannoma commonly had a huge size, sometimes involving the adjacent structures.
Male ; Humans

To elucidate the effect of copper on the 3'-methyl-4-dimethylaminoazobenzene(3'-MeDAB) induced hepatic carcinogenesis, Sprague-Dawley rats were divided into 4 groups according to 3'-MeDAB and copper administration: I. noraml control, II. copper only, III. 3'-MeDAB only, IV. 3'-MeDAB plus copper. The animals of groups III and IV were fed experimental diet containing 0.06% 3'-MeDAB. Copper was administrated intraperitoneally in a dose of 0.5 mg, twice a weak. Animals were sacrificed at different intervals. Liver weight, hepatic copper content and gross and microscopical changes of the liver were examined and the cell kinetics of various lesions in the hepatic carcinogenesis was studied by applying the immunohistochemical method for bromodeoxyuridine(BrdU). The hepatic copper content was significantly increased in animals given copper but returned to the normal value after cessation of adminstration. 3'-MeDAB administration caused oval cell proliferation and produced hyperplastic nodules, cholangiofibrosis and carcinoma of the liver. Simultaneous administration of copper did not alter the incidence of 3'-MeDAB induced lesions, except for carcinoma. The liver weight and the size of hepatic nodules and masses were smaller in group IV than in group III. The liver weight as well as the nodularity and the mass formation continued to increase affect cessation of 3'-MeDAB administration. Copper did not affect the BrdU labelling indices of the hepatic lesions induced by 3'-MeDAB. The oval cell proliferation and the BrdU labelling indices of the oval cell and the hyperplastic nodule were decreased, but the incidence of cholangiofibrosis and its BrdU labelling index were still elevated after cessation of 3'MeDAB administration. These findings indicate that copper could delay the developement of 3'-MeDAB induced hepatic lesions, but not suppress, since copper does not stay long enough to accumulate in the rat liver, and that copper could not affect the proliferation of 3'-MeDAB induced hepatic lesions once developed.
Rats ; Animals ; Incidence