Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We clinicopathologically studied 23 surgically resected cases of combined hepatocellular and cholangiocarcinoma (HCC-CC). The frequency of this cancer in our subjects, who had primary liver cancer and who underwent hepatectomy, was 6.3%. The mean age of patients was 64.0 years old and the male: female ratio was 1.9:1. Serum alpha-fetoprotein was positive in 70% of cases and its levels were relatively low (< or = 1000 ng/mL) in most cases. The positive rate of serum carcinoembryonic antigen was 18% and its levels were also low. In regard to hepatitis virus markers, 17% of the 20 combined HCC-CC cases were positive to HBs antigen and 70% were positive to the HCV antibody. Of the 23 combined HCC-CC cases, 9 cases (39%) were associated with liver cirrhosis. Tumours were classified macroscopically into a separated type (HCC and CC are clearly separated 17%), a HCC-predominant type (resembles HCC 49%), and a CC-predominant type (resembles CC 34%). The separated and HCC-predominant types were associated with liver cirrhosis in 50 and 55% of cases, respectively. These cases with liver cirrhosis presented the features of HCC more apparently, while those without liver cirrhosis presented the features of CC. Histologically, all cases were classified into either Type I (HCC and CC were clearly distinguished; 17%), Type II (HCC and CC were contiguous and shared transitional features; 66%), and Type III (cancer cells were able to be evaluated as either HCC or CC and were considered to be an intermediate type; 17%). Immunohistological stains for cytokeratin were useful to distinguish HCC and CC. Specifically, CC was positive to cytokeratin 7 and 19. The tumour, in which HCC and CC were almost indistinguishable, such as Type III), indicates the presence of intermediate tumour cells that can differentiate either to HCC or CC.
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PMID:A clinicopathological study on combined hepatocellular and cholangiocarcinoma. 887 74

Immunohistochemical study was carried out on D-galactosamine hydrochloride (GaIN)-induced subacute hepatitis in rats of JCL: Wistar-TGN (ARGHGEN) 1Nts strain (Mini rats), in which the expression of growth hormone gene is suppressed by the presence of an antisense transgene. Mini rats were given 1000 mg/kg of GaIN once a week for 4 consecutive weeks and killed at 1, 2, 3 and 4 weeks after the first administration. At 1 week after the first administration, proliferation of small epithelial cells positive for both alpha-fetoprotein and cytokeratin 7, i.e. so-called oval cells, was observed in the whole area of each hepatic lobule, and prominent deposition of fibronectin, laminin and type IV collagen was detected around these oval cells. Together with these extracellular matrix components, many activated Ito cells positive for both desmin and alpha-smooth muscle actin were observed. With time, most of the oval cells formed duct-like structures and lost their positive stainability for alpha-fetoprotein, and many Ito cells became inactive. Deposition of fibronectin decreased rapidly from 2 weeks after the first administration. At 4 weeks after the first administration, deposition of laminin was detected only around the duct-like structures, where that of type IV collagen was also still prominent. These results suggest that a large population of oval cells differentiated into bile duct epithelial cells and that Ito cells and extracellular matrix components might play a role in this process.
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PMID:Immunohistochemical study on galactosamine-induced subacute hepatitis in rats of JCL: Wistar-TGN (ARGHGEN) 1 Nts strain (Mini rats). 925 Apr 81

Histopathological and immunohistochemical studies were carried out on D-galactosamine (GalNAc)-induced acute hepatitis in rats of the JCI: Wistar TgN (ARGHGEN) 1 Nts strain (Mini rats), in which expression of the growth hormone gene is suppressed by an antisense transgene. Hepatitis characterized by hepatocellular acidophilic necrosis with inflammatory cell infiltration was most prominent at 2 days after GalNAc (1000 mg/kg)-injection, when proliferation of Ito cells and deposition of fibronectin and laminin were found along the sinusoidal linings. At 72 hours after GalNAc-injection, Ito cell proliferation with deposition of laminin and fibronectin became more prominent, and marked proliferation of small epithelial cells was observed in the periportal area. At 7 days after GalNAc-injection, quite a number of alpha-smooth muscle actin-positive Ito cells, surrounded by abundant fibronectin, laminin and type IV collagen, were still observed in close juxtaposition to rapidly proliferating small epithelial cells. The small epithelial cells were found to be positive for both alpha-fetoprotein and cytokeratin 7 and were therefore considered to be so-called oval cells. The results suggest that there may be some relation between oval cell proliferation, Ito cell activation and extracellular matrix accumulation in GalNAc-induced acute hepatitis in Mini rats.
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PMID:Prolonged oval cell proliferation with Ito cell activation and extracellular matrix accumulation in galactosamine-induced acute hepatitis in mini rats. 930 54

To characterize cellular responses during hepatic regeneration, we examined 13 explant livers and 5 liver allografts by immunohistochemistry for cytokeratin 7, HepPar1, CD68, alpha-smooth muscle actin (alpha-SMA) and proliferating cell nuclear antigen as well as reticulin and Masson-trichrome staining. Within a week after liver damage, elongated CD68-positive cells were detected along the border of necrotic area. The number of alpha-SMA-positive cells was slightly increased along the sinusoids. Ductular proliferation or fibrosis was negligible. After one or two weeks, the size and number of CD68-positive cells were markedly increased. alpha-SMA-positive cells increased in number within lobules and portal tracts. Ductular proliferation occurred predominantly at the limiting plate or along the border of necrotic areas. After one month, necrotic parenchyma was replaced by many ductules, CD68-positive cells, alpha-SMA-positive cells. Nodules of regenerating hepatocytes and irregular fibrosis were diffusely present. Other nonparenchymal cells were not significantly changed. These observations indicate that chronological interaction between nonparenchymal and parenchymal cells occur during the course of human hepatic regeneration and suggest extensive porto-periportal fibrosis more than a few months after the onset of fulminant hepatitis is a major indicator of chronic functional impairment necessitating liver transplantation.
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PMID:Parenchymal and nonparenchymal cellular responses in human hepatic regeneration. 1151 89

We studied nondiagnostic liver biopsy specimens from 20 patients with definite primary biliary cirrhosis (PBC) and 18 with definite autoimmune hepatitis (AIH) to identify distinguishing features. All patients had early-stage disease; biopsy specimens were devoid of granulomas or diagnostic features of PBC or AIH. Diagnoses were based on serologic and clinical variables. Sixteen specimens from each group were immunostained with cytokeratin 7. The density of portal tract eosinophils and number with cytokeratin 7-reactive periportal hepatocytes were quantified. Sixteen of 18 patients with AIH and 13 of 20 with PBC had no or minimal bile duct injury. Histologic activity index scores were 5.8 in AIH and 5.7 in PBC. The mean portal eosinophil score was greater in PBC than in AIH. Cytokeratin 7 identified many central bile ducts that were obscured by portal inflammation. The mean periportal cytokeratin 7-reactive hepatocyte score was greater in PBC than in AIH. Portal eosinophils and cytokeratin 7 reactivity in periportal hepatocytes are supportive of PBC rather than AIH. No morphologic features were supportive of AIH. Cytokeratin 7 reactivity in periportal hepatocytes may be an early response to PBC-induced biliary obstruction in other regions of the liver.
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PMID:Portal tract eosinophils and hepatocyte cytokeratin 7 immunoreactivity helps distinguish early-stage, mildly active primary biliary cirrhosis and autoimmune hepatitis. 1176 73

We report a surgical case of liver tumor, 40 x 35 mm in size, with squamous cell carcinoma (SCC) and hepatocellular carcinoma (HCC) components in a 60-year-old Japanese man with steatohepatitis. Most of the SCC component showed typical intercellular bridge and keratinization, while most of the HCC components showed a thick trabecular pattern with mild to moderate nuclear atypia. Both components transit each other without undifferentiated foci; however, a small foci showing glandular structure was intermediated. No cyst formation was found in the liver. The primary site of the squamous cell carcinoma was not detected in general clinical and radiological examination. Immunohistochemical analysis revealed that part of the HCC components neighboring the SCC showed patchy and weak expression of cytokeratin 7. There are several possibilities for the origin of squamous cell carcinoma in this case: marked squamous metaplastic change of cholangiocarcinoma and/or HCC, and carcinoma originating from pleuripotential stem cells. Irregular fatty changes, scattered giant mitochondria and acellular fibrosis with bridging were seen in the liver; however, this patient had no episode of hepatitis-associated viral infection. This is an interesting case of combined hepatocellular and cholangiocarcinoma with marked SCC components arising in a non-cirrhotic fibrotic liver.
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PMID:Combined hepatocellular and cholangiocarcinoma with marked squamous cell carcinoma components arising in non-cirrhotic liver. 1258 36

During fibrosis, the extracellular matrix (ECM) is continuously remodeled and increases in volume due to the production of various proteins. We studied the distribution of tenascin-C (TN-C) and the correlation of TN-C with the necro-inflammatory activity and expression of alpha-smooth muscle actin (alpha-SMA), cytokeratin 7 (CK7), and CD3+ T-lymphocytes in canine chronic hepatitis. This was analyzed using immunohistochemistry and semiquantitative scoring. We used 3 groups (n = 19) of dogs: group 1 (n = 5) with neonatal hepatitis/lobular dissecting hepatitis (NH/LDH), group 2 (n = 8) with chronic hepatitis/cirrhosis (CH/CIRR), and group 3 (n = 6) consisting of healthy animals. In normal livers, TN-C was localized in Disse's space and around bile ducts and blood vessels. In CH/CIRR livers, TN-C was localized at the periphery of the regenerating nodules and was conspicuous in the bridging fibrous bands. In NH/LDH, TN-C was diffusely distributed along the reticular fibers that dissected between single cells or groups of hepatocytes. alpha-SMA in the normal hepatic parenchyma showed an irregular distribution along the perisinusoidal linings. In other groups, alpha-SMA was increased in fibrotic septa and perisinusoidal linings. In normal livers, CK7 was positive in bile ducts. In other groups, CK7-expressing cells were conspicuous in the portal-parenchymal interface, the periphery of the regenerative nodules, and the degenerated parenchyma. The pattern of CD3+ lymphocytes was inversely proportional to that of TN-C. These results also showed that TN-C is strongly correlated with increased fibrotic stage, inflammatory activity, and expression of CK7 and alpha-SMA. TN-C, CK7, and CD3 expression did not differ between diagnostic groups.
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PMID:Tenascin-C in chronic canine hepatitis: immunohistochemical localization and correlation with necro-inflammatory activity, fibrotic stage, and expression of alpha-smooth muscle actin, cytokeratin 7, and CD3+ cells. 1803 93

We present a case of a 7-year-old boy who had cholestasis after trimethoprim-sulfamethoxazole combination therapy. Liver biopsy was performed 36 days after the onset of jaundice because of no evidence of improving cholestasis. Liver histology revealed portal inflammation, bile plug, and biliary stasis around the central vein with the loss of the interlobular bile ducts. Immunohistochemical stains for cytokeratin 7 and 19 were negative. These findings were consistent with those of vanishing bile duct syndrome (VBDS). Chlestasis was progressively improved with dose increment of urosodeoxycholic acid from conventional to high dose. This is the first case report of trimethoprime-sulfamethoxazole associated VBDS in Korean children. The case suggests that differential diagnosis of VBDS should be considered in case of progressive cholestatic hepatitis with elevation of alkaline phosphatase and gamma-glutamyl transpeptidase after or during taking medicine to treat nonhepatobiliary diseases illness.
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PMID:Urosodeoxycholic Acid Therapy in a Child with Trimethoprim-Sulfamethoxazole-induced Vanishing Bile Duct Syndrome. 2451 25